دورية أكاديمية

PRMT5 promotes chemotherapy‐induced neuroendocrine differentiation in NSCLC

التفاصيل البيبلوغرافية
العنوان: PRMT5 promotes chemotherapy‐induced neuroendocrine differentiation in NSCLC
المؤلفون: Qi Shen, Yi Liu, Xuehong Deng, Chang‐Deng Hu
المصدر: Thoracic Cancer, Vol 14, Iss 18, Pp 1764-1773 (2023)
بيانات النشر: Wiley, 2023.
سنة النشر: 2023
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: acquired resistance, chemotherapy, NED, neuroendocrine differentiation, PRMT5, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: Abstract Background In response to therapeutic treatments, cancer cells can exhibit a variety of resistance phenotypes including neuroendocrine differentiation (NED). NED is a process by which cancer cells can transdifferentiate into neuroendocrine‐like cells in response to treatments, and is now widely accepted as a key mechanism of acquired therapy resistance. Recent clinical evidence has suggested that non‐small cell lung cancer (NSCLC) can also transform into small cell lung cancer (SCLC) in patients treated with EGFR inhibitors. However, whether chemotherapy induces NED to confer therapy resistance in NSCLC remains unknown. Methods We evaluated whether NSCLC cells can undergo NED in response to chemotherapeutic agents etoposide and cisplatin. By Knock‐down of PRMT5 or pharmacological inhibition of PRMT5 to identify its role in the NED process. Results We observed that both etoposide and cisplatin can induce NED in multiple NSCLC cell lines. Mechanistically, we identified protein arginine methyltransferase 5 (PRMT5) as a critical mediator of chemotherapy‐induced NED. Significantly, the knock‐down of PRMT5 or pharmacological inhibition of PRMT5 suppressed the induction of NED and increased the sensitivity to chemotherapy. Conclusion Taken together, our results suggest that targeting PRMT5 may be explored as a chemosensitization approach by inhibiting chemotherapy‐induced NED.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1759-7714
1759-7706
Relation: https://doaj.org/toc/1759-7706; https://doaj.org/toc/1759-7714
DOI: 10.1111/1759-7714.14921
URL الوصول: https://doaj.org/article/da8d3537b4d74adb9318ad7703e46e36
رقم الأكسشن: edsdoj.8d3537b4d74adb9318ad7703e46e36
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:17597714
17597706
DOI:10.1111/1759-7714.14921