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MARK2 inhibits the growth of HeLa cells through AMPK and reverses epithelial-mesenchymal transition

Ge Xu1, Yinggang Ge2, Xiaohong Tao3

  • 1Institute of Life Science, Chongqing Medical University, Chongqing 400016, P.R. China.

Oncology Reports
|June 1, 2017
PubMed

Insights

Microtubule affinity-regulating kinases (MARKs) regulate cell growth and epithelial‑mesenchymal transition (EMT). MARK2 overexpression inhibits cell growth and EMT, suggesting anti-metastatic potential.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Microtubule affinity-regulating kinases (MARKs) are downstream of the tumor suppressor LKB1.
  • MARKs' functions are primarily linked to cell polarity.
  • Their role in cellular growth control is largely unexplored.

Purpose of the Study:

  • To investigate MARKs' functions beyond cell polarity.
  • To characterize MARKs' role in cellular growth and epithelial‑mesenchymal transition (EMT).
  • To elucidate MARK2's mechanisms in LKB1-deficient cells.

Main Methods:

  • Utilized an inducible lentiviral expression system in LKB1-deficient HeLa cells.
  • Overexpressed MARK2 and analyzed effects on cell growth, cell cycle, and colony formation.
  • Assessed MARK2's role in F-actin reorganization, cell migration, invasion, and EMT.

Main Results:

  • MARK2 overexpression decreased cell growth, inhibited colony formation, and caused G1 cell cycle arrest.
  • AMP-activated protein kinase (AMPK) was identified as a downstream effector, upregulating p21 and p16.
  • MARK2 promoted F-actin reorganization and reversed EMT, reducing cell migration and invasion.

Conclusions:

  • MARK2 plays a coordinated role in regulating cell growth and EMT.
  • MARK2 exhibits anti-metastatic activity by inhibiting cell invasion and migration.
  • Findings provide new insights into MARK2's mechanisms in cancer progression.

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