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TERT attenuated ER stress-induced cell death.
Toru Hosoi1, Yuki Inoue1, Kanako Nakatsu1
1Department of Pharmacotherapy, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Biochemical and Biophysical Research Communications
|April 22, 2014
Summary
Cancer cells survive nutrient deprivation by activating endoplasmic reticulum (ER) stress, which increases telomerase reverse transcriptase (TERT) expression. This ER stress-TERT axis helps tumor cells withstand harsh conditions, promoting cancer progression.
Area of Science:
- Molecular Biology
- Cancer Research
- Cellular Stress Response
Background:
- Tumor cells often exist in nutrient-deprived microenvironments.
- Mechanisms enabling tumor cell survival under stress are not fully understood.
- Endoplasmic reticulum (ER) stress is a cellular response to environmental challenges.
Purpose of the Study:
- To investigate the role of glucose deprivation in inducing ER stress in breast cancer cells.
- To explore the relationship between ER stress and telomerase reverse transcriptase (TERT) expression.
- To elucidate the survival mechanisms of tumor cells under nutrient-deprived conditions.
Main Methods:
- Utilized the MCF-7 breast cancer cell line.
- Induced ER stress by depriving cells of glucose.
- Measured TERT expression in response to ER stress.
- Assessed the impact of TERT overexpression on ER stress-induced cell death.
Main Results:
- Glucose deprivation led to significant ER stress in MCF-7 cells.
- ER stress specifically activated the expression of TERT.
- Overexpression of TERT reduced ER stress-induced cell death, indicating a protective role.
Conclusions:
- ER stress induces TERT expression as a survival mechanism for tumor cells.
- The 'ER stress-TERT axis' is a novel pathway contributing to tumor progression under stress.
- Targeting this axis may offer new therapeutic strategies for cancers in stressed environments.
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