# FANCA facilitates G1/S cell cycle advancement, proliferation, migration and invasion in gastric cancer: FANCA’s role in G1/S cell cycle progression and beyond in GC

## TL;DR

This study shows that the FANCA gene promotes cancer growth and spread in gastric cancer by advancing the cell cycle, suggesting it could be a target for treatment.

## Contribution

The study reveals FANCA's role in driving gastric cancer progression through cell cycle regulation, identifying it as a potential therapeutic target.

## Key findings

- FANCA expression is elevated in gastric cancer and correlates with advanced stages and metastasis.
- FANCA knockdown reduces cancer cell proliferation, migration, and invasion while causing cell cycle arrest.
- FANCA overexpression promotes tumor growth in vivo and activates cell cycle pathways.

## Abstract

The present study explores the function of
FANCA gene, a pivotal member of the Fanconi anaemia (FA) pathway crucial for preserving genomic stability and preventing cancer, particularly in the context of gastric cancer (GC). Using immunohistochemistry, quantitative real-time PCR, and western blot analysis, we evaluate FANCA mRNA and protein expressions in GC cell lines. The relationship between FANCA expression and clinicopathological characteristics is also explored. Various assays, including CCK8, colony formation, wound healing, and Transwell assays, are used to assess functional changes in cells associated with FANCA. Flow cytometry is utilized to evaluate alterations in the cell cycle resulted from
FANCA knockdown and overexpression. Our findings show elevated FANCA expression in GC cell lines, with levels correlated with pathologic stage and lymphatic metastasis.
FANCA knockdown impedes cell proliferation, migration, and invasion and induces G1/S phase cell cycle arrest. Conversely,
FANCA overexpression stimulates cell proliferation, migration, and invasion.
In vivo xenograft experiments confirm the promotional role of FANCA in GC tumor progression. Moreover,
FANCA overexpression is associated with the activation of cell cycle. Collectively, our results suggest that FANCA drives malignant cell behaviors in GC through the cell cycle pathway, highlighting its potential as a therapeutic target for the treatment of GC.