ADAM10 is overexpressed in human hepatocellular carcinoma and contributes to the proliferation, invasion and migration of HepG2 cells

Abstract

Abstract.The overexpression of A disintegrin and metalloproteinase 10 (ADAM10) has been found to be closely associated with the development and progression of various types of tumors. However, ADAM10 expression in hepatocellular carcinoma (HCC) and its significance remain largely unknown. The present study aimed to investigate the expression of ADAM10 in human HCC and the effect of ADAM10 gene silencing by siRNA on the proliferation, invasion and migration of HepG2 human hepatoma cells. Immunohistochemistry was performed to examine the expression of ADAM10 in human HCC tissues and in the adjacent non-cancer tissues from 30 patients with HCC. RNA interference was used to knock down ADAM10 expression in HepG2 human hepatoma cells and the proliferation and migration as well as the invasive ability of the treated cells were observed in vitro. The expression of ADAM10 protein in HCC tissues was significantly higher when compared to that in adjacent non-tumor tissues (P<0.05). The high expression of ADAM10 in cancer was significantly correlated with clinical outcomes (P<0.05). Silencing of ADAM10 resulted in inhibition of proliferation and migration as well as invasion of HepG2 human hepatoma cells (P<0.05). These studies suggest that ADAM10 plays an important role in regulating proliferation, invasion and migration of HepG2 cells. High expression of ADAM10 may be a valuable predictive factor for HCC prognosis, and ADAM10 is potentially an important therapeutic target for the prevention of tumor development and progression in HCC.

Silencing ADAM10 inhibits the in vitro and in vivo growth of hepatocellular carcinoma cancer cells

“…Bai et al (22) found that expression of microRNA-122, as a negative regulator of ADAM10, sensitizes HCC cells to sorafenib, a multikinase inhibitor clinically effective against HCC. Yuan et al (23) observed that ADAM10 silencing resulted in inhibition of proliferation and migration as well as HepG2 human hepatoma cell invasion (P<0.05), a finding that is in concordance with the results of the present study. However, Yuan et al (23) did not investigate responses in an in vivo model.…”

“…Yuan et al (23) observed that ADAM10 silencing resulted in inhibition of proliferation and migration as well as HepG2 human hepatoma cell invasion (P<0.05), a finding that is in concordance with the results of the present study. However, Yuan et al (23) did not investigate responses in an in vivo model. The results from the present study revealed that downregulation of ADAM10 expression using the RNA silencing approach in HepG2 tumor cells significantly suppressed cell proliferation, cell migration and cell invasion in vitro, and tumor growth in vivo.…”

MicroR-140-5p suppresses tumor cell migration and invasion by targeting ADAM10-mediated Notch1 signaling pathway in hypopharyngeal squamous cell carcinoma

“…ADAM10 has been shown to be overexpressed in malignant tumors and may be related to the malignant behavior. For instance, overexpression of ADAM10 was detected and to promote cancer cell migration and invasion in non-small cell lung cancer, hepatocellular carcinoma, oral squamous cell carcinoma and bladder cancer (Fu et al, 2014;Guo et al, 2012;Jones et al, 2013;Yuan et al, 2013). Our data are in line with previous reports showing that ADAM10 is correlated with the migration and invasion of tumor cells.…”

High Resolution Proteomic Analysis of the Cervical Cancer Cell Lines Secretome Documents Deregulation of Multiple Proteases

“…ADAM10 is significantly overexpressed in breast cancer and colorectal cancer (40). Furthermore, ADAM10 has been reported to be secreted from pancreatic cancer cells (41) and is up-regulated in human hepatocellular carcinoma with an additional role in cancer cell migration and malignant transformation (42). In our study, ΑDAM10 displayed a qualitative difference in SiHa and HeLa cell lines and this pattern was actually validated by western blot analysis (Figure 8).…”