دورية أكاديمية

MiR-141-3p promotes malignant progression in prostate cancer through AlkB homolog 5-mediated m6A modification of protein arginine methyltransferase 6

التفاصيل البيبلوغرافية
العنوان: MiR-141-3p promotes malignant progression in prostate cancer through AlkB homolog 5-mediated m6A modification of protein arginine methyltransferase 6
المؤلفون: Xun Li, Bide Liu, Shuheng Wang, Jiuzhi Li, Xiaohu Ge
المصدر: Chinese Journal of Physiology, Vol 66, Iss 1, Pp 43-51 (2023)
بيانات النشر: Wolters Kluwer Medknow Publications, 2023.
سنة النشر: 2023
المجموعة: LCC:Physiology
مصطلحات موضوعية: mir-141-3p, prostate cancer, alkb homolog 5, m6a, protein arginine methyltransferase 6, Physiology, QP1-981
الوصف: Prostate cancer (PCa) is one of the leading causes of cancer-related death in males worldwide and exploring more reliable biomarkers for PCa is essential for the diagnosis and therapeutics for the disease. Although the functions of miR-141-3p and AlkB homolog 5 (ALKBH5) were identified in some cancers, whether they were involved in the development of PCa remains unclear. In this study, reverse transcription-quantitative polymerase chain reaction unveiled that the expression of ALKBH5 was reduced in PCa tissues and was negatively correlated with miR-141-3p. ALKBH5 attenuated the malignant development of PCa through suppressing the growth, migration, invasion, and sphere formation abilities of PCa cells. In addition, the luciferase activity assay identified that ALKBH5 was corroborated as a downstream target of miR-141-3p. Moreover, miR-141-3p expression was boosted in PCa tissues and cells and inhibition of miR-141-3p suppressed the tumor growth of PCa in vivo. Moreover, ALKBH5 was confirmed to suppress protein arginine methyltransferase 6 (PRMT6) expression through N6-methyladenosine (m6A) modification. We further identified that miR-141-3p-modulated PRMT6 level through mediating ALKBH5. Furthermore, PRMT6 level was positively correlated with miR-141-3p level and negatively associated with ALKBH5 level. Finally, rescue assays also uncovered that miR-141-3p aggravated PCa development by regulating PRMT6. In conclusion, miR-141-3p accelerated the malignant progression of PCa through ALKBH5-mediated m6A modification of PRMT6, which might offer a novel insight into the role of miR-141-3p and ALKBH5 in the treatments of PCa patients.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 0304-4920
2666-0059
Relation: http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2023;volume=66;issue=1;spage=43;epage=51;aulast=Li; https://doaj.org/toc/0304-4920; https://doaj.org/toc/2666-0059
DOI: 10.4103/cjop.CJOP-D-22-00071
URL الوصول: https://doaj.org/article/336269bae2024efeb1842a7b00971bb3
رقم الأكسشن: edsdoj.336269bae2024efeb1842a7b00971bb3
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:03044920
26660059
DOI:10.4103/cjop.CJOP-D-22-00071