The AT1/Raf/ERK1/2 signaling pathway is involved in Angiotensin II-enhanced proliferation of hepatic carcinoma cells

Qi, Ran; Bai, Y.; Tang, Na; Xue, Xindong

doi:10.4149/neo_2018_171213n816

Cited by 7 publications

(3 citation statements)

References 43 publications

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“…Ang II clearly stimulated primary tumor growth and increased the expressions of c-Myc and cyclin D1. Since several reports have shown that Ang II can stimulate cancer cell proliferation by upregulating c-Myc expression in hepatocellular carcinoma cells (Ji et al, 2016;Qi et al, 2019) and cyclin D1 expression in breast cancer cells (Du et al, 2012), these cell proliferation-related proteins may be involved in Ang II-stimulated primary tumor growth in our model.…”

Section: Discussionmentioning

confidence: 92%

Angiotensin II promotes primary tumor growth and metastasis formation of murine TNBC 4T1 cells through the fibroblasts around cancer cells

Takiguchi

Takahashi-Yanaga

Ishikane

et al. 2021

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 92%

Angiotensin II promotes primary tumor growth and metastasis formation of murine TNBC 4T1 cells through the fibroblasts around cancer cells

Takiguchi

Takahashi-Yanaga

Ishikane

et al. 2021

European Journal of Pharmacology

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“…Both hepatic stellate cells (HSCs) activation and extracellular matrix (ECM) deposition can induce the occurrence of liver fibrosis, while transforming growth factor-β (TGF-β)-mediated Smad and MAPK signals play an important role in this process [ 38 – 40 ]. TNF-α, Akt, mTOR, PI3K, ERK1/2 and IGF-1 are important signaling molecules affecting the growth of HCC, and activation of Raf protein by Ang II binding to AT1R was found to promote the proliferation of HCC cells [ 41 ]. However, losartan and other ARBs can inhibit the growth of HCC cells through inducing apoptosis [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of PLC-β1/CaM signaling pathway mediated by AT1R on the occurrence and development of hepatocellular carcinoma

Liu

Wang

et al. 2021

Cancer Cell Int

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Objective To study the roles of AT1R, PLC-β1, CaM and other related signal molecules in the formation and development of hepatocellular carcinoma (HCC) and their correlation. Methods ELISA and immunohistochemistry were used to analyze the expressions of target proteins in serum and liver tissue of HCC patients, and the correlation between AT1R, PLC-β1 and CaM and postoperative survival status of patients was followed up and determined. CCK-8 method was used to screen the doses of Ang II and candesartan sensitive to HepG2 and HCCLM3 cells. Transwell experiment was used to observe the effects of different drugs on the migration and invasion activity of HCC cells. Meanwhile, flow cytometry and Western blot were used to detect the expression levels of AT1R, PLC-β1 and CaM in the cells. Then PLC-β1 siRNA was selected to transfect HCC cells, so as to further clarify the mechanism of the above signal proteins. HepG2 cells were inoculated under the hepatic capsule of mice to induce the formation of HCC in situ. Ang II and candesartan were used to stimulate HCC mice to observe the difference in liver appearance and measure the liver index. Finally, ELISA and immunofluorescence experiments were selected to analyze the levels of target proteins in mouse serum and liver tissue. Results The expression levels of target proteins in serum and liver tissue of HCC patients were significantly increased, and the postoperative survival time of patients with high expression of AT1R, PLC-β1 or CaM was obviously shortened. Ang II and candesartan could significantly promote and inhibit the motility of HCC cells, and had different effects on the levels of AT1R, PLC-β1 and CaM in cells. However, in hepatocellular carcinoma cells transfected with PLC-β1 siRNA, the intervention ability of drugs was obviously weakened. Ang II could significantly promote the formation and progression of mouse HCC, while candesartan had the opposite effect. Meanwhile, medications could affect the expressions of target proteins in mouse serum and liver tissue. Conclusion AT1R, PLC-β1 and CaM may be risk factors affecting the formation and prognosis of HCC, and the PLC-β1/CaM signaling pathway mediated by AT1R is an important way to regulate the migration and invasion activity of HCC cells.

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“…[ 24 ] Additionally, S100A9 has been shown to be upregulated in HepG2 HCC cells via activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) signal-transduction pathways, which subsequently contribute to the proliferation, invasion, and development of liver cancer cells. [ 25 – 27 ] Liang et al have also suggested that the expression of S100A9 was higher in HCC. [ 26 – 28 ] Furthermore, Arai et al have demonstrated that S100A9 upregulation is correlated with poorly differentiated liver carcinomas.…”

Section: Introductionmentioning

confidence: 99%

S100 family members: potential therapeutic target in patients with hepatocellular carcinoma

et al. 2021

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Proteins in S100 family exhibit different expressions patterns and perform different cytological functions, playing substantial roles in certain cancers, carcinogenesis, and disease progression. However, the expression and role of S100 family members in the prognosis of hepatocellular carcinoma (HCC) remains unclear. To investigate the effect of S100 family members for the prognosis of liver cancer, we assessed overall survival (OS) using a Kaplan–Meier plotter (KM plotter) in liver cancer patients with different situation. Our results showed that 15 members of the S100 family exhibited high levels of expression and these levels were correlated with OS in liver cancer patients. The higher expression of S100A5, S100A7, S100A7A, S100A12, S100Z, and S100G was reflected with better survival in liver cancer patients. However, worse prognosis was related to higher levels of expression of S100A2, S100A6, S100A8, S100A9, S100A10, S100A11, S10013, S100A14, and S100P. We then evaluated the prognostic values of S100 family members expression for evaluating different stages of AJCC-T, vascular invasion, alcohol consumption, and the presence of hepatitis virus in liver cancer patients. Lastly, we studied the prognostic values of S100 family members expression for patients after sorafenib treatment. In conclusion, our findings show that the proteins of S100 family members exhibit differential expression and may be useful as targets for liver cancer, facilitating novel diagnostic and therapeutic strategies in cancer.

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The AT1/Raf/ERK1/2 signaling pathway is involved in Angiotensin II-enhanced proliferation of hepatic carcinoma cells

Cited by 7 publications

References 43 publications

Angiotensin II promotes primary tumor growth and metastasis formation of murine TNBC 4T1 cells through the fibroblasts around cancer cells

Angiotensin II promotes primary tumor growth and metastasis formation of murine TNBC 4T1 cells through the fibroblasts around cancer cells

Effect of PLC-β1/CaM signaling pathway mediated by AT1R on the occurrence and development of hepatocellular carcinoma

S100 family members: potential therapeutic target in patients with hepatocellular carcinoma

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