Endotoxing Cancer

If you read the science, you’ll see that bacterial endotoxin (LPS) has been shown to promote the growth and spread of cancer. But only when it comes to leukemia, melanoma, lymph node metastasis, oral squamous cell carcinoma, lung, breast, pancreatic, colorectal, liver, gastric, gallbladder, esophageal, cervical, bone and prostate cancer.

Truth is, all cancers likely get a boost, one way or another, from endotoxin, and though you might not know it, this is good news. Maybe not the be all end all solution to every disease problem, but it means more than most realize. Endotoxin exposure is an important part of the puzzle regarding the progression of metabolic illness, and an awareness of it can open the way to better understanding of what leads to cancer, and what helps prevent or treat it.

I’m not a doctor, and this article is not intended as advice for the treatment of cancer, or disease of any kind. I’m also not suggesting that all you need to do is deal with endotoxin, and just like that, cancer is solved. But when you look at the vast amounts of high quality biological evidence relating to the subject of bacterial endotoxin (lipopolysaccharide/LPS) and cancer, it makes you wonder why people don’t know about it, and that includes many health professionals.

If I were to say to you that stress causes cancer, or that chronic low level inflammation is a powerful driver of cancer spread, you probably wouldn’t blink an eyelid. But mention lipopolysaccharides in conversation, and people start to look at you like you’re speaking Greek or Latin, or a combination of both. (Ok, you are, but you know what I mean.)

You see, there’s a powerful relationship between bacterial endotoxin issues, stress, and the stimulation of chronic inflammation and metabolic dysfunction, and all these things have been shown to be directly involved in the development and metastasis of cancer, as well as inflammatory disease in general. And this makes a lot of sense when you examine it more closely. And making sense of cancer seems like a worthwhile objective.

“…low levels of circulating Gram-negative bacterial endotoxin lipopolysaccharide (LPS) appear to be one of the key culprits in provoking a non-resolving low-grade inflammation…low-grade endotoxemia may skew host immune environment into a mild non-resolving pro-inflammatory state, which eventually leads to the pathogenesis and progression of inflammatory diseases…”

“Inflammation is a potent promoter of tumor metastasis…Lipopolysaccharide (LPS) is a major structural component of the outer membrane of Gram-negative bacteria and is a potent inducer of inflammation through the production of various cytokines, growth factors and inflammatory mediators…LPS promoted lung metastasis of breast cancer…”

The mediators of inflammation, toll-like receptor (TLR) proteins, nuclear factor-kappa B (NF-κB) transcription factor proteins, tumor necrosis factor-α (TNF-α), interleukins and other cytokines and inflammatory things, play a role in the metabolic response to bacteria and bacterial toxins (such as endotoxin), and have been shown to be involved in cancer development and progression.

“TLRs, a family of pattern recognition receptors, have been shown to be closely related to cancer progression…In our study, it seems that treatment of LPS, a ligand of TLR4, increased TLR4 expression, thereby promoting MCF7 breast cancer cell migration or invasion.

“…NF-kappaB is one of the key factors connecting inflammation with cancer progression….lipopolysaccharide (LPS) promotes NF-kappaB activation in colon cancer cells and pancreatic cancer cells…Blockade of TLR4…decreased the LPS-dependent increased invasive ability…results suggest…TLR/NF-kappaB signaling pathway plays a significant role in connecting inflammation and cancer invasion and progression.”

“Chronic inflammation is a well-documented risk for carcinogenesis, particularly in the pancreas and gastrointestinal tract…LPS…induces…cells to produce proinflammatory cytokines, such as tumor necrosis factor (TNF), interleukins, inducible nitric oxide synthase, and cyclooxygenase-2…”

Although there’s probably an endless number of ways that the inflammatory substances can interact with and promote each other (and knowing all of these ways would probably be useful), what I am most interested in is the overall picture.

The inflammatory process can have a protective role, but nobody is suggesting (I don’t think) that chronic inflammation is something to strive for, and much can be gained from a general understanding of things (like endotoxin) that can connect stress, metabolic energy system suppression and inflammation, with cancer development.

