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AMPKα phosphatase Ppm1E upregulation in human gastric cancer is required for cell proliferation

Min-Bin Chen1, Yuan-Yuan Liu1, Li-Bo Cheng2

  • 1Department of Radiotherapy and Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.

Oncotarget
|April 21, 2017
PubMed

Insights

Increased Ca2+/calmodulin-dependent protein kinase phosphatase (Ppm1E) promotes gastric cancer growth by inhibiting AMP-activated protein kinase (AMPK) and activating mTORC1. Downregulation of miR-135b-5p further contributes to this process.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • AMP-activated protein kinase (AMPK) activation is a promising anti-cancer strategy.
  • Ca2+/calmodulin-dependent protein kinase phosphatase (Ppm1E) dephosphorylates and inactivates AMPK.
  • The role of Ppm1E in human gastric cancer remains largely unexplored.

Purpose of the Study:

  • To investigate the expression and functional significance of Ppm1E in human gastric cancer.
  • To elucidate the relationship between Ppm1E, AMPK, and mTOR complex 1 (mTORC1) signaling in gastric tumorigenesis.
  • To explore the potential role of microRNA-135b-5p (miR-135b-5p) in regulating Ppm1E in gastric cancer.

Main Methods:

  • Quantitative analysis of Ppm1E and p-AMPKα (Thr-172) expression in human gastric cancer tissues and adjacent normal tissues.
  • Western blot analysis to assess Ppm1E, AMPK, and mTORC1 pathway components in gastric cancer cell lines (AGS, HGC-27, SNU601).
  • RNA interference (shRNA) to knockdown Ppm1E and transfection with miR-135b-5p mimics in AGS cells to evaluate functional effects on cell proliferation, AMPK activation, and mTORC1 signaling.

Main Results:

  • Ppm1E expression was significantly elevated in human gastric cancer tissues compared to normal tissues.
  • Elevated Ppm1E correlated with decreased AMPK phosphorylation (p-AMPKα, Thr-172) and increased mTORC1 activation in tumors.
  • Ppm1E knockdown suppressed gastric cancer cell proliferation by activating AMPK and inhibiting mTORC1.
  • Overexpression of Ppm1E enhanced proliferation through AMPK inhibition and mTORC1 activation.
  • miR-135b-5p was downregulated in gastric cancer tissues and cells; its restoration inhibited Ppm1E, activated AMPK, and reduced proliferation.

Conclusions:

  • Ppm1E upregulation is a key event in human gastric cancer development and progression.
  • Ppm1E promotes gastric cancer cell proliferation by inhibiting the AMPK pathway and activating mTORC1 signaling.
  • miR-135b-5p acts as a tumor suppressor by downregulating Ppm1E, suggesting a potential therapeutic target.
Keywords:
AMPKαPpm1Egastric cancermTORmiR-135b-5p

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