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Long non-coding RNA MEG3 induces renal cell carcinoma cells apoptosis by activating the mitochondrial pathway

Miao Wang1, Tao Huang2, Gang Luo1

  • 1Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban
|July 31, 2015
PubMed

Insights

Long non-coding RNA MEG3 is downregulated in renal cell carcinoma (RCC). Overexpressing MEG3 inhibits RCC cell viability and promotes apoptosis, suggesting therapeutic potential.

Area of Science:

  • Molecular Biology
  • Oncology

Background:

  • Renal cell carcinoma (RCC) is a significant health concern.
  • Long non-coding RNAs (LncRNAs) play crucial roles in cancer development.
  • The role of LncRNA MEG3 in RCC requires further investigation.

Purpose of the Study:

  • To investigate the effect of LncRNA MEG3 on the biological behaviors of RCC cells.
  • To elucidate the underlying mechanism of MEG3's action in RCC.

Main Methods:

  • MEG3 expression was quantified using RT-qPCR in RCC tissues and cell lines.
  • MEG3 was overexpressed in 786-0 RCC cells via plasmid transfection.
  • Cell viability, apoptosis rates, and protein/mRNA expression (Bcl-2, caspase-9, cytochrome c) were assessed.

Main Results:

  • MEG3 expression was significantly downregulated in RCC tissues and cell lines.
  • MEG3 overexpression reduced 786-0 cell viability and increased apoptosis.
  • MEG3 overexpression affected apoptosis-related proteins and Bcl-2 mRNA levels, indicating mitochondrial pathway activation.

Conclusions:

  • LncRNA MEG3 is downregulated in RCC.
  • MEG3 induces apoptosis in RCC cells, likely through the mitochondrial pathway.
  • MEG3 may serve as a potential therapeutic target for RCC.

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