Volume 44 Issue 11
Nov.  2023
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Ming ZHANG, Chenglong YU, Jinpeng CAO. ZNF384 Regulates Metastasis of Hepatocellular Carcinoma via GCLM[J]. Journal of Kunming Medical University, 2023, 44(11): 56-62. doi: 10.12259/j.issn.2095-610X.S20231108
Citation: Ming ZHANG, Chenglong YU, Jinpeng CAO. ZNF384 Regulates Metastasis of Hepatocellular Carcinoma via GCLM[J]. Journal of Kunming Medical University, 2023, 44(11): 56-62. doi: 10.12259/j.issn.2095-610X.S20231108

ZNF384 Regulates Metastasis of Hepatocellular Carcinoma via GCLM

doi: 10.12259/j.issn.2095-610X.S20231108
  • Received Date: 2023-09-05
    Available Online: 2023-11-04
  • Publish Date: 2023-11-30
  •   Objective  To investigate the effect of ZNF384 on the proliferation and metastasis of HCC by regulating GCLM and demonstrate the specific mechanism.   Methods  si-ZNF384 and pcDNA-GCLM were transfected into HepG2 and HuH7 cell lines of HCC, respectively. Western blot was carried out to detect the expressions of ZNF384 and GCLM proteins as well as the expressions of EMT-markers N-cadherin, Vimentin and E-cadherin. CCK-8 assessed cell proliferative activity. Transwell assay was conducted to measure cell migration. Dual-luciferase experiment verified the binding relationship between ZNF384 and GCLM. The localization of ZNF384 and GCLM in HepG2 cells was detected by FISH assay.   Results  The expressions of ZNF384 and GCLM in HepG2 and HuH7 cells were increased(P < 0.05). Knockdown of ZNF384 inhibited the proliferation(P < 0.001) and migration(P < 0.001) of HepG2 and HuH7 cells, suppressed the expression of interstitial markers N-cadherin(P < 0.01) and Vimentin(P < 0.01), and promoted the expression of epithelial marker E-cadherin(P < 0.01). Database and dual-luciferase experiments confirmed that ZNF384 is bound to the promoter of GCLM. Overexpression of GCLM reversed the inhibitory effect of knocking down ZNF384 on the proliferation, migration and EMT of HepG2 and HuH7 cells(P < 0.05).   Conclusion  Knocking down ZNF384 can repress the proliferation and metastasis of HCC cells by inhibiting GCLM.
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