The thing is, you can’t really talk about stress, inflammation and metabolic disease, without talking about bacterial endotoxin issues, and you can’t talk about excessive endotoxin exposure, without also talking about the inflammatory stress substances like serotonin, estrogen, nitric oxide (NO), histamine and lactate. 

Rising levels of these and other related things are involved in the promotion of what has been referred to as the cancer metabolism, and they have a tendency to rise in response to ongoing stress, thyroid suppression and inflammation, as well as being able to promote inflammation and biochemical stress. It can be a bit of a circular problem.

When stress is high and blood sugar supplies run low, metabolic energy system function is interfered with in a manner which can promote bacterial excess, and which can eventually lead to rising systemic circulation of endotoxin. Endotoxin is itself directly inflammatory, as well as being able to interfere with cellular energy metabolism, increasing many of the inflammatory stress substances which have been shown to encourage cancer.

“Gram-negative bacteria significantly promoted lung cancer development including growth and metastasis in dose dependent manner. Mechanistically, Gram-negative bacteria activate TLR4 and TLR9 signaling and enhance lipid synthesis in human lung cancer cells.”

“TLR4 and the intestinal microbiota were…required for…HCC promotion, mediating increased proliferation…and prevention of apoptosis…the intestinal microbiota and TLR4 represent therapeutic targets for HCC prevention in advanced liver disease.”

“TLR4 protein was increased in ESCC [esophageal squamous cell carcinoma] tumor tissues compared with the adjacent normal tissues. TLR4 over-expression was significantly correlated with tumor differentiation grade, lymph node metastasis, and UICC stage. LPS-induced activation of TLR4 signaling promoted cancer cell proliferation, increased production of proinflammatory or immunosuppressive cytokines TNF-α, TGF-β and inhibited the anti-inflammatory cytokine IL-10.”

A suppressed thyroid metabolism is likely to promote cortisol and adrenaline release, as well as increased levels of estrogen, serotonin, NO, lactate, histamine, and greater circulation of polyunsaturated free fatty acids, encouraging the potential for systemic inflammatory issues. Subclinical hypothyroidism can activate TLR4 and can increase levels of NF-κB, TNF-α, IL-6 and IL-1β. All of these things promote inflammation and can further interfere with metabolism, creating even more opportunity for bacteria to feed and multiply, and for endotoxin to circulate through to the main system. All have been shown to be connected to cancer development.

As silly as it would be to argue that energy system suppression and unresolved low level inflammation is something to aim for, many of the substances of stress still get interpreted in a positive light. But don’t ignore science showing how rising levels of things like NO, serotonin, estrogen, lactate and the polyunsaturated fats (PUFAs) are involved with the progression of cancer and disease. And don’t ignore how all of this ties in with bacterial issues, and other things like the various cytokines that also promote inflammatory conditions like cancer.

“Chronic inflammation is a key contributor to carcinogenesis in various organs including the stomach, colon, lung and liver. Given the relationship between inflammation and carcinogenesis, recent studies have addressed the role of TLRs in inflammation-associated carcinogenesis in various cancers including GC [gastric cancer]…Our results described the involvement of TLR4 signaling in promoting tumor development by showing that LPS can significantly induce human GC cells to proliferate.”

“The link between systemic inflammation and promotion of tumor metastasis is well established…IL-6 contributes to lung and breast cancer cell malignancy and effusion…LPS promotes…up-regulation…of IL-6…in a dose-dependent manner…human breast cancer cells showed significant biological changes after LPS stimulation…and a tendency that TLR4 overexpression in tumor tissue was related with lymph node metastasis…TLR4 played a significant role in breast cancer metastasis…”

LPS (endotoxin) itself, through activation of toll-like receptor 4 (TLR4), activates multiple cells to release proinflammatory cytokines (cell signaling proteins), including TNF-alpha, interleukin (IL)-1β, and IL-6 (mostly from monocytes and macrophages). Endotoxin promotes NO (nitric oxide), which also encourages TNF-alpha, a powerful regulator of immune response. TNF production dysregulation has been implicated in inflammatory disease including cancer.

