ARCHITTAPON NOKKEAW^1,2,3,#, PANNATHON THAMJAMRASSRI^1,2,3,#, NAPHAT CHANTARAVISOOT^1,4, PISIT TANGKIJVANICH^1,2,*, CHAIYABOOT ARIYACHET^1,2,*

Oncology Research, Vol.31, No.6, pp. 989-1005, 2023, DOI:10.32604/or.2023.030395

Abstract Hepatocellular carcinoma (HCC) is the leading cause of cancer death worldwide; nevertheless, current therapeutic options are limited or ineffective for many patients. Therefore, elucidation of molecular mechanisms in HCC biology could yield important insights for the intervention of novel therapies. Recently, various studies have reported dysregulation of long non-coding RNAs (lncRNAs) in the initiation and progression of HCC, including H19; however, the biological function of H19 in HCC remains unclear. Here, we show that knockdown of H19 disrupted HCC cell growth, impaired the G1-to-S phase transition, and promoted apoptosis, while overexpression of H19 yielded the opposite results. Screening for expression… More > Graphic Abstract

Junfeng Lu^*, Zhongsong Zhao^†, Yanhong Ma^‡

Oncology Research, Vol.28, No.5, pp. 509-518, 2020, DOI:10.3727/096504020X15954139263808

Abstract The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of hepatocellular carcinoma (HCC). In this work, miR-186 was downregulated in HCC tissues and cells, and low miR-186 level helped predict the occurrence of vascular invasion and poor prognosis in patients with HCC. miR-186 overexpression inhibited cell proliferation and tumor growth in nude mice, repressed migration and invasion abilities, and enhanced apoptosis in HCC cells. miR-186 also retarded progression of EMT. miR-186 directly bound to the 3 -untranslated regions of cyclin-dependent kinase 6 (CDK6) to inhibit its expression. Overexpression of CDK6 markedly… More >