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FOXK2 downregulation suppresses EMT in hepatocellular carcinoma

Jian Kong1, Qingyun Zhang2, Xuefeng Liang3

  • 1Department of Hepatobiliary Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100043, China.

Open Medicine (Warsaw, Poland)
|December 14, 2020
PubMed

Insights

Forkhead box K2 (FOXK2) downregulation suppresses hepatocellular carcinoma (HCC) progression by inhibiting epithelial-mesenchymal transition (EMT). This occurs partly via the Akt signaling pathway, impacting cell proliferation and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Forkhead box K2 (FOXK2) has a dual role as an oncogene or tumor suppressor.
  • The specific role and regulatory mechanisms of FOXK2 in hepatocellular carcinoma (HCC) epithelial-mesenchymal transition (EMT) are not fully understood.

Purpose of the Study:

  • To investigate the functional role of FOXK2 in EMT in HCC.
  • To elucidate the regulatory mechanisms of FOXK2 in HCC progression.

Main Methods:

  • FOXK2 expression was downregulated using siRNA in Hep3B and HCCLM3 cells.
  • Cell proliferation, migration, and invasion were assessed using MTT, colony formation, and Transwell assays.
  • Protein expression related to EMT and Akt signaling was analyzed via Western blot.

Main Results:

  • FOXK2 downregulation inhibited cell proliferation, colony formation, migration, and invasion in HCC cells.
  • E-cadherin expression increased, while snail and p-Akt expression decreased upon FOXK2 suppression.
  • The Akt pathway activator SF1670 partially reversed the effects of FOXK2 downregulation, promoting EMT markers and cell invasion.

Conclusions:

  • FOXK2 downregulation suppresses EMT in HCC.
  • This suppression is partly mediated through the inhibition of the Akt signaling pathway.
  • Targeting FOXK2 may offer a therapeutic strategy for HCC.
Keywords:
AktFOXK2epithelial–mesenchymal transitionhepatocellular carcinoma

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