Searching for just a few words should be enough to get started. If you need to make more complex queries, use the tips below to guide you.
Article type: Research Article
Authors: Xu, Zhi-Honga | Liu, Cai-Honga | Hang, Jun-Biaob | Gao, Bei-Lic | Hu, Jia-Ana; *
Affiliations: [a] Department of Geriatrics, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China | [b] Department of Thoracic Surgery, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China | [c] Department of Respiration, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China
Correspondence: [*] Corresponding: Jia-an Hu, Department of Geriatrics, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China. Tel.: +86 21 64370045; E-mail: [email protected].
Abstract: Tyrosine kinase inhibitors (TKIs), a novel group of target-specific anti lung cancer drugs, have recently been found to resistant to some NSCLC cells which have the T790M EGFR mutation. However, recent investigations on the therapies of resistance to EGFR-TKIs are very limited. Therefore, it is important to develop more effective therapies to reverse EGFR-TKIs resistance. In our present study, erlotinib was used as the TKIs drug and the effects of the erlotinib on cell growth were evaluated. Cell viability and concentration dependent studies were performed using HCI-H1975 and HCI-H1299 cells alone with erlotinib, respectively. Further combined with rituximab, the results showed that erlotinib and rituximab were significantly inhibited the cell growth. Furthermore, the combination of erlotinib and rituximab greatly decreased the expression of p-mTOR and p-EGFR. Additional results from western blotting and immunofluorescence assays demonstrated that the accumulation of rictor was also decreased on MAM. Thus, all these results suggested that EGFR-TKIs combined with CD20 mono-antibody significantly decrease the cell growth of H1975 cells and H1299, with T790M EGFR mutation, and inhibit the localization of the key mTOR pathway proteins to MAM. So, it may be a promising strategy for overcoming EGFR TKI resistance in NSCLC patients.
Keywords: Rituximab, tyrosine kinase inhibitors, ER-membrane, NSCLC cells
DOI: 10.3233/CBM-170575
Journal: Cancer Biomarkers, vol. 20, no. 4, pp. 581-588, 2017
IOS Press, Inc.
6751 Tepper Drive
Clifton, VA 20124
USA
Tel: +1 703 830 6300
Fax: +1 703 830 2300
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
IOS Press
Nieuwe Hemweg 6B
1013 BG Amsterdam
The Netherlands
Tel: +31 20 688 3355
Fax: +31 20 687 0091
[email protected]
For editorial issues, permissions, book requests, submissions and proceedings, contact the Amsterdam office [email protected]
Inspirees International (China Office)
Ciyunsi Beili 207(CapitaLand), Bld 1, 7-901
100025, Beijing
China
Free service line: 400 661 8717
Fax: +86 10 8446 7947
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
如果您在出版方面需要帮助或有任何建, 件至: [email protected]