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UPR-Induced miR-616 Inhibits Human Breast Cancer Cell Growth and Migration by Targeting c-MYC
Vahid Arabkari1,2, Afrin Sultana1, David Barua1
1Discipline of Pathology, Cancer Progression and Treatment Research Group, Lambe Institute for Translational Research, School of Medicine, University of Galway, H91 TK33 Galway, Ireland.
International Journal of Molecular Sciences
|September 9, 2023
Summary
MicroRNA-616, found within the CHOP gene, inhibits breast cancer cell growth by targeting c-MYC. Both CHOP protein and miR-616 cooperate to suppress cancer progression.
Area of Science:
- Molecular Biology
- Cancer Biology
- Gene Regulation
Background:
- C/EBP homologous protein (CHOP) is induced by unfolded protein response (UPR) and triggers ER stress-induced apoptosis.
- MicroRNA-616 (miR-616) is encoded within the CHOP gene, but its UPR regulation and function in breast cancer remain unclear.
Purpose of the Study:
- To investigate the regulation of miR-616 during ER stress and its role in breast cancer.
- To elucidate the mechanism by which miR-616 affects cancer cell proliferation.
Main Methods:
- Analysis of miR-616 and CHOP expression in human breast cancer.
- Induction of ER stress and monitoring of miR-616 expression via PERK pathway.
- Overexpression and knockout of miR-616 in cancer cells.
- Assessment of cell proliferation and colony formation.
- Identification of miR-616 targets using bioinformatics and experimental validation.
Main Results:
- miR-616 and its host gene CHOP are downregulated in human breast cancer.
- ER stress increases miR-616 expression, primarily via the PERK pathway.
- miR-616 suppresses breast cancer cell proliferation and colony formation.
- miR-616 inhibits c-MYC expression by binding to its coding region.
Conclusions:
- The CHOP locus has a dual function: CHOP protein induces apoptosis, while miR-616 inhibits proliferation.
- miR-616 acts as a tumor suppressor in breast cancer by targeting c-MYC.
- CHOP and miR-616 cooperate to inhibit cancer progression.
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