Academic Journal
MYSM1 induces apoptosis and sensitizes TNBC cells to cisplatin via RSK3–phospho-BAD pathway
العنوان: | MYSM1 induces apoptosis and sensitizes TNBC cells to cisplatin via RSK3–phospho-BAD pathway |
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المؤلفون: | Xiaolin Guan, Xin Meng, Keyu Zhu, Jinyan Kai, Yixuan Liu, Qian Ma, Ying Tong, Hui Zheng, Suhong Xie, Xiaolu Ma, Yanchun Wang, Renquan Lu, Lin Guo |
المصدر: | Cell Death Discovery, Vol 8, Iss 1, Pp 1-11 (2022) |
بيانات النشر: | Nature Publishing Group, 2022. |
سنة النشر: | 2022 |
المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens LCC:Cytology |
مصطلحات موضوعية: | Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671 |
الوصف: | Abstract Breast cancer is one of the leading causes of mortality among women. Triple-negative breast cancer (TNBC) is responsible for a large percentage of all breast cancer deaths in women. This study demonstrated the function of Myb-like, SWIRM, and MPN domains 1 (MYSM1), an H2A deubiquitinase (DUB), in TNBC. MYSM1 expression was drastically decreased in breast cancer, especially in TNBC, suggesting a potential anticancer effect. Overexpressing and suppressing MYSM1 expression in TNBC cell lines led to significant biological changes in cell proliferation. Furthermore, MYSM1 overexpression increased cisplatin-induced apoptosis, which might be attributed to RSK3 inactivation and the subsequently decreased phosphorylation of Bcl-2 antagonist of cell death (BAD) (Ser 112). The findings suggest that MYSM1 is a potential target for regulating cell apoptosis and suppressing resistance to cisplatin in TNBC. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2058-7716 |
Relation: | https://doaj.org/toc/2058-7716 |
DOI: | 10.1038/s41420-022-00881-1 |
URL الوصول: | https://doaj.org/article/438b94b038eb42068849b5371c1fee78 |
رقم الانضمام: | edsdoj.438b94b038eb42068849b5371c1fee78 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 20587716 |
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DOI: | 10.1038/s41420-022-00881-1 |