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TW37 enhances the pro-apoptosis and anti-migration ability of gefitinib in Non-Small Cell Lung Cancer
- Source :
- Cellular and Molecular Biology. 64:6-10
- Publication Year :
- 2018
- Publisher :
- CMB Association, 2018.
-
Abstract
- B cell leukemia-2 (Bcl-2) plays important roles in the development of tumor and drug resistance. The growth of tumor cells can be inhibited by downregulating the abnormal expression of Bcl-2 protein. TW37, an effective inhibitor of Bcl-2 protein, has now been widely studied in many tumors. In our study, it was found that TW37 exerted a significant effect on the proliferation, apoptosis and migration of Non-Small Cell Lung Cancer cells. Bcl-2 is also a key downstream factor of many signaling pathways such as Epidermal Growth Factor Receptor (EGFR). TW37 enhanced the inhibition of tumorigenesis by gefitinib, an EGFR-Tyrosine Kinase Inhibitor drug. Moreover, TW37 can promote apoptosis ability by inhibiting the phosphorylation level of EGFR protein in H1975 cells. Overall, TW37 enhances the pro-apoptosis and anti-migration ability of gefitinib in Non-Small Cell Lung Cancer.
- Subjects :
- 0301 basic medicine
Apoptosis
Respiratory Mucosa
medicine.disease_cause
03 medical and health sciences
Gefitinib
Cell Movement
Cell Line, Tumor
Antineoplastic Combined Chemotherapy Protocols
medicine
Humans
Sulfones
Epidermal growth factor receptor
Phosphorylation
Lung cancer
B cell
Cell Proliferation
Dose-Response Relationship, Drug
030102 biochemistry & molecular biology
biology
Chemistry
Kinase
Drug Synergism
Epithelial Cells
General Medicine
medicine.disease
ErbB Receptors
Gene Expression Regulation, Neoplastic
medicine.anatomical_structure
Proto-Oncogene Proteins c-bcl-2
Benzamides
Quinazolines
Cancer