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DEPDC1 up-regulates RAS expression to inhibit autophagy in lung adenocarcinoma cells

Wei Wang1, Aili Li1, Xiaodan Han1

  • 1Laboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.

Journal of Cellular and Molecular Medicine
|October 6, 2020
PubMed

Insights

DEP domain containing 1 (DEPDC1) promotes lung adenocarcinoma (LUAD) by up-regulating RAS-ERK1/2 signaling, inhibiting autophagy, and correlating with poor prognosis in LUAD patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • DEP domain containing 1 (DEPDC1) is implicated in various cancers.
  • Its specific role in lung adenocarcinoma (LUAD) tumorigenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role and underlying mechanisms of DEPDC1 in LUAD development.
  • To analyze DEPDC1 expression, prognostic value, and its impact on cell behavior and signaling pathways.

Main Methods:

  • Analysis of public databases (TCGA) for DEPDC1 expression and prognostic value.
  • Gene enrichment analysis using Gene Set Enrichment Analysis (GSEA).
  • In vitro assays (colony formation, Transwell, wound healing) and Western blot analysis in LUAD cell lines (A549, HCC827, H1993) following DEPDC1 modulation.

Main Results:

  • DEPDC1 expression is significantly upregulated in LUAD tissues and associated with unfavorable patient prognosis.
  • DEPDC1 knockdown inhibits proliferation, migration, and invasion of LUAD cells.
  • DEPDC1 upregulates RAS expression, enhances ERK1/2 activity, and subsequently inhibits autophagy.

Conclusions:

  • DEPDC1 acts as an oncogene in LUAD, promoting tumor development.
  • DEPDC1 inhibits autophagy via the RAS-ERK1/2 signaling pathway in LUAD cells, presenting a potential therapeutic target.
Keywords:
A549 cellsDEPDC1H1993 cellsHCC827 cellsRASautophagylung adenocarcinoma

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