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Toll like receptor 4 and Lipopolysaccharide in hepatocellular carcinoma

Yuan-Hsi Wang, Yuh-Ching Twu, Chung-Kwe Wang, Fu-Zhen Lin, Chun-Ya Lee, Yi-Jen Liao
Liver fibrosis is the first step toward the progression to cirrhosis, portal hypertension, and hepatocellular carcinoma. A high-cholesterol diet is associated with liver fibrosis via the accumulation of free cholesterol in hepatic stellate cells (HSCs). Niemann-Pick type C2 (NPC2) plays an important role in the regulation of intracellular free cholesterol homeostasis via direct binding with free cholesterol. Previously, we reported that NPC2 was downregulated in liver cirrhosis tissues. Loss of NPC2 enhanced the accumulation of free cholesterol in HSCs and made them more susceptible to transforming growth factor (TGF)-β1...
June 5, 2018: International Journal of Molecular Sciences
Yi Lu, Jianliang Xu, Shuxian Chen, Zheng Zhou, Nan Lin
Angiogenesis plays a key role in the progression of hepatocellular carcinoma (HCC). This study aimed to investigate whether lipopolysaccharide (LPS) could promote HCC angiogenesis and the role of hepatic stellate cell (HSC) in this process. In vivo orthotopic HCC model and the effect of LPS on HSC in vitro were studied. Our results demonstrated that LPS-induced HSC activation during the promotion of HCC growth and angiogenesis in mice. The LPS-TLR4 (Toll-like receptor 4) pathway in HSC is responsible for HCC angiogenesis...
November 1, 2017: Acta Biochimica et Biophysica Sinica
Cuiyuan Huang, Hong Zhang, Ruidan Bai, Li Wang, Jian Lv
Toll-like receptor 4 (TLR4) appears to play an important role in the development and progression of hepatocellular carcinoma (HCC), but it is unclear whether single-nucleotide polymorphisms (SNPs) in the TLR4 gene influence HCC. In this study, we investigated the effects of TLR4 SNPs on HepG2 cell survival and proliferation, migration, and invasion. Plasmids carrying wild-type or mutant versions of the TLR4 gene (A896G and/or C1196T) were stably transfected into HepG2 cells, and cell viability and proliferation were analyzed using the Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assays, whereas apoptosis was assessed using flow cytometry...
November 2017: DNA and Cell Biology
Hideto Kawaratani, Kei Moriya, Tadashi Namisaki, Masakazu Uejima, Mitsuteru Kitade, Kousuke Takeda, Yasushi Okura, Kousuke Kaji, Hiroaki Takaya, Norihisa Nishimura, Shinya Sato, Yasuhiko Sawada, Kenichiro Seki, Takuya Kubo, Akira Mitoro, Junichi Yamao, Hitoshi Yoshiji
Excessive alcohol consumption is the most common cause of liver disease in the world. Chronic alcohol abuse leads to liver damage, liver inflammation, fibrosis and hepatocellular carcinoma. Inflammatory cytokines, such as tumor necrosis factor-α and interferon-γ, induce liver injury, which leads to the develo-pment of alcoholic liver disease (ALD). Hepatoprotective cytokines, such as interleukin (IL)-6 and IL-10, are also associated with ALD. IL-6 improves ALD via the activation of STAT3 and the subsequent induction of a variety of hepatoprotective genes in hepatocytes...
June 9, 2017: International Journal of Molecular Medicine
Rui Zhang, Catherine I Real, Chao Liu, Hideo A Baba, Guido Gerken, Mengji Lu, Ruth Broering
Previous studies have shown that hepatocellular carcinoma (HCC) develops more frequently in hepatitis B virus surface antigen (HBsAg)-transgenic mice (Alb/HBs) than in wild-type (WT) mice. However, the mechanism of this HCC model has not been well documented. Toll-like receptor 4 (Tlr4) signaling probably links innate immunity and HCC progression. This study was designed to investigate the role of innate immunity in hepatocarcinogenesis in Alb/HBs mice. Immunohistochemical analysis of liver specimens from Alb/HBs mice (16 per group) showed that the oncogenes Bmi1 (16/16, 100%) and Dkk1 (13/16, 81...
