Epithelial-mesenchymal transition mediates anoikis resistance and enhances invasion in pleural effusion-derived human lung cancer cells.
Epithelial-mesenchymal transition mediates anoikis resistance and enhances invasion in pleural effusion-derived human lung cancer cells.
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DOI：
10.3892/ol.2013.1108
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发表时间：
2013-03
期刊：
影响因子：
2.9
通讯作者：
Chanvorachote P
中科院分区：
文献类型：
--
作者：
Chunhacha P;Sriuranpong V;Chanvorachote P
上皮-间质转化（EMT）参与了肿瘤的病理过程，尤其是肿瘤的侵袭和转移。目前的研究表明，EMT是从患者中分离的肺癌细胞的转移潜力的关键。发现P1原代肺癌细胞与已建立的A549、H23和H460肺癌细胞相比表现出增加的失巢凋亡抗性。迁移和侵袭实验结果显示，P1和A549细胞的侵袭能力高于H23和H460细胞。P1细胞的迁移能力与H23和H460细胞相似，而A549细胞的迁移能力较强，具有上级迁移能力。蛋白质印迹分析表明，虽然在所有肺癌细胞中的E-钙粘蛋白水平被确定为可比的，P1细胞表达的N-钙粘蛋白的最高水平。在本研究中，首次证明了细胞的脱离刺激E-钙粘蛋白进一步转变为N-钙粘蛋白。此外，这种观察在P1细胞中更为明显。这些观察结果突出了EMT在癌症转移中的重要性。为了研究种族对癌细胞行为的影响，将来必须分析大量泰国患者来源的细胞系。
Epithelial-mesenchymal transition (EMT) is implicated in cancer pathological processes, particularly cancer invasion and metastasis. The present study demonstrated that EMT was critical for the metastasic potential of lung cancer cells isolated from a patient. P1 primary lung cancer cells were found to exhibit increased anoikis resistance compared with established A549, H23 and H460 lung cancer cells. Results of migration and invasion assays revealed that the invasion capability of P1 and A549 cells was higher than that of H23 and H460 cells. However, the migration of P1 cells was similar to that of H23 and H460 cells while A549 demonstrated a superior migrating ability. Western blot analysis indicated that while E-cadherin levels in all lung cancer cells were identified as comparable, P1 cells expressed the highest levels of N-cadherin. In the present study, detachment of cells was demonstrated for the first time to stimulate further transition of E-cadherin to N-cadherin. In addition, this obervation was more pronounced in P1 cells. These observations highlight the importance of EMT in cancer metastasis. In order to study the effect of ethnicity on cancer cell behavior, in the future a large number of Thai patient-derived cell lines must be analyzed.
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影响因子：
4.8
作者：
Luanpitpong, Sudjit;Talbott, Siera Jo;Chanvorachote, Pithi
通讯作者：
Chanvorachote, Pithi
影响因子：
2.9
作者：
Chanvorachote, Pithi;Luanpitpong, Sudjit;Sriuranpong, Virote
通讯作者：
Sriuranpong, Virote
影响因子：
2.4
作者：
Vatanasapt, V;Sriamporn, S;Vatanasapt, P
通讯作者：
Vatanasapt, P
影响因子：
5.2
作者：
Ko, Hyeonseok;Kim, Seongrak;Kim, Kunhong
通讯作者：
Kim, Kunhong
影响因子：
11.2
作者：
Tsuji T;Ibaragi S;Hu GF
通讯作者：
Hu GF