Related Experiment Video
Updated: Nov 27, 2025
Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
SNHG6 Interacted with miR-325-3p to Regulate Cisplatin Resistance of Gastric Cancer by Targeting GITR
Tuanhe Sun1, Kang Li1, Kun Zhu1
1Department of Surgical Oncology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Background:
Cisplatin resistance results in the failure of platinum-based chemotherapy and relapse of gastric cancer. We aimed to investigate the potential regulating role of SNHG6/miR-325-3p/GITR in reversing cisplatin resistance.
Patients And Methods:
A total of 137 gastric cancer patients were recruited. qRT-PCR and ELISA were used to test the expression of target genes. CCK-8 and caspase 3/7 kit were used to test the cell viability and apoptosis rate. Dual luciferase reporter gene and RNA-pull down assay were used to investigate the potential interaction between target genes.
Results:
SNHG6 and GITR were up regulated in gastric cancer; however, miR-325-3p was down-regulated. Besides, SNHG6, miR-325-3p and GITR expression were associated with gastric cancer prognosis. Then, we found that GITR and SNHG6 promoted proliferation and inhibited apoptosis of MKN45 and MKN45 cisplatin resistance cell line; however, miR-325-3p inhibited proliferation and promoted apoptosis of these cell lines. Furthermore, SNHG6 might bind to miR-325-3p to regulate its expression, and miR-325-3p directly interacted with the 3`UTR of GITR.
Conclusion:
SNHG6 binds to miR-325-3p, which directly interacted with GITR to regulate cisplatin resistance of gastric cancer.
Insights
Gastric cancer cisplatin resistance involves SNHG6, miR-325-3p, and GITR. SNHG6 and GITR promote resistance, while miR-325-3p reverses it by targeting GITR, offering a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cisplatin resistance is a major cause of gastric cancer treatment failure and relapse.
- Identifying novel molecular mechanisms is crucial for overcoming therapeutic resistance.
Purpose of the Study:
- To investigate the regulatory role of the SNHG6/miR-325-3p/GITR axis in reversing cisplatin resistance in gastric cancer.
Main Methods:
- Gene expression analysis (qRT-PCR, ELISA) in 137 gastric cancer patients.
- Cell viability and apoptosis assays (CCK-8, caspase 3/7).
- Molecular interaction studies (dual luciferase reporter, RNA-pull down).
Main Results:
- SNHG6 and GITR were upregulated, while miR-325-3p was downregulated in gastric cancer.
- SNHG6 and GITR promoted proliferation and inhibited apoptosis; miR-325-3p had opposite effects.
- SNHG6 regulates miR-325-3p, and miR-325-3p directly targets GITR.
Conclusions:
- The SNHG6/miR-325-3p/GITR pathway plays a significant role in regulating cisplatin resistance in gastric cancer.
- SNHG6 sponges miR-325-3p, which in turn targets GITR, modulating chemoresistance.
