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TNFAIP8 promotes prostate cancer cell survival by inducing autophagy

Suryakant Niture1,2, Malathi Ramalinga2, Habib Kedir1,2

  • 1Julius L. Chambers Biomedical Biotechnology Research Institute, North Carolina Central University Durham, 27707 NC, USA.

Oncotarget
|June 22, 2018
PubMed

Insights

Tumor necrosis factor-α-inducible protein 8 (TNFAIP8) promotes prostate cancer cell survival and drug resistance by inducing autophagy. This protein dysregulates the cell cycle and enhances resistance to chemotherapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor necrosis factor-α-inducible protein 8 (TNFAIP8) is an anti-apoptotic protein implicated in tumor growth.
  • The precise mechanisms by which TNFAIP8 promotes cancer cell survival are not fully understood.
  • TNFAIP8's role in prostate cancer, particularly concerning cell cycle, autophagy, and drug resistance, requires further investigation.

Purpose of the Study:

  • To elucidate the function of TNFAIP8 in regulating cell cycle, autophagy, cell survival, and neuroendocrine differentiation in prostate cancer cells.
  • To investigate the association between TNFAIP8 expression, autophagy induction, and apoptosis.
  • To determine the impact of TNFAIP8 on neuroendocrine differentiation and drug resistance in prostate cancer.

Main Methods:

  • Investigated TNFAIP8's effects on cell-cycle-related proteins in PC3 prostate cancer cells.
  • Assessed autophagy induction by measuring the expression of key autophagy effectors (LC3β I/II, Beclin1, 4EBP1, p62, SIRT1).
  • Examined TNFAIP8's interaction with autophagy-related protein 3 (ATG3) and its influence on neuroendocrine markers (synaptophysin, chromogranin A) and drug resistance.

Main Results:

  • TNFAIP8 dysregulates cell-cycle-related proteins in PC3 cells.
  • TNFAIP8 significantly increases the expression of autophagy effectors, indicating autophagy induction.
  • TNFAIP8 interacts with ATG3, enhances autophagy, decreases apoptosis, increases neuroendocrine differentiation markers, and confers resistance to docetaxel and doxorubicin.

Conclusions:

  • TNFAIP8 promotes prostate cancer cell survival and drug resistance through the induction of cellular autophagy.
  • TNFAIP8 plays a critical role in dysregulating the cell cycle and enhancing chemoresistance in prostate cancer.
  • Targeting TNFAIP8-induced autophagy may represent a therapeutic strategy for overcoming drug resistance in prostate cancer.
Keywords:
TNFAIP8autophagycell survivalneuroendocrine differentiationprostate cancer

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