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Targeting CXCR4 and FAK reverses doxorubicin resistance and suppresses invasion in non-small cell lung carcinoma
Author(s) -
Miodrag Dragoj,
Zorica Milošević,
Jasna Banković,
Nikola Tanić,
Milica Pešić,
Tijana Stanković
Publication year - 2016
Publication title -
cellular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.698
H-Index - 40
eISSN - 2211-3436
pISSN - 2211-3428
DOI - 10.1007/s13402-016-0304-6
Subject(s) - cancer research , cxcr4 , doxorubicin , focal adhesion , viability assay , flow cytometry , metastasis , lung cancer , abcc1 , chemokine receptor , biology , medicine , cell culture , cancer , chemokine , pathology , signal transduction , receptor , immunology , microbiology and biotechnology , chemotherapy , gene , biochemistry , genetics , atp binding cassette transporter , transporter
Current high lung cancer mortality rates are mainly due to the occurrence of metastases and therapeutic resistance. Therefore, simultaneous targeting of these processes may be a valid approach for the treatment of this type of cancer. Here, we assessed relationships between CXC chemokine receptor type 4 (CXCR4) and focal adhesion kinase (FAK) gene expression levels and expression levels of the drug resistance-related genes ABCB1 and ABCC1, and tested the potential of CXCR4 and FAK inhibitors to reverse doxorubicin (DOX) resistance and to decrease the invasive capacity of non-small cell lung carcinoma (NSCLC) cells.

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