Hypoxia-induced miR-424 decreases tumor sensitivity to chemotherapy by inhibiting apoptosis
Open accessAbstract
Chemotherapy resistance of tumor cells is a big challenge. Adaption to hypoxia is an essential cellular response that is controlled by the master oxygen-sensitive transcription factor HIF1 (hypoxia-inducible factor 1). The mechanism by which tumor cells acquire resistance to chemotherapy under hypoxic conditions is not fully understood. In this study, we found that hypoxia induces miR-424 expression and that miR-424 in turn suppresses the level of PDCD4 protein, a tumor suppressor that is involved in apoptosis, by targeting its 3' untranslated region. Functionally, miR-424 overexpression decreases the sensitivity of cancer cells (HCT116 and A375) to doxorubicin (Dox) and etoposide. In contrast, the inhibition of miR-424 enhanced apoptosis and increased the sensitivity of cancer cells to Dox. In a xenograft tumor model, miR-424 overexpression promoted tumor growth following Dox treatment, suggesting that miR-424 promotes tumor cell resistance to Dox. Furthermore, miR-424 levels are inversely correlated with PDCD4 expression in clinical breast cancer samples. These results suggest that miR-424 is a potential molecular target for tumor therapy.
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Inhibition of HIF-1α could overcome resistance of tumor cells to chemotherapy.
“Numerous reports demonstrated that inhibition of HIF-1α could overcome resistance of tumor cells to chemotherapy [25, 26].”
From Inhibition of HIF-1α by PX-478 enhances the anti-tumor effect of gemcitabine by inducing immunogenic cell death in pancreatic ductal adenocarcinoma (2015) · cites this paper as [26]
The Discussion (page not available in our copy) reports that HIF1α regulates miR-424 expression and that hypoxia-induced miR-424 contributes to chemotherapy resistance. The paper reports increased sensitivity to doxorubicin after inhibiting miR-424, not after inhibiting HIF1α; it therefore supports the proposed pathway but not the specific intervention attributed to it. (LLM, conf=0.82)
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- Authors
- Zhang, D., Shi, Z., Li, M., & Mi, J.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Dalian Medical University (CN)
- Corresponding author
- Li, M
- Mi, J
- Venue
- Cell Death & Disease
- Published
- 2014-06-26
- Volume
- 5
- Issue
- 6
- Pages
- e1301-e1301
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC4611715
- OpenAlex
- W1997934991
- Cited by
- 81
- References
- 18
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 6 · 2023: 2 · 2022: 6 · 2021: 7 · 2020: 13 · 2019: 8 · 2018: 11 · 2017: 6 · 2016: 8 · 2015: 9 · 2014: 2
- FWCI
- 2.67
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Death and Disease (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (973 Program, 81372194)
- National Key Research and Development Program of China (2012CB910102)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- miR-424, PDCD4, tumor hypoxia, chemoresistance, doxorubicin, apoptosis, HIF-1, microRNA, 3' untranslated region, breast cancer, xenograft tumor growth, etoposide
- MeSH terms
- Animals, Antibiotics, Antineoplastic, Antineoplastic Agents, Phytogenic, Doxorubicin, Etoposide, Humans, Mice, Nude, Neoplasms, RNA, Neoplasm, Cell Hypoxia, Apoptosis, Drug Resistance, Neoplasm, MicroRNAs, Cell Line, Tumor, Mice
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