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Ad5-EMC6 mediates antitumor activity in gastric cancer cells through the mitochondrial apoptosis pathway

Riyong Li1, Xiaokun Wang2, Xuan Zhang1

  • 1Department of Immunology, Peking University School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China.

Biochemical and Biophysical Research Communications
|April 16, 2019
PubMed

Insights

Endoplasmic reticulum membrane protein complex subunit 6 (EMC6) overexpression induces apoptosis in gastric cancer cells by activating the mitochondrial pathway. This finding supports EMC6

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Endoplasmic reticulum membrane protein complex subunit 6 (EMC6), also known as transmembrane protein 93 (TMEM93), is an autophagy-related protein.
  • The precise cellular functions and interaction partners of EMC6 are not fully elucidated.
  • Previous studies indicate EMC6 overexpression can inhibit cancer cell growth and induce apoptosis.

Purpose of the Study:

  • To investigate the role of EMC6 in gastric cancer.
  • To elucidate the molecular mechanisms underlying EMC6-induced apoptosis in gastric cancer cells.
  • To evaluate the therapeutic potential of EMC6 in gastric cancer treatment.

Main Methods:

  • Adenovirus-mediated ectopic overexpression of EMC6 (Ad5-EMC6) in BGC823 and SGC7901 gastric cancer cell lines.
  • Analysis of apoptosis-related signaling pathways, including ERK1/2, BCL-2, tBID, and BAX.
  • Assessment of mitochondrial membrane potential.
  • In vivo studies using a xenograft tumor model in nude mice.
  • Evaluation of EMC6's effect on sensitivity to etoposide chemotherapy.

Main Results:

  • Ad5-EMC6 overexpression decreased ERK1/2 activity and BCL-2 levels while increasing tBID and BAX expression.
  • EMC6 induced apoptosis through the mitochondrial pathway, evidenced by decreased mitochondrial membrane potential.
  • Ad5-EMC6 impaired gastric cancer cell tumorigenesis in a xenograft model.
  • EMC6 enhanced the sensitivity of gastric cancer cells to etoposide.

Conclusions:

  • EMC6-induced apoptosis in gastric cancer cells is mediated, at least in part, by the mitochondrial apoptosis pathway.
  • EMC6 demonstrates potential as a therapeutic agent for gastric cancer.
  • Further clinical investigation of Ad5-EMC6 for gastric cancer treatment is warranted.
Keywords:
ApoptosisBCL-2EMC6ERK1/2Gastric cancer

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