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The Long Noncoding RNA D63785 Regulates Chemotherapy Sensitivity in Human Gastric Cancer by Targeting miR-422a

Zhixia Zhou1, Zhijuan Lin2, Yuqi He3

  • 1Center for Tumor Molecular Biology, Institute for Translational Medicine, Qingdao University, Qingdao 266021, China.

Molecular Therapy. Nucleic Acids
|September 10, 2018
PubMed

Insights

Targeting long intergenic non-protein-coding RNA D63785 (lncR-D63785) may overcome chemotherapy resistance in gastric cancer. Suppressing lncR-D63785 enhances drug sensitivity and inhibits tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Gastric cancer is a prevalent malignancy with limited treatment options due to chemotherapy resistance and side effects.
  • Long noncoding RNAs (lncRNAs) play crucial roles in cancer development and progression.
  • Aberrant expression of lncRNAs is implicated in various stages of gastric cancer.

Purpose of the Study:

  • To investigate the role of the oncogenic lncRNA, long intergenic non-protein-coding RNA D63785 (lncR-D63785), in gastric cancer.
  • To explore the potential of lncR-D63785 as a therapeutic target for overcoming chemoresistance.

Main Methods:

  • Quantitative real-time PCR to assess lncR-D63785 and miR-422a expression in gastric cancer tissues and cells.
  • In vitro assays (cell proliferation, migration, invasion) and in vivo studies (tumor xenografts in mice) to evaluate the functional role of lncR-D63785.
  • Western blotting to determine MEF2D expression.
  • Analysis of the regulatory relationship between lncR-D63785, miR-422a, and MEF2D.

Main Results:

  • lncR-D63785 was highly expressed in gastric cancer tissues and cells.
  • Silencing lncR-D63785 inhibited gastric cancer cell proliferation, migration, invasion, and reduced tumor growth in mice.
  • lncR-D63785 acted as a competing endogenous RNA (ceRNA) for miR-422a, leading to the downregulation of MEF2D.
  • Knockdown of lncR-D63785 increased miR-422a expression and sensitized gastric cancer cells to doxorubicin (DOX)-induced apoptosis.

Conclusions:

  • lncR-D63785 promotes gastric cancer progression and chemoresistance by sponging miR-422a and upregulating MEF2D.
  • Therapeutic suppression of lncR-D63785, alone or with chemotherapy, presents a promising strategy for gastric cancer treatment.
Keywords:
DOXMEF2Dgastric cancerlncRNAmiR-422a

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