SNHG3 Affects Gastric Cancer Development by Regulating SEPT9 Methylation

Area of Science:

• Oncology
• Molecular Biology
• Epigenetics

Background:

• Gastric cancer (GC) involves tumor suppressor gene silencing via methylation.
• SEPT9 methylation is a tumor marker that downregulates gene expression.
• Long noncoding RNA small nucleolar host gene 3 (lncRNA SNHG3) is implicated in cancer development.

Purpose of the Study:

• Investigate the mechanism by which SNHG3 regulates SEPT9 methylation.
• Determine the effects of SNHG3 on gastric cancer cell growth, metastasis, and spread.

Main Methods:

• Quantitative real-time PCR (qRT-PCR) for SNHG3 and miR-448 detection.
• Dual-luciferase assays to verify interactions between SNHG3, miR-448, and DNMT1.
• Methylation-specific PCR, Western blotting, Transwell, scratch, and CCK-8 assays to assess methylation, protein expression, and cell behavior.

Main Results:

• SNHG3 was found to be upregulated in gastric cancer tissues.
• Knockdown of SNHG3 or overexpression of miR-448 inhibited SEPT9 methylation.
• This inhibition led to increased SEPT9 expression, suppressing gastric cancer cell growth, migration, and invasion.

Conclusions:

• lncRNA SNHG3 promotes gastric cancer progression by regulating SEPT9 methylation.
• The mechanism involves SNHG3 targeting the miR-448/DNMT1 axis.
• This pathway influences the occurrence and development of gastric cancer.