FAM172A affects cell proliferation and apoptosis not by targeting β-tubulin in HepG2 cells

Ai-Min Xu1, Chuan-Jiang He1, Zureguli Tuerxun1

  • 1Department of Laboratory, The First People's Hospital of Kashgar, Kashi, Kashi 844000, China.

Abstract

Insights

Family with sequence similarity 172, member A (FAM172A) inhibits liver cancer cell proliferation and invasion by affecting cell cycle and apoptosis, not by interacting with tubulin. This suggests FAM172A acts as a tumor suppressor gene.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Microtubules are crucial for chromosome segregation during mitosis, making spindle microtubule formation a target for anti-cancer therapies.
  • Previous research indicated that Family with sequence similarity 172, member A (FAM172A) inhibits proliferation and promotes apoptosis in colorectal cancer cells.
  • The role and interaction mechanism of FAM172A in liver cancer cells remained unexplored.

Purpose of the Study:

  • To investigate the biological effects of FAM172A on liver cancer cells (HepG2).
  • To elucidate the interaction mechanism between FAM172A and tubulin in liver cancer.
  • To assess FAM172A's impact on cell proliferation, migration, invasion, cell cycle, and apoptosis.

Main Methods:

  • STRING software and immunoprecipitation were used to predict and verify interactions between FAM172A and β-tubulin.
  • Real-Time qPCR and Western blot analyzed β-tubulin mRNA and protein expression.
  • Immunofluorescence microscopy examined β-tubulin distribution and dynamics.
  • MTT, wound healing, Transwell, and flow cytometry assays assessed proliferation, migration, invasion, cell cycle, and apoptosis.

Main Results:

  • No direct interaction was found between FAM172A and β-tubulin.
  • FAM172A modulation did not significantly alter β-tubulin mRNA or protein levels or its cellular dynamics.
  • Overexpression of FAM172A significantly inhibited HepG2 cell proliferation, migration, and invasion, inducing S phase arrest and apoptosis.
  • Interfering with FAM172A produced opposite effects.

Conclusions:

  • FAM172A exhibits tumor-suppressive properties in liver cancer cells.
  • FAM172A influences cell cycle control and proliferation independently of direct tubulin interaction.
  • Further research is needed to fully understand the specific mechanism of FAM172A's action.

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