Related Experiment Video
Updated: Dec 5, 2025

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
LncRNA-SNHG7 interferes with miR-34a to de-sensitize gastric cancer cells to cisplatin
Li-Juan Pei1,1, Peng-Jun Sun1,1, Kui Ma2,1
1Department of General Surgery, The Fourth Medical Center of PLA General Hospital, Beijing, China.
Abstract:
Gastric cancer (GC) remains poor prognosis and survival issues due to the resistance of chemotherapies, such as cisplatin. The long non-coding RNA small nucleolar RNA host gene 7 (lncRNA-SNHG7) is known as an oncogenic molecule in diverse cancers. Here, we demonstrate that SNHG7 was significantly upregulated in gastric cancer and positively correlated with cisplatin resistance of gastric cancer cells that SNHG7 was significantly upregulated in cisplatin resistant cells. Silencing SNHG7 dramatically sensitized cisplatin resistant cells. In contrast, a negative correlation between lncRNA-SNHG7 and miR-34a was found that miR-34a was downregulated in gastric cancer patient tissues and significantly sensitized cisplatin resistant gastric cancer cells. Intriguingly, bioinformatical analysis indicated miR-34a has putative biding site for SNHG7 and such negative association between SNHG7 and miR-34a was verified in gastric cancer tissues. The cisplatin resistant cells displayed increased glycolysis rate and SNHG7 promoted cellular glycolysis rate of gastric cancer cells. Luciferase assay illustrated LDHA, a glycolysis enzyme, was the direct target of miR-34a. Importantly, inhibiting SNHG7 successfully suppressed LDHA expressions and sensitized cisplatin resistant cells and such inhibitory effects could be recovered by further anti-miR-34a. These findings suggest an important regulator mechanism for the SNHG7-mediated cisplatin resistance via miR-34a/LDHA-glycolysis axis.
Insights
Gastric cancer (GC) cisplatin resistance is linked to increased SNHG7. Targeting SNHG7 and its miR-34a/LDHA-glycolysis axis can overcome chemoresistance in GC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric cancer (GC) exhibits poor prognosis, often due to chemotherapy resistance, particularly to cisplatin.
- Long non-coding RNAs (lncRNAs) play critical roles in cancer progression, with SNHG7 identified as an oncogenic molecule.
Purpose of the Study:
- To investigate the role of lncRNA-SNHG7 in cisplatin resistance in gastric cancer.
- To elucidate the regulatory mechanism involving SNHG7, miR-34a, and LDHA in GC chemoresistance.
Main Methods:
- Quantitative real-time PCR to measure SNHG7 and miR-34a expression.
- Cell viability assays to assess cisplatin sensitivity.
- Bioinformatical analysis and luciferase reporter assays to confirm interactions.
- Glycolysis rate assays and Western blotting for protein expression.
Main Results:
- SNHG7 was significantly upregulated in GC tissues and cisplatin-resistant cells, correlating with poor prognosis.
- Silencing SNHG7 sensitized GC cells to cisplatin, while its overexpression enhanced resistance.
- SNHG7 negatively regulated miR-34a, which was downregulated in GC.
- SNHG7 promoted glycolysis by targeting the miR-34a/LDHA axis, and inhibiting SNHG7 reversed cisplatin resistance.
Conclusions:
- SNHG7 promotes cisplatin resistance in gastric cancer by upregulating glycolysis via the miR-34a/LDHA pathway.
- The SNHG7/miR-34a/LDHA axis represents a potential therapeutic target for overcoming cisplatin resistance in GC.
Related Concept Videos
MicroRNAs
MicroRNAs
lncRNA - Long Non-coding RNAs
Experimental RNAi
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

