Abstract
Background In our previous study, we found that the FAM172A recombinant protein could promote proliferation of L02 cells. However, the underlying mechanisms are still unknown. The present study was aimed at investigating the effect of FAM172A on proliferation of HepG2 cells and exploring the possible molecular mechanisms and its role in hepatocellular carcinoma (HCC). Methods Cell proliferation was measured by MTT assay. Western blot test was carried out to investigate the mechanism. Rabbit antibodies against FAM172A and membrane proteins isolated from lysate of HepG2 cell were coprecipitated and the resultant precipitates were analyzed by mass spectrum. Results The MTT assay showed that recombinant protein FAM172A isoform 1 (FAM172A-1) could induce HepG2 cell proliferation at the concentration of 10-100 ng/mL, while protein FAM172A isoform 3 (FAM172A-3) was at the concentration of 80-100 ng/mL. Western blot demonstrated that both FAM172A-1 and FAM172A-3 could activate the mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) pathway and the phosphatidylinositol 3-kinase/threonine-protein kinase (PI3K/Akt) pathway. Mass spectrum analysis suggested that there were some membrane proteins interacting with FAM172A. Several candidate interacting proteins might mediate proliferation signals induced by FAM172A recombinant protein, including seven membrane proteins. Conclusion In conclusion, FAM172A recombinant protein could induce proliferation of HepG2 cells, in which the MAPK/ERK and PI3K/Akt signaling pathways might be involved. The role of FAM172A in HepG2 cell proliferation also indicated its possible involvement in HCC. The receptor of FAM172A on cells still needs to be exploited.
Highlights
Liver cancer is the fourth among the most common causes of cancer deaths (782,000 deaths, 8.2%) as published by the International Agency for Research on Cancer in 2018 [1]
Dulbecco’s modified Eagle’s medium (DMEM), penicillin, streptomycin, and fetal bovine serum were purchased from Hyclone (Logan, UT)
Rabbit polyclonal antibodies against total MAPK/ERK, phosphoMAPK/ERK, total-Akt, phospho-Akt, and phosphatase inhibitor cocktail were obtained from Cell Signaling Technology (Boston, MA). 3-(4,5-Dimethylthiazol)-2,5-diphenyltetra-zolium bromide (MTT), aprotinin, and leupeptin were from Amresco (Solon, OH)
Summary
Liver cancer is the fourth among the most common causes of cancer deaths (782,000 deaths, 8.2%) as published by the International Agency for Research on Cancer in 2018 [1]. Disease at the advanced stage or with progression after locoregional therapy has a dismal prognosis and systemic therapy has not improved survival in patients with advanced hepatocellular carcinoma, sorafenib and lenvatinib are the drugs mostly used with little success at this stage [5, 6] These data provide evidence that the pathogenesis and progression of HCC are mediated by a number of molecular defects and dysregulated pathways. The present study was aimed at investigating the effect of FAM172A on proliferation of HepG2 cells and exploring the possible molecular mechanisms and its role in hepatocellular carcinoma (HCC). FAM172A recombinant protein could induce proliferation of HepG2 cells, in which the MAPK/ERK and PI3K/Akt signaling pathways might be involved. The receptor of FAM172A on cells still needs to be exploited
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