“Proinflammatory cytokines and growth factors such as IL-6…have been established as important NO-induced biomarkers that are up-regulated in breast cancer…and correlate with poor prognosis…NO also induced TNFα…reports have shown elevated levels of TNFα in cancer patients… The ability of NO…to regulate different cytokines…elucidates their crosstalk in the promotion of tumor growth and metastasis…the participation of inflammatory factors such as TNFα and other cytokines…can have a major effect on survival.”

“Activation of TLR triggers a cascade of intracellular events, including innate immune responses through NF-κB–dependent and interferon regulating factor (IRF)-dependent signaling pathways. This is known to recruit and activate leukocytes to sites…melanoma cells responding to TLR activation cause innate immune responses that may set the stage for an active inflammatory state favoring tumor promotion and suppression of host-specific immunity…TLR ligand activation in melanoma cells induced migration.”

LPS (endotoxin) and NO (nitric oxide) promote activation of NF-κB, and NF-κB has been suggested to act like an “on signal” for the catabolic proinflammatory cytokines and growth factors. Interaction between bacteria and immune cells (neutrophils), can also increase the release of inflammatory cytokines, promoting tumor growth. LPS instigated NF-κB activation can stimulate tumor progression by promoting increased resistance to apoptosis as well as contributing to angiogenesis in tumors.

“Triggering of TLR4 by LPS induced tumor promotion by the induction of proliferation, activation of NF-κB…accompanied by the increased production of proinflammatory cytokines…”

“LPS or endotoxin…may have a direct effect on tumor progression by promoting tumor cell adhesion and invasion. This effect is mediated by LPS-induced…activation of NF-κB…neutralization of LPS and modulation of NF-κB may be considered therapeutic strategies for the prevention of tumor relapse and metastasis…”

“…exposure to lipopolysaccharide (LPS) is associated with accelerated metastatic colorectal tumour growth. LPS directly affects cells through Toll-like receptor 4 (TLR-4) and the transcription factor NF-kappaB…”

“The induction of angiogenesis by LPS has been…shown…LPS might have noticeable effect in leukemia progression through stimulation of pathologic angiogenesis…avoidance/treatment of bacterial infections especially their LPS could be essential in management of tumors such as leukemia in which pathologic angiogenesis has played considerable role.”

Stress and inflammation also increase estrogen levels, and estrogen is known to promote cancer. Estrogen increases NO and enhances TLR4 activation and the dangerous effects of endotoxin, as well as the production of inflammatory mediators and cytokines, including IL-1beta, IL-6, and TNF-alpha. Progesterone is likely to be protective.

“…chronic E2 administration…increased both cytokine (IL-1beta, IL-6, and TNF-alpha) and inducible NO synthase…The proinflammatory action of E2 was also evidenced at the level of released IL-1beta and IL-6 by ex vivo LPS-activated macrophages…estrogens…enhance…ability to produce inflammatory mediators and cytokines upon subsequent TLR activation.”

Endotoxin (and other TLR4 agonists) help to shift cellular metabolism in the direction of aerobic glycolysis seen in cancer (much like Warburg metabolism), increasing lactate production.

Lactate has been shown to play an important role in the promotion of inflammation and cancer development, as well as in the activation of TLR4 and stimulation of the effects of endotoxin on cytokine expression and other inflammatory mediators, including prostaglandins and polyunsaturated free fatty acids, as well as nitric oxide and hypoxia inducible factor.

PUFAs interfere with oxidative metabolism, promoting lactic acid production and exacerbating the negative impact of endotoxin circulation, further increasing cancer progression. Sugar helps to reduce exposure to PUFAs, endotoxin and lactate, and is generally protective against stress, inflammation and metabolic suppression, and hence cancer.

