Academic Journal

METTL3 promotes colorectal cancer metastasis by promoting the maturation of pri-microRNA-196b

التفاصيل البيبلوغرافية
العنوان: METTL3 promotes colorectal cancer metastasis by promoting the maturation of pri-microRNA-196b
المؤلفون: Huang, Lanlan, Liang, Danlu, Zhang, Yu, Chen, Xiaoting, Chen, Junxiong, Wen, Chuangyu, Liu, Huanliang, Yang, Xiaorong, Yang, Xiangling, Lin, Shaoqiang
المساهمون: National Natural Science Foundation of China, Key discipline project of Guangdong Province
المصدر: Journal of Cancer Research and Clinical Oncology ; volume 149, issue 8, page 5095-5108 ; ISSN 0171-5216 1432-1335
بيانات النشر: Springer Science and Business Media LLC
سنة النشر: 2022
الوصف: Purpose Methyltransferase-like 3 (METTL3), a key member of the m6A methyltransferase complex, is upregulated in multiple human malignancies and plays a role in regulating tumor migration. This study aimed to reveal the underlying mechanism by which METTL3 in regulates the metastasis of colorectal cancer (CRC). Methods We compared METTL3 expression levels in CRC tumor tissues and adjacent nontumor tissues by immunohistochemistry (IHC). The functional roles of METTL3 in CRC were assessed by real-time cell migration assays, wound-healing assays and Transwell assays. miRNA sequencing (miRNA-seq), RNA-binding protein immunoprecipitation (RIP) assays and N6-methyladenosine immunoprecipitation (MeRIP) assays were performed to confirm the molecular mechanism underlying the involvement of METTL3 in CRC cell metastasis. Results We found that METTL3 was overexpressed in CRC tissues. METTL3 knockdown significantly inhibited CRC cell migration and invasion, while METTL3 overexpression had the opposite effects. Furthermore, we demonstrated that METTL3 regulates miR-196b expression via an N6-methyladenosine (m6A)-pri-miR-196b-dependent mechanism and thereby promotes CRC metastasis. Conclusion This study shows the important role of METTL3 in CRC metastasis and provides novel insight into m6A modification in CRC metastasis.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1007/s00432-022-04429-9
DOI: 10.1007/s00432-022-04429-9.pdf
DOI: 10.1007/s00432-022-04429-9/fulltext.html
الاتاحة: http://dx.doi.org/10.1007/s00432-022-04429-9
https://link.springer.com/content/pdf/10.1007/s00432-022-04429-9.pdf
https://link.springer.com/article/10.1007/s00432-022-04429-9/fulltext.html
Rights: https://creativecommons.org/licenses/by/4.0 ; https://creativecommons.org/licenses/by/4.0
رقم الانضمام: edsbas.688F4006
قاعدة البيانات: BASE
الوصف
DOI:10.1007/s00432-022-04429-9