دورية أكاديمية
Adaptor protein LNK promotes anaplastic thyroid carcinoma cell growth via 14-3-3 ε/γ binding
| العنوان: | Adaptor protein LNK promotes anaplastic thyroid carcinoma cell growth via 14-3-3 ε/γ binding |
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| المؤلفون: | Zhao-Ming Zhong, Xue Chen, Xiao Qi, Xue-Min Wang, Chun-Yan Li, Ru-Jia Qin, Shi-Qi Wang, Jin Liang, Mu-Sheng Zeng, Chuan-Zheng Sun |
| المصدر: | Cancer Cell International, Vol 20, Iss 1, Pp 1-12 (2020) |
| بيانات النشر: | BMC, 2020. |
| سنة النشر: | 2020 |
| المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens LCC:Cytology |
| مصطلحات موضوعية: | Adaptor protein, Anaplastic thyroid carcinoma, Cell growth, LNK, 14-3-3 ε/γ, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671 |
| الوصف: | Abstract Background Rapid progression contributes to treatment failure in anaplastic thyroid carcinoma (ATC) patients. In a preliminary study, we demonstrated that some hematopoietic factors may be involved in the progression of ATC. The adaptor protein LNK, which is a negative regulator of hematopoietic cytokine signalling, has been studied extensively in malignant hematopoietic cells. However, there are few studies on LNK in solid tumours. Methods Real-time PCR, immunohistochemistry (IHC) and western blot analysis of LNK were performed on ATC cells, differentiated thyroid cancer (DTC) cells and normal thyroid cells. In vitro assays (including pull-down, liquid chromatography-mass spectrometry (LC–MS), co-IP, MTT and colony formation) were performed to validate the effect of LNK on ATC progression and elucidate the molecular mechanisms. Results Compared with DTC cells and normal thyroid cells, ATC cells exhibit overexpression of LNK. In addition, LNK overexpression results in increased proliferation of ATC cells. Conversely, LNK knockdown significantly suppresses ATC cell proliferation. LC–MS identified the 14-3-3 ε/γ protein as a LNK binding partner. Finally, the results indicate that LNK overexpression significantly enhances the anti-apoptotic ability of ATC cells via the Akt-NFκB-Bcl-2/Bcl-xL pathway and that the oncogenic effect of LNK largely depends on 14-3-3 ε/γ binding. Conclusions The present study elucidated the important role of LNK in the growth of ATC opposite to its behaviour in the hematopoietic system and indicates that LNK is a potential target for the treatment of ATC. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1475-2867 |
| Relation: | https://doaj.org/toc/1475-2867 |
| DOI: | 10.1186/s12935-019-1090-9 |
| URL الوصول: | https://doaj.org/article/1c0e3a8e79ba422aa4b469ac693913c8 |
| رقم الأكسشن: | edsdoj.1c0e3a8e79ba422aa4b469ac693913c8 |
| قاعدة البيانات: | Directory of Open Access Journals |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 14752867 |
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| DOI: | 10.1186/s12935-019-1090-9 |