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FAM83A signaling induces epithelial-mesenchymal transition by the PI3K/AKT/Snail pathway in NSCLC

Fengrui Zhou1, Jianxiong Geng1, Shanqi Xu1

  • 1Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150081, China.

Aging
|August 25, 2019
PubMed

Insights

Family with sequence similarity 83, member A (FAM83A) promotes non-small cell lung cancer (NSCLC) metastasis by inducing epithelial-mesenchymal transition. Targeting FAM83A may offer a new therapeutic strategy for NSCLC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Family with sequence similarity 83, member A (FAM83A) is implicated as a tumor promoter in various cancers.
  • The role of FAM83A in the invasion and metastasis of non-small cell lung cancer (NSCLC) is not well understood.

Purpose of the Study:

  • To investigate the role of FAM83A in NSCLC progression, specifically focusing on its contribution to invasion and metastasis.
  • To elucidate the underlying molecular mechanisms by which FAM83A influences NSCLC metastasis.

Main Methods:

  • Analysis of FAM83A expression in NSCLC tissues and correlation with clinical outcomes.
  • In vitro and in vivo functional assays to assess the impact of FAM83A knockdown or overexpression on NSCLC cell migration and invasion.
  • Investigation of the epithelial-mesenchymal transition (EMT) pathway, including the PI3K/AKT/Snail signaling cascade.

Main Results:

  • FAM83A expression is significantly elevated in NSCLC tissues and correlates with increased metastasis and poorer patient survival.
  • FAM83A knockdown inhibits, while overexpression enhances, NSCLC cell migration and invasion.
  • FAM83A promotes NSCLC metastasis by inducing EMT via the PI3K/AKT/Snail signaling pathway.
  • Inhibition of AKT or Snail partially reverses the pro-metastatic effects of FAM83A.

Conclusions:

  • Increased FAM83A expression is linked to EMT and metastasis in NSCLC.
  • FAM83A plays a crucial role in promoting NSCLC cell migration and invasion.
  • FAM83A represents a potential novel therapeutic target for NSCLC treatment.
Keywords:
EMTFAM83Anon-small cell lung cancer

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