Academic Journal

Inhibition of cell-adhesion protein DPYSL3 promotes metastasis of lung cancer

التفاصيل البيبلوغرافية
العنوان: Inhibition of cell-adhesion protein DPYSL3 promotes metastasis of lung cancer
المؤلفون: Yang Yang, Yan Jiang, Dong Xie, Ming Liu, Nan Song, Junjie Zhu, Jiang Fan, Chenfang Zhu
المصدر: Respiratory Research, Vol 19, Iss 1, Pp 1-7 (2018)
بيانات النشر: BMC, 2018.
سنة النشر: 2018
المجموعة: LCC:Diseases of the respiratory system
مصطلحات موضوعية: DPYSL3, LLC cells, EMT, Lung cancer, Metastasis, Diseases of the respiratory system, RC705-779
الوصف: Abstract Background Our previous screening study suggested that the cell-adhesions protein Dihydropyrimidinase-like 3 (DPYSL3) was a candidate metastatic lung cancer related molecule. This study aimed to analyze the correlation between DPYSL3 and metastatic lung cancer. Methods Stable DPYSL3 knockdown Lewis lung carcinoma (LLC) cells were constructed with a retroviral system. Cell migration and invasion assays were performed to determine the role of DPYSL3 in LLC cells’ migration and invasion changes. A metastatic lung tumor model in which the stable DPYSL3 knockdown LLC cells were injected through tail vein was used to analyze the role of DPYSL3 in tumor metastasis in vivo. The correlation between DPYSL3 expression and the survival time of lung cancer patients were analyzed in KMPLOT database. Results Knockdown of DPYSL3 promoted the migratory and invasive of LLC cells compared to the control group. Meanwhile, the motility of LLC cells was also increased with the inhibition of DPYSL3. The TGFβ-induced EMT increased when DPYSL3 was inhibited. The expression of EMT markers, TWIST1 and N-cadherin, significantly increased to almost two times with the knockdown of DPYSL3. Furthermore, inhibition of DPYSL3 promoted the progression of metastatic xenograft in C57BL/6 mice. The expression level of DPYSL3 decreased in lung cancer patients with distant metastasis. Conclusions Knockdown of DPYSL3 promoted the metastatic ability of LLC cells in vitro and in vivo.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1465-993X
Relation: http://link.springer.com/article/10.1186/s12931-018-0740-0; https://doaj.org/toc/1465-993X
DOI: 10.1186/s12931-018-0740-0
URL الوصول: https://doaj.org/article/c160a132265d4f9e88c7c8115d8922d1
رقم الانضمام: edsdoj.160a132265d4f9e88c7c8115d8922d1
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:1465993X
DOI:10.1186/s12931-018-0740-0