July 15, 2017: International Journal of Cancer. Journal International du Cancer
Xiaoyu Zhang, Shuchen Li, Mingrong Li, Haiying Huang, Jingyuan Li, Changwei Zhou
Hypoxia-inducible factor-1α (HIF-1α) and toll-like receptor 4 (TLR4) are involved in numerous mechanisms of cancer biology, including cell proliferation and survival; however the interaction of the two factors under hypoxic conditions remains unclear. The present study investigated the in vitro mechanism that results in the suppression of tumor cell growth and cellular functions when HIF-1α is silenced. In the present study, the human hepatocellular carcinoma HepG2 cell line was transfected with short hairpin RNA (shRNA) against HIF-1α and cultured under hypoxic conditions (1% O2 for 24 h)...
August 2016: Oncology Letters
Junsheng Gu, Ranran Sun, Shen Shen, Zujiang Yu
OBJECTIVE: This study was designed to explore the influence of Toll-like receptor 4 (TLR4) agonist lipopolysaccharides (LPS) on liver cancer cell and the feasibility to perform liver cancer adjuvant therapy. METHODS: Human liver cancer cell lines HepG2, H7402, and PLC/PRF/5 were taken as models, and the expression of TLRs mRNA was detected by real time-polymerase chain reaction method semiquantitatively. WST-1 method was used to detect the influence of LPS on the proliferation ability of liver cancer cells; propidium iodide (PI) single staining and Annexin V/PI double staining were used to test the influence of LPS on the cell cycle and apoptosis, respectively, on human liver cancer cell line H7402...
2015: OncoTargets and Therapy
Chih-Cheng Hsiao, Po-Han Chen, Cheng-I Cheng, Ming-Shian Tsai, Chih-Yang Chang, Shang-Chieh Lu, Ming-Chu Hsieh, Yu-Chun Lin, Po-Huang Lee, Ying-Hsien Kao
Toll-like receptor-4 (TLR4) is known to influence growth and migration of hepatocellular tumors; however, its role in hepatoblastoma remains poorly understood. This study investigated the regulatory role of TLR4 in proliferation and chemoresistance of HepG2 hepatoblastoma cells. Treatment with lipopolysaccharide (LPS), a TLR4 agonist, was found to significantly upregulate TLR4 expression in HepG2 cells, but not in malignant Huh-7 and Sk-Hep1 hepatocellular carcinoma cells. Additionally, IL-6 enhanced LPS-induced TLR4 upregulation...
November 1, 2015: Cancer Letters
Wen-Ting Liu, Ying-Ying Jing, Guo-Feng Yu, Zhi-Peng Han, Dan-Dan Yu, Qing-Min Fan, Fei Ye, Rong Li, Lu Gao, Qiu-Dong Zhao, Meng-Chao Wu, Li-Xin Wei
Cancer stem cells (CSCs) or tumor-initiating cells (TICs), a small subset of tumor cells, are involved in tumor initiation, progression, recurrence and metastasis. In human hepatocellular carcinoma (HCC), TICs are enriched with cell surface markers and play a key role in chemotherapy resistance, tumor invasion and migration. Toll like receptor 4 (TLR4), acting as a receptor for lipopolysaccharide (LPS), has been reported to be responsible for carcinogenesis, invasion, metastasis and cancer progression. In our study, two HCC cell lines and a splenic vein metastasis of the nude mouse model were used to study the invasive ability of TLR4 positive HCC cells in vitro and in vivo...
March 28, 2015: Cancer Letters
Yiting Wang, Qunfei Tu, Wei Yan, Dan Xiao, Zhimin Zeng, Yuming Ouyang, Long Huang, Jing Cai, Xiaoli Zeng, Ya-Jie Chen, Anwen Liu
CXC195 showed strong protective effects in neuronal apoptosis by exerting its antioxidant activity. However, the anti-cancer effects of CXC195 is still with limited acquaintance. Here, we investigated the role of CXC195 in lipopolysaccharide (LPS)-induced human hepatocellular carcinoma (HCC) cells lines (HepG2) and the possible signaling pathways. CXC195 exhibited significant anti-proliferative effect and induced cell cycle arrest in LPS-induced HepG2 cells. In addition, CXC195 suppressed the release of pro-inflammatory mediators in LPS-induced HepG2 cells, including TNF-α, iNOS, IL-1β, IL-6, CC chemokine ligand (CCL)-2, CCL-22 and epidermal growth factor receptor (EGFR)...
