Knockdown of RAD51AP1 suppressed cell proliferation and invasion in esophageal squamous cell carcinoma

Yang-Yang Hu1, Chen-Chao Ma1, Kai-Xing Ai2

  • 1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, No.507, Zhengmin Road, Shanghai, 200433, China.

Discover Oncology
|October 5, 2022
PubMed
Abstract

Insights

RAD51AP1 is highly expressed in esophageal squamous cell carcinoma (ESCC) and drives cancer progression. Silencing RAD51AP1 inhibits ESCC cell proliferation and invasion, suggesting it as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Bioinformatics

Background:

  • Esophageal cancer, particularly esophageal squamous cell carcinoma (ESCC), is a significant global health concern.
  • Identifying key molecular drivers is crucial for developing effective ESCC treatments.

Purpose of the Study:

  • To identify novel hub genes implicated in ESCC pathophysiology using bioinformatics and experimental validation.
  • To investigate the functional role of RAD51-associated protein 1 (RAD51AP1) in ESCC progression.

Main Methods:

  • Utilized Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases for differential gene expression analysis.
  • Constructed a protein-protein interaction (PPI) network using Cytoscape to identify hub genes.
  • Performed in vitro functional assays (CCK-8, colony formation, flow cytometry, Transwell) to assess the impact of RAD51AP1 knockdown on ESCC cells.

Main Results:

  • RAD51AP1 was significantly upregulated in ESCC tissues and associated with poorer patient survival.
  • RAD51AP1 knockdown inhibited ESCC cell proliferation, induced cell cycle arrest, and promoted apoptosis.
  • Silencing RAD51AP1 suppressed ESCC cell migration and invasion.

Conclusions:

  • RAD51AP1 plays a critical role in promoting ESCC cell proliferation and invasion.
  • RAD51AP1 represents a promising novel therapeutic target for esophageal squamous cell carcinoma treatment.

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