“…bacterial infection and LPS increase lactate production…and lactate boosted LPS signaling-mediated inflammatory gene expression as shown by the present study. These findings…reveal a molecular mechanism by which the actions of LPS and lactate lead to a vicious cycle that promotes TLR4-mediated inflammation and contributes to a number of diseases…”

“Lactate is not only consumed by tumor cells for their survival, but it also stimulates angiogenesis…lactate has an immunosuppressive role, affecting several immune cell functions such as T-cell proliferation, cytokine production, and cytotoxic activity…lactate is needed not only for survival but also for promoting tumor growth…”

“Uncontrolled growth of cervical cancer cells is closely related to the excessive activation of…transcription factor, hypoxia-inducible factor-1α (HIF-1α)…TLR4 signaling pathway is positively correlated with high expression of HIF-1α….TLR4/iNOS pathway is highly expressed in cervical cancer…NF-κB…downstream of TLR4 signaling…promoted the production of the immunosuppressive cytokines…which promoted the growth of…cells and enhanced their resistance to apoptosis…”

But all you probably need to know, for starters, is that the inflammatory things all tie in together, and one of the important changes that can significantly increase protection from the cancer promoting impact of stress and metabolic suppression, is a reduction in exposure to the harmful effects of endotoxin. Dealing with digestion issues to improve cancer prognosis, is far from being a new idea.

These days, most people are probably aware of the fact that chronic inflammation helps drive cancer, but that’s often as far as it goes. The information that comes after that tends to not be very helpful, to say the least, and is rarely understood in a legitimately holistic manner.

“Recent evidence demonstrated an enhanced metastasis of non-small cell lung cancer (NSCLC) cells induced by lipopolysaccharide (LPS) stimulation, which reflected an important role of inflammation in tumor progression…We found that LPS stimulation of NSCLC cells facilitates their metastasis…”

“Monocytes are the major inflammatory cells that infiltrate most solid tumors in humans…infiltrating monocytes…play a significant role in altering the tumor to become more aggressive…exposure to lipopolysaccharide (LPS) was suggested to promote cancer cell adhesion to monocytes…LPS…is specifically recognized by TLR4. LPS-mediated signaling has been shown to play an important role in regulating cancer progression…”

Endotoxin is connected one way or another, to the inflammatory things that suppress proper metabolic function, and promote oxidative stress, aerobic glycolysis, hypoxia, and cancer risk. That includes NO, serotonin, estrogen, lactic acid, the inflammatory cytokines and growth factors, and PUFA breakdown products.

There are a number of simple things that have been shown to be be preventative and curative, and one way or another they involve improving metabolism, lowering stress, assisting with digestive function, intestinal barrier function, liver performance, and as such, reducing exposure to endotoxin and other inflammation promoting things such as the PUFAs. You don’t need to be a biologist to benefit from this kind of information, and you don’t need to know all of it to get results.

The beauty of approaches that effectively reduce bacterial endotoxin issues is that they have a natural tendency to also improve thyroid energy metabolism and inflammation issues, lowering overall stress and susceptibility to inflammatory disease, including cancer.

“Robust evidence supports a strong link between inflammation and cancer, including HCC [liver cancer]…TLR4 activation by LPS and other pathogen‐associated molecular patterns (PAMPs) induces NF‐κB signaling and subsequent secretion of several cytokines (e.g., interleukin‐1) and other inflammatory molecules (e.g., tumor necrosis factor α), which regulate multiple reactions in hepatocytes, Kupffer cells, and hepatic stellate cells.”

The same can be true in reverse. Things that improve thyroid energy system function, also then reduce exposure to stress substances, such as the polyunsaturated free fatty acids, nitric oxide, estrogen and lactate, eventually improving digestive function and reducing the potential for exposure to endotoxin as well as the inflammatory things stimulated by endotoxin. And before you jump to any conclusions, reducing exposure to other kinds of bacteria that do not produce endotoxin, can also be beneficial.

