Downregulation of PHF6 inhibits cell proliferation and migration in hepatocellular carcinoma

• Verfasst von: Yu, Qiangfeng [VerfasserIn]
• Verfasst von: Yin, Libo [VerfasserIn]
• Titel: Downregulation of PHF6 inhibits cell proliferation and migration in hepatocellular carcinoma
• Verf.angabe: Qiangfeng Yu, Libo Yin, Yizeng Jian, Pengtao Li, Wenlong Zeng and Jianyin Zhou
• E-Jahr: 2019
• Jahr: 8 May 2019
• Umfang: 7 S.
• Fussnoten: Gesehen am 24.06.2020
• Titel Quelle: Enthalten in: Cancer biotherapy and radiopharmaceuticals
• Ort Quelle: Larchmont, NY : Liebert, 1996
• Jahr Quelle: 2019
• Band/Heft Quelle: 34(2019), 4, Seite 245-251
• ISSN Quelle: 1557-8852
• DOI: doi:10.1089/cbr.2018.2671
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1692445707

Abstract

Background: The plant homeodomain finger 6 (PHF6) was originally identified as single gene mutated in Börjeson-Forssman-Lehmann syndrome, which was reported to be a tumor suppressor in T-cell acute lymphoblastic leukemia. However, the biological function of PHF6 in hepatocellular carcinoma (HCC) has been poorly characterized.Materials and Methods: In this study, we first determined the mRNA levels of PHF6 in HCC tissues and adjacent normal tissues using quantitative real-time PCR. Then the expression of PHF6 was knocked down in HCC cell lines (HepG2, SMMC-7721, and Bel-7402) by siRNA transfection. A series of functional experiments, including EdU proliferation assay, colony formation assay, and Transwell assay, were performed in HCC cells. Western blot analysis was used to detect the expression of PHF6, E-cadherin, and Vimentin.Results: We found that PHF6 was significantly elevated in HCC tissues and positively correlated with TNM stage, differentiation, and lymph node metastasis. Silencing PHF6 significantly inhibited cell proliferation, colony formation, and migration in HCC cells. Furthermore, silencing PHF6 obviously increased E-cadherin and decreased Vimentin expression.Conclusions: These findings suggest that PHF6 plays a positive role in the growth of HCC cells, and targeting PHF6 could serve as a promising therapeutic strategy for human HCC.