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Published on: February 16, 2015
Apoptosis induced by adenosine involves endoplasmic reticulum stress in EC109 cells
Ling-Fei Wu1, Bi-Liu Wei, Yi-Tian Guo
1Department of Gastroenterology, The Second Affiliated Hospital, Shantou University Medical College, Shantou 515041, PR China. lingfeiwu@21cn.com
International Journal of Molecular Medicine
|August 4, 2012
Summary
Adenosine induces apoptosis in esophageal cancer cells by triggering endoplasmic reticulum stress (ERS). This study reveals adenosine inhibits proliferation and activates key ERS proteins, offering new insights into cancer therapy.
Area of Science:
- Oncology
- Cell Biology
- Molecular Mechanisms
Background:
- Apoptosis is crucial for organism development and homeostasis.
- Endoplasmic reticulum stress (ERS) is an intrinsic pathway initiating apoptosis.
- Adenosine is known to induce apoptosis in cancer cells, but the mechanism is unclear.
Purpose of the Study:
- To investigate if adenosine triggers apoptosis in EC109 esophageal carcinoma cells via ERS.
- To elucidate the molecular pathways involved in adenosine-induced apoptosis.
Main Methods:
- MTT assay for cell proliferation.
- Flow cytometry (FCM) and TUNEL assay for apoptosis.
- Western blot for ERS-related proteins (GRP78, cleaved caspase-3, cleaved caspase-4, CHOP, NF-κB p65).
- Electrophoretic mobility shift assay (EMSA) for NF-κB activation.
Main Results:
- Adenosine inhibited EC109 cell proliferation in a dose- and time-dependent manner.
- Adenosine induced cell cycle arrest and increased apoptosis.
- Adenosine upregulated GRP78, cleaved caspase-4, CHOP, NF-κB p65, and cleaved caspase-3 expression.
- Adenosine activated NF-κB p65.
Conclusions:
- Adenosine inhibits EC109 cell proliferation and induces apoptosis through ERS.
- The study demonstrates adenosine's role in upregulating GRP78 and NF-κB p65.
- Adenosine-induced apoptosis involves CHOP and caspase-4 pathways, mediated by ERS.
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