“Gram positive bacteria do not have endotoxin, but the presence of these bacteria in tissues provokes an inflammatory response that is similar to that triggered by Gram negative LPS…The same cytokines elicited by LPS are released and the same types of physiological effects are seen….largely via the initiation of an inflammatory response through the stimulation of monocytes and macrophages and the subsequent release of proinflammatory cytokines, especially tumour necrosis factor-alpha (TNF-α) and interleukin-1…”

A diet avoiding the PUFAs, and limiting intake of difficult to digest starchy and fibrous grains, seeds, nuts, beans, legumes and under cooked vegetables, with enough protein from milk, cheese and gelatin, and plenty of sugar from sweet ripe fruits and juices, white sugar and honey, is one possible way to reduce exposure to bacteria, endotoxin and many interrelated cancer promoting inflammatory substances.

Some things that have been used to deal with endotoxin, TLR4 activation, inflammation and cancer, include minocycline, doxycycline, penicillin and some other antibiotics, cyproheptadine and famotidine, glycine and gelatin, methylene blue, vitamin C, A and D, activated charcoal, coconut oil, aspirin, taurine, Cascara Sagrada and Emodin, magnesium, coffee and caffeine, thyroid hormone, progesterone, pregnenolone and niacinamide.

Whole body hyperthermia, iron restriction, methionine restriction, occasional calorie restriction, improved calcium to phosphorous ratio, raw carrots and well cooked mushrooms, have also been shown to be cancer protective for reasons that can be seen as directly or indirectly related to bacteria and endotoxin.

See More Here

The Pancreatic Cancer Microbiome Promotes Oncogenesis by Induction of Innate and Adaptive Immune Suppression

Human Monocytes Engage an Alternative Inflammasome Pathway

Causes and consequences of low grade endotoxemia and inflammatory diseases.

Lipopolysaccharide (LPS) increases the invasive ability of pancreatic cancer cells through the TLR4/MyD88 signaling pathway.

LPS Up-Regulates ICAM-1 Expression in Breast Cancer Cells by Stimulating a MyD88-BLT2-ERK-Linked Cascade, Which Promotes Adhesion to Monocytes

Inflammatory stimuli promote growth and invasion of pancreatic cancer cells through NF-κB pathway dependent repression of PP2Ac

Role of TOPK in lipopolysaccharide-induced breast cancer cell migration and invasion

Lipopolysaccharide modulates p300 and Sirt1 to promote PRMT1 stability via an SCFFbxl17-recognized acetyldegron

LPS-induced TLR4 signaling in human colorectal cancer cells increases beta1 integrin-mediated cell adhesion and liver metastasis.

Gram negative bacteria increase non‐small cell lung cancer metastasis via toll‐like receptor 4 activation and mitogen‐activated protein kinase phosphorylation

Effect of lipopolysaccharide on toll-like receptor-4 signals in mouse cancer cells.

Functional Toll-Like Receptor 4 Conferring Lipopolysaccharide Responsiveness Is Expressed in Thyroid Cells

Effect of TLR4 on the growth of SiHa human cervical cancer cells via the MyD88-TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways

Targeting gut flora to prevent progression of hepatocellular carcinoma.

Gram-negative bacteria facilitate tumor outgrowth and metastasis by promoting lipid synthesis in lung cancer patients

The role of TLRs in cervical cancer with HPV infection: a review

Store-operated Ca2+ Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells

Macrophages mediate colon carcinoma cell adhesion in the rat liver after exposure to lipopolysaccharide

LPS induced miR-181a promotes pancreatic cancer cell migration via targeting PTEN and MAP2K4.

Lipopolysaccharide-pathway proteins are associated with gallbladder cancer among adults in Shanghai, China with mediation by systemic inflammation

Toll-Like Receptors in Esophageal Cancer

Activation of TLR4 signaling promotes gastric cancer progression by inducing mitochondrial ROS production

NF-κB, inflammation and metabolic disease

NADPH oxidase 1-dependent ROS is crucial for TLR4 signaling to promote tumor metastasis of non-small cell lung cancer.

Protective effects of Isofraxidin against lipopolysaccharide-induced acute lung injury in mice.

Mechanisms of bacterial pathogenicity.

Lipopolysaccharides increase the amount of CXCR4, and modulate the morphology and invasive activity of oral cancer cells in a CXCL12-dependent manner.

