scholarly journals Adenomatous polyposis coli determines sensitivity to the EGFR tyrosine kinase inhibitor gefitinib in colorectal cancer cells

2014 ◽  
Vol 31 (4) ◽  
pp. 1811-1817 ◽  
Author(s):  
YINING ZHANG ◽  
QINGHUAN XIAO ◽  
HUIJING ZHANG ◽  
XUREN SUN ◽  
HUIJUAN GE ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Kinase Inhibitor ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Egfr Tyrosine Kinase Inhibitor ◽  
Colorectal Cancer Cells

scholarly journals Therapeutic targeting truncated adenomatous polyposis coli (APC) proteins for the selective killing of colorectal cancer cells

BMC Genomics ◽  
2014 ◽  
Vol 15 (Suppl 2) ◽  
pp. O3 ◽  
Author(s):  
Lu Zhang ◽  
Sang B Kim ◽  
Ugur Eskiocak ◽  
Bruce Posner ◽  
Priyabrata Das ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Therapeutic Targeting ◽  
Colorectal Cancer Cells

scholarly journals Secreted Phosphoprotein 1 (SPP1) Contributes to Second-Generation EGFR Tyrosine Kinase Inhibitor Resistance in Non-Small Cell Lung Cancer

2019 ◽  
Vol 27 (8) ◽  
pp. 871-877 ◽  
Author(s):  
Xinwen Wang ◽  
Fupeng Zhang ◽  
Xi Yang ◽  
Meiping Xue ◽  
Xiaoli Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Cancer Cells ◽  
Second Generation ◽  
Kinase Inhibitor ◽  
Lung Cancer Cells ◽  
Egfr Tyrosine Kinase Inhibitor ◽  
Egfr Tyrosine Kinase ◽  
Secreted Phosphoprotein 1

Second-generation irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), afatinib, has been approved for treating EGFR mutant lung cancer patients, but the mechanism of acquired resistance to afatinib has not been well studied. In this study, we established afatinib acquired resistant cell lines. Gene array technology was used to screen changes in gene expression between afatinib-resistant lung cancer cells and parental cells. Our results showed that secreted phosphoprotein 1 (SPP1) was significantly increased in afatinib-resistant lung cancer cells. To study the effect of SPP1 on afatinib resistance, siSPP1 was used to knock down SSP1 in afatinib-resistant lung cancer cells. Then sensitivity to afatinib and invasive ability were studied. We found that knockdown of SPP1 increased sensitivity of lung cancer cells to afatinib and decrease the ability of invasion. Of clinical significance, we found that SSP1 was upregulated in lung cancer tissues compared with adjacent normal tissues, and low level of SSP1 was strongly associated with better overall survival. Our results suggest that SPP1 enhanced the second-generation EGFR TKI resistance in lung cancer, and inhibiting SPP1 might be a therapeutic target to overcome afatinib resistance.

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