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Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Biol+Int 2020 ; 44 (8): 1616-1627 Nephropedia Template TP
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Plantamajoside inhibits the proliferation and epithelial-to-mesenchymal transition in hepatocellular carcinoma cells via modulating hypoxia-inducible factor-1alpha-dependent gene expression #MMPMID32239594
Yin W; Xu J; Li C; Dai X; Wu T; Wen J
Cell Biol Int 2020[Aug]; 44 (8): 1616-1627 PMID32239594show ga
As a potential antitumor herbal medicine, plantamajoside (PMS) benefits the treatment of many human malignances. However, the role of PMS in the progression of hepatocellular carcinoma (HCC) and the related molecular mechanisms is still unknown. Here, we proved that the cell viabilities of HepG2 cells were gradually decreased with the increasing concentrations of CoCl(2) and/or PMS via cell counting kit-8 assay. Meanwhile, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and western blot assays were used to further confirm that PMS inhibited the CoCl(2) -induced cell proliferation in HepG2 cells via suppressing the Ki67 and proliferating cell nuclear antigen expressions. We also performed wound-healing and transwell assays and demonstrated that PMS inhibited CoCl(2) -induced migration and invasion in HepG2 cells via suppressing the epithelial-mesenchymal transition (EMT) process. In addition, the use of 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole further proved that PMS inhibited the malignant biological behaviors of HepG2 cells under hypoxic condition by suppressing the hypoxia-inducible factor-1alpha (HIF-1alpha) expression. Besides, we further confirmed that PMS suppressed the growth and metastasis of implanted tumors in vivo. Given that PMS suppressed the proliferation and EMT induced by CoCl(2) in HCC cells via downregulating HIF-1alpha signaling pathway, we provided evidence that PMS might be a novel anti-cancer drug for HCC treatment.