Targeting Toll-like receptors against cancer

Toll-like receptor–induced changes in glycolytic metabolism regulate dendritic cell activation

Toll-like receptor 4 in lymphatic endothelial cells contributes to LPS-induced lymphangiogenesis by chemotactic recruitment of macrophages

Lipopolysaccharide-induced toll-like receptor 4 signaling enhances the migratory ability of human esophageal cancer cells in a selectin-dependent manner.

Expression of Toll-Like Receptors on Human Rectal Adenocarcinoma Cells

Role of toll-like receptor 4 on the immune escape of human oral squamous cell carcinoma and resistance of cisplatin-induced apoptosis

Lipopolysaccharide-induced toll-like receptor 4 signaling in esophageal squamous cell carcinoma promotes tumor proliferation and regulates inflammatory cytokines expression.

Toll-Like Receptor 4 Prompts Human Breast Cancer Cells Invasiveness via Lipopolysaccharide Stimulation and Is Overexpressed in Patients with Lymph Node Metastasis

Melanoma cell lines are responsive in vitro to lipopolysaccharide and express TLR-4.

S100A8 facilitates the migration of colorectal cancer cells through regulating macrophages in the inflammatory microenvironment

Propofol suppresses LPS-induced nuclear accumulation of HIF-1α and tumor aggressiveness in non-small cell lung cancer

Lipopolysaccharide Effect on Vascular Endothelial Factor and Matrix Metalloproteinases in Leukemic Cell Lines In vitro

Hypertonic Saline Attenuates the Pro-metastatic Effects of LPS by Reducing Tumor Cell Migration, Proliferation and MMP-9 Expression

Enhanced TLR4 Expression on Colon Cancer Cells After Chemotherapy Promotes Cell Survival and Epithelial-Mesenchymal Transition Through Phosphorylation of GSK3β.

Activation of toll-like receptors 2, 3, and 4 on human melanoma cells induces inflammatory factors

Links between Toll-like receptor 4 and breast cancer

Endotoxin/Lipopolysaccharide Activates NF-κB and Enhances Tumor Cell Adhesion and Invasion Through a β1 Integrin-Dependent Mechanism

Role of bacterial infections in pancreatic cancer

Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Production by Human Monocytes Involves the Raf-1/MEK1-MEK2/ERK1-ERK2 Pathway

Exposure to bacterial products lipopolysaccharide and flagellin and hepatocellular carcinoma: a nested case-control study

Aspirin inhibited the metastasis of colon cancer cells by inhibiting the expression of toll -like receptor 4

LPS/TLR4 Signaling Enhances TGF-β Response Through Downregulating BAMBI During Prostatic Hyperplasia

Toll-like receptor 4 signaling promotes the migration of human melanoma cells.

Activation of TOPK by lipopolysaccharide promotes induction of inducible nitric oxide synthase through NF-κB activity in leukemia cells.

p53 protects against LPS-induced lung endothelial barrier dysfunction

Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle.

Aging predisposes to acute inflammatory induced pathology after tumor immunotherapy

Mechanism and Regulation of NLRP3 Inflammasome Activation

High-fat Diet Accelerates Intestinal Tumorigenesis Through Disrupting Intestinal Cell Membrane Integrity

The role of the liver in the response to LPS: experimental and clinical findings.

Involvement of oncogenic protein β-catenin in LPS-induced cytotoxicity in mouse mononuclear leukemia RAW 264.7 cells.

IκB kinase β Mediating the Downregulation of p53 and p21 by Lipopolysaccharide in Human Papillomavirus 16+ Cervical Cancer Cells

Lipopolysaccharide promoted the growth rate of MG-63 cells via the extracellular regulated kinase pathway

The gut microbiota: A new potential driving force in liver cirrhosis and hepatocellular carcinoma

Puerarin suppresses LPS-induced breast cancer cell migration, invasion and adhesion by blockage NF-κB and Erk pathway.

Lipopolysaccharide promotes tumorigenicity of hepatic progenitor cells by promoting proliferation and blocking normal differentiation.

Therapeutic Targeting of Toll-Like Receptors for Infectious and Inflammatory Diseases and Cancer

Systemic inflammation promotes lung metastasis via E-selectin upregulation in mouse breast cancer model

The role of lipopolysaccharide/toll-like receptor 4 signaling in chronic liver diseases

Multiple Roles of Toll-Like Receptor 4 in Colorectal Cancer

Macrophage conditioned medium promotes colorectal cancer stem cell phenotype via the hedgehog signaling pathway

Bacterial endotoxin enhances colorectal cancer cell adhesion and invasion through TLR-4 and NF-κB-dependent activation of the urokinase plasminogen activator system

Alleviation of Lipopolysaccharide-Induced Acute Liver Injury in Propionibacterium acnes-Primed IFN-γ-Deficient Mice by a Concomitant Reduction of TNF-α, IL-12, and IL-18 Production

Role of nonresolving inflammation in hepatocellular carcinoma development and progression

Lipopolysaccharide Effect on Vascular Endothelial Factor and Matrix Metalloproteinases in Leukemic Cell Lines In vitro

Possible pro-carcinogenic association of endotoxin on lung cancer among Shanghai women textile workers

Association of plasma endotoxin, inflammatory cytokines and risk of colorectal adenomas

Lipopolysaccharide increases the release of VEGF-C that enhances cell motility and promotes lymphangiogenesis and lymphatic metastasis through the TLR4- NF-κB/JNK pathways in colorectal cancer

The role of intestinal endotoxin in liver injury: A long and evolving history

Interleukin-1β and tumor necrosis factor-α mediation of endotoxin action on growth hormone

Lipopolysaccharide enhances mouse lung tumorigenesis: A model for inflammation-driven lung cancer

TNF-alpha in promotion and progression of cancer.

TNF-α promotes colon cancer cell migration and invasion by upregulating TROP-2

LPS-induced CXCR4-dependent migratory properties and a mesenchymal-like phenotype of colorectal cancer cells

Toll-Like Receptor 4 Prompts Human Breast Cancer Cells Invasiveness via Lipopolysaccharide Stimulation and Is Overexpressed in Patients with Lymph Node Metastasis

Role of TOPK in lipopolysaccharide-induced breast cancer cell migration and invasion

Expression of functional toll like receptor 4 in estrogen receptor/progesterone receptor-negative breast cancer

Accelerated inflammation and oxidative stress induced by LPS in acute lung injury: Inhibition by ST1926

Inflammation induced oxidative stress mediates gene fusion formation in prostate cancer

The role of the gut microbiome in the development and progression of liver cirrhosis and hepatocellular carcinoma

Endotoxin induces proliferation of NSCLC in vitro and in vivo: role of COX-2 and EGFR activation

LPS Upregulated VEGFR-3 Expression Promote Migration and Invasion in Colorectal Cancer via a Mechanism of Increased NF-κB Binding to the Promoter of VEGFR-3

Lipopolysaccharide‐induced metastatic growth is associated with increased angiogenesis, vascular permeability and tumor cell invasion

Treating cancer with heat: hyperthermia as promising strategy to enhance apoptosis.

Bacteria Peptidoglycan Promoted Breast Cancer Cell Invasiveness and Adhesiveness by Targeting Toll-Like Receptor 2 in the Cancer Cells

Aspirin inhibited the metastasis of colon cancer cells by inhibiting the expression of toll-like receptor 4

Inhibition of iNOS as a novel effective targeted therapy against triple-negative breast cancer

Lung inflammation promotes metastasis through neutrophil protease-mediated degradation of Tsp-1

The endotoxin of Helicobacter pylori is a modulator of host-dependent gastritis.

The role of tumour-derived iNOS in tumour progression and angiogenesis

Taurine alleviates lipopolysaccharide‑induced liver injury by anti‑inflammation and antioxidants in rats

Function of inducible nitric oxide synthase in the regulation of cervical cancer cell proliferation and the expression of vascular endothelial growth factor

The role of hyperthermia in the battle against cancer.

