دورية أكاديمية

SIK2 promotes ovarian cancer cell motility and metastasis by phosphorylating MYLK

التفاصيل البيبلوغرافية
العنوان: SIK2 promotes ovarian cancer cell motility and metastasis by phosphorylating MYLK
المؤلفون: Xiu Shi, Xuejiao Yu, Juan Wang, Shimin Bian, Qiutong Li, Fengqing Fu, Xinwei Zou, Lin Zhang, Robert C. Bast Jr., Zhen Lu, Lingchuan Guo, Youguo Chen, Jinhua Zhou
المصدر: Molecular Oncology, Vol 16, Iss 13, Pp 2558-2574 (2022)
بيانات النشر: Wiley, 2022.
سنة النشر: 2022
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: cell motility, metastasis, MYLK, ovarian cancer, phosphorylation, SIK2, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: Salt‐inducible kinase 2 (SIK2; also known as serine/threonine‐protein kinase SIK2) is overexpressed in several cancers and has been implicated in cancer progression. However, the mechanisms by which SIK2 regulates cancer cell motility, migration and metastasis in ovarian cancer have not been fully discovered. Here, we identify that SIK2 promotes ovarian cancer cell motility, migration and metastasis in vitro and in vivo. Mechanistically, SIK2 regulated cancer cell motility and migration by myosin light chain kinase, smooth muscle (MYLK)‐meditated phosphorylation of myosin light chain 2 (MYL2). SIK2 directly phosphorylated MYLK at Ser343 and activated its downstream effector MYL2, promoting ovarian cancer cell motility and metastasis. In addition, we found that adipocytes induced SIK2 phosphorylation at Ser358 and MYLK phosphorylation at Ser343, enhancing ovarian cancer cell motility. Moreover, SIK2 protein expression was positively correlated with the expression of MYLK‐pS343 in ovarian cancer cell lines and tissues. The co‐expression of SIK2 and MYLK‐pS343 was associated with reduced median overall survival in human ovarian cancer samples. Taken together, SIK2 positively regulates ovarian cancer motility, migration and metastasis, suggesting that SIK2 is a potential candidate for ovarian cancer treatment.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1878-0261
1574-7891
العلاقة: https://doaj.org/toc/1574-7891Test; https://doaj.org/toc/1878-0261Test
DOI: 10.1002/1878-0261.13208
الوصول الحر: https://doaj.org/article/79adc25e6b85439bb2e5bb149f97ac33Test
رقم الانضمام: edsdoj.79adc25e6b85439bb2e5bb149f97ac33
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:18780261
15747891
DOI:10.1002/1878-0261.13208