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LncRNA-mediated regulation of cisplatin response in breast cancer
S. Azizidoost, M. Sheykhi-Sabzehpoush, MAG. Dari, M. Józkowiak, J. Niebora, D. Domagała, K. Data, P. Dzięgiel, P. Mozdziak, M. Farzaneh, B. Kempisty
Language English Country Germany
Document type Journal Article, Review
- MeSH
- Drug Resistance, Neoplasm * genetics MeSH
- Cisplatin * therapeutic use pharmacology MeSH
- Humans MeSH
- Breast Neoplasms * drug therapy genetics pathology metabolism MeSH
- Antineoplastic Agents * therapeutic use pharmacology MeSH
- Gene Expression Regulation, Neoplastic * drug effects MeSH
- RNA, Long Noncoding * genetics metabolism MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
Breast cancer is a prevalent and aggressive disease characterized by high metastasis, recurrence, and mortality rates. While cisplatin is an effective chemotherapy drug, its use is limited by its toxic effects on the body. Despite advancements in therapeutic strategies, the therapeutic response is often unsatisfactory due to drug resistance, leading to poor prognosis. Recent studies have shown that cisplatin interacts with long non-coding RNAs (lncRNAs) and accelerates the development of resistance in tumor cells to therapy. This interaction highlights the complex mechanisms involved in the response of cancer cells to chemotherapy. Several lncRNAs have been identified as key players in mediating cisplatin resistance in breast cancer. These lncRNAs include SNHG15, HULC, HCP5, MT1JP, LncMat2B, DLX6-ASL, Linc00665, CARMN, and Lnc-EinRP44-3:6. These lncRNAs have been shown to target microRNAs and mRNAs and modulate the expression of genes involved in cisplatin resistance, which is important in treating breast cancer.
Atherosclerosis Research Center Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran
Department of Toxicology Poznan University of Medical Sciences Poznan Poland
Graduate Physiology Program North Carolina State University Raleigh NC 27695 USA
Prestage Department of Poultry Science North Carolina State University Raleigh NC 27695 USA
References provided by Crossref.org
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- $a Breast cancer is a prevalent and aggressive disease characterized by high metastasis, recurrence, and mortality rates. While cisplatin is an effective chemotherapy drug, its use is limited by its toxic effects on the body. Despite advancements in therapeutic strategies, the therapeutic response is often unsatisfactory due to drug resistance, leading to poor prognosis. Recent studies have shown that cisplatin interacts with long non-coding RNAs (lncRNAs) and accelerates the development of resistance in tumor cells to therapy. This interaction highlights the complex mechanisms involved in the response of cancer cells to chemotherapy. Several lncRNAs have been identified as key players in mediating cisplatin resistance in breast cancer. These lncRNAs include SNHG15, HULC, HCP5, MT1JP, LncMat2B, DLX6-ASL, Linc00665, CARMN, and Lnc-EinRP44-3:6. These lncRNAs have been shown to target microRNAs and mRNAs and modulate the expression of genes involved in cisplatin resistance, which is important in treating breast cancer.
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