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Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
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Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

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FAM107A Inactivation Associated with Promoter Methylation Affects Prostate Cancer Progression through the

Shuai Ke1, Zelin Liu1, Qinghua Wang1

  • 1Department of Urology, Renmin Hospital of Wuhan University, 99 Zhangzhidong Road, Wuhan 430060, China.

Cancers
|August 26, 2022
PubMed

Insights

FAM107A gene downregulation in prostate cancer (PCa) is caused by hypermethylation. Overexpressing FAM107A inhibits PCa cell growth and migration via the FAK/PI3K/AKT pathway, suggesting it as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer (PCa) is a leading cause of cancer mortality in men, necessitating novel therapeutic strategies.
  • The FAM107A gene is frequently downregulated in PCa, correlating with poor prognosis, but its regulatory mechanisms and functional impact are unclear.

Purpose of the Study:

  • To investigate the mechanisms underlying FAM107A downregulation in prostate cancer.
  • To elucidate the functional role of FAM107A in PCa progression and its associated signaling pathways.

Main Methods:

  • Analysis of FAM107A expression levels in PCa tissues.
  • Investigation of CpG island methylation and DNA methyltransferase 1 (DNMT1) involvement.
  • Functional assays assessing the impact of FAM107A overexpression on tumor cell proliferation, migration, invasion, and apoptosis.
  • Exploration of the FAK/PI3K/AKT signaling pathway.

Main Results:

  • FAM107A downregulation in PCa is attributed to hypermethylation of its CpG islands, with DNMT1 maintaining this hypermethylation.
  • FAM107A overexpression significantly inhibits PCa cell proliferation, migration, and invasion.
  • FAM107A promotes apoptosis in PCa cells.
  • FAM107A functions as a molecular brake on the FAK/PI3K/AKT signaling pathway.

Conclusions:

  • FAM107A downregulation in prostate cancer is epigenetically regulated by DNA hypermethylation.
  • FAM107A exerts tumor-suppressive effects by inhibiting cell proliferation, migration, and invasion through the FAK/PI3K/AKT pathway.
  • FAM107A represents a promising novel therapeutic target for prostate cancer treatment.
Keywords:
EMTFAK/PI3K/AKT pathwayFAM107Amethylationprostate cancer

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