Helicobacter pylori Augments Growth of Gastric Cancers via the Lipopolysaccharide-Toll-like Receptor 4 Pathway whereas Its Lipopolysaccharide Attenuates Antitumor Activities of Human Mononuclear Cells

Potential of fecal microbiota for early-stage detection of colorectal cancer

Actions of NO and INOS on endotoxin induced rat acute lung injury and effect of rhubarb on them.

Genetic Alterations in Gastric Cancer Associated with Helicobacter pylori Infection

Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation

Hyperthermia as an immunotherapy strategy for cancer

Bacterial overgrowth and diversification of microbiota in gastric cancer

Acute Renal Failure in Endotoxemia Is Caused by TNF Acting Directly on TNF Receptor-1 in Kidney

Toll-like Receptor 4 on Macrophage Promotes the Development of Steatohepatitis-related Hepatocellular Carcinoma in Mice

Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia.

Aging predisposes to acute inflammatory induced pathology after tumor immunotherapy

Hyperthermia protects mice against the lethal effects of endotoxin.

The Clinical Evidence Linking Helicobacter pylori to Gastric Cancer

Consumption of pomegranate decreases plasma lipopolysaccharide-binding protein levels, a marker of metabolic endotoxemia, in patients with newly diagnosed colorectal cancer: a randomized controlled clinical trial.

Hyperthermia-related clinical trials on cancer treatment within the ClinicalTrials.gov registry.

Doxycycline as Potential Anti-cancer Agent.

Pathogenic Microorganisms and Pancreatic Cancer

Lipopolysaccharide induces inflammation and facilitates lung metastasis in a breast cancer model via the prostaglandin E2-EP2 pathway

Cancer immunity and therapy using hyperthermia with immunotherapy, radiotherapy, chemotherapy, and surgery

Minocycline: far beyond an antibiotic

Sesamin inhibits lipopolysaccharide-induced proliferation and invasion through the p38-MAPK and NF-κB signaling pathways in prostate cancer cells.

HCC Is promoted by bacterial translocation and TLR‐4 signaling: A new paradigm for chemoprevention and management

Gastric nitric oxide synthase expression during endotoxemia: Implications in mucosal defense in rats

Doxycycline induces apoptosis via ER stress selectively to cells with a cancer stem cell-like properties: importance of stem cell plasticity

The role of endotoxin in infection: Helicobacter pylori and Campylobacter jejuni.

Induction of proinflammatory response in prostate cancer epithelial cells by activated macrophages

The Impact of Hyperthermia on Receptor-Mediated Interleukin-6 Regulation in Mouse Skeletal Muscle

Elevated lipopolysaccharide in the colon evokes intestinal inflammation, aggravated in immune modulator-impaired mice

Inhibition of proliferation of cervical and leukemic cancer cells by penicillin G.

Doxycycline reduces lipopolysaccharide-induced inflammatory mediator secretion in macrophage and ex vivo human whole blood models.

The physiological expression of inducible nitric oxide synthase (iNOS) in the human colon

Coexpression of NOS2 and COX2 accelerates tumor growth and reduces survival in estrogen receptor-negative breast cancer

Lactate Boosts TLR4 Signaling and NF-κB Pathway-Mediated Gene Transcription in Macrophages via Monocarboxylate Transporters and MD-2 Up-Regulation

Lactate Contribution to the Tumor Microenvironment: Mechanisms, Effects on Immune Cells and Therapeutic Relevance

17Beta-estradiol promotes TLR4-triggered proinflammatory mediator production through direct estrogen receptor alpha signaling in macrophages in vivo.

NOS1-derived nitric oxide promotes NF-κB transcriptional activity through inhibition of suppressor of cytokine signaling-1

The effects of subclinical hypothyroidism on serum lipid level and TLR4 expression of monocyte in peripheral blood of rats.

Increased Toll-Like Receptors Activity and TLR Ligands in Patients with Autoimmune Thyroid Diseases


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1 Response

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