January 2, 2015: Biochemical and Biophysical Research Communications
Hangyu Li, Yan Li, Dan Liu, Jingang Liu
The endotoxin level in the portal and peripheral veins of hepatocellular carcinoma (HCC) patients is higher and lipopolysaccharide (LPS), has been reported to inhibit tumor growth. However, in this study, we found that LPS-induced Toll-like receptor 4 (TLR4) signaling was involved in tumor invasion and the molecular mechanism was investigated. The HCC cells were used to study the invasion ability of LPS-induced HCC cells and the epithelial-mesenchymal transition (EMT) in vitro. The in vitro experiments demonstrated that LPS could significantly enhance the invasive potential and induce EMT in HCC cells with TLR4 dependent...
October 2014: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Donghua Xu, Xiaochen Wang, Shushan Yan, Yin Yin, Jiajie Hou, Xuehao Wang, Beicheng Sun
Protein tyrosine phosphatase receptor type O (PTPRO) has been identified as a tumor suppressor in a number of cancers including hepatocellular carcinoma (HCC). Toll-like receptor 4 (TLR4) plays diverse roles in HCC tumorigenesis and progression. The association between PTPRO and TLR4 signaling in HCC remains largely unknown. We aimed to clarify the interaction between PTPRO and TLR4 in HCC. Surprisingly, we found reduced and positive-related expression of TLR4 and PTPRO in 84 human HCC specimens. Increased TLR4 expression and activity was found in PTPRO-overexpressed HCC cells stimulated with lipopolysaccharide (LPS)...
October 2014: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Mohammad Zare-Bidaki, Kyoko Tsukiyama-Kohara, Mohammad Kazemi Arababadi
Hepatitis B virus (HBV) infection mainly causes liver disease, including inflammation, cirrhosis, and hepatocellular carcinoma (HCC). It has been documented that prolonged hepatitis B-infected patients are unable to clear HBV from hepatocytes completely. Previous investigations have suggested that various genetic and immunologic parameters may be responsible for the induction of prolonged infection forms. Toll-like receptors (TLRs), as members of pathogen recognition receptors (PRRs), play critical roles in the recognition of viruses and the induction of appropriate immune responses...
September 2014: Viral Immunology
Yoon Seok Roh, Ekihiro Seki
Activation of innate immune systems including Toll-like receptor (TLR) signaling is a key in chronic liver disease. Recent studies suggest that gut microflora-derived bacterial products (i.e. lipopolysaccharide [LPS], bacterial DNA) and endogenous substances (i.e. high-mobility group protein B1 [HMGB1], free fatty acids) released from damaged cells activate hepatic TLRs that contribute to the development of alcoholic (ASH) and non-alcoholic steatohepatitis (NASH) and liver fibrosis. The crucial role of TLR4, a receptor for LPS, has been implicated in the development of ASH, NASH, liver fibrosis, and hepatocellular carcinoma...
August 2013: Journal of Gastroenterology and Hepatology
Lili Wang, Rong Zhu, Zhiquan Huang, Haigang Li, Hongguang Zhu
BACKGROUND: Recent studies have shown that toll-like receptor 4 (TLR4) is involved in hepatocarcinogenesis. However, the significance of TLR4 signaling in cancer development and progression remains unclear. AIM: The purpose of this study was to investigate the role of TLR4 in cancer cell survival and proliferation in hepatocellular carcinoma (HCC). METHODS: Fifty-three HCC and ten normal liver specimens were analyzed by immunohistochemistry, and three cell lines (HL-7702, PLC/PRF/5 and HepG2) were used for in vitro studies...
