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.

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.

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