August 2013: Digestive Diseases and Sciences
Laman K Mamedova, Kai Yuan, Amber N Laudick, Sherry D Fleming, Douglas G Mashek, Barry J Bradford
Saturated free fatty acids (FFA) can activate inflammatory cascades including the toll-like receptor 4 (TLR4) pathway. TLR4 is expressed by hepatocytes and may help link FFA to altered hepatic gluconeogenesis in type 2 diabetes mellitus. This study examined the role of TLR4 in mediating palmitate effects on the expression of phosphoenolpyruvate carboxykinase (PCK1) and the catalytic subunit of glucose-6-phosphatase (G6PC), rate-determining gluconeogenic enzymes. Human hepatocellular carcinoma cells (HepG2 and HuH7) were incubated in media including 2% bovine serum albumin and 250 to 1000 μM palmitate for 24 h...
August 2013: Journal of Nutritional Biochemistry
Ying-Ying Jing, Zhi-Peng Han, Kai Sun, Shan-Shan Zhang, Jing Hou, Yan Liu, Rong Li, Lu Gao, Xue Zhao, Qiu-Dong Zhao, Meng-Chao Wu, Li-Xin Wei
BACKGROUND: The endotoxin level in the portal and peripheral veins of hepatocellular carcinoma (HCC) patients is higher and lipopolysaccharide (LPS), a cell wall constituent of gram-negative bacteria, has been reported to inhibit tumor growth. However, in this study, we found that LPS-induced toll-like receptor 4 (TLR4) signaling was involved in tumor invasion and survival, and the molecular mechanism was investigated, METHODS: Four HCC cell lines and a splenic vein metastasis of the nude mouse model were used to study the invasion ability of LPS-induced HCC cells and the epithelia-mesenchymal transition (EMT) in vitro and in vivo...
2012: BMC Medicine
Jing Yang, Jin-Xiang Zhang, Hui Wang, Guo-Liang Wang, Qing-Gang Hu, Qi-Chang Zheng
AIM: To investigated the interaction between toll-like receptor 4 (TLR4)-activated hepatoma cells and macrophages in the induction of tumor-immune suppression mediated by CD4+CD25(high) family of transcription factor P3 (FOXP3) regulatory T cells (Tregs). METHODS: The proportion of FOXP3+ Tregs was identified in peripheral blood and tumor tissues of 60 hepatocellular carcinoma (HCC) patients. TLR4 expression was examined in tumor tissues and cell lines. The correlation was examined between FOXP3+ Tregs in peripheral blood and TLR4 expression of HCC tissues...
June 21, 2012: World Journal of Gastroenterology: WJG
Yan Lin, Le-Xing Yu, He-Xin Yan, Wen Yang, Liang Tang, Hui-Lu Zhang, Qiong Liu, Shan-Shan Zou, Ya-Qin He, Chao Wang, Meng-Chao Wu, Hong-Yang Wang
Robust clinical and epidemiologic data support the role of inflammation as a key player in hepatocellular carcinoma (HCC) development. Our previous data showed that gut-derived lipopolysaccharide (LPS) promote HCC development by activating Toll-like receptor 4 (TLR4) expressed on myeloid-derived cells. However, the effects of gut-derived LPS on other types of liver injury models are yet to be studied. The purpose of this study was to determine the importance of gut-derived LPS and TLR4 signaling in a T-cell-mediated hepatitis-Con A-induced hepatitis model, which mimic the viral hepatitis...
September 2012: Cancer Prevention Research
Wei Gong, Jiu Liang Zhang, Xiao Juan Yan, Qing Zhou, Zhi Yong Wang, Tie Nan Yi
LPS can induce TACE upregulation via signaling from TLR4-derived EGFR activation in tumor cells. The regulation and activity of TACE have been investigated with the observation that gene expression is upregulated in response to LPS followed by EGFR activation, however, the process remains poorly understood. In this study, we examined the effects of LPS on H22 hepatocarcinoma cells that displayed constitutively active TLR4 expression. Upon TLR4 shRNA transfection into H22 cells, HSP70 expression significantly increased...
December 2011: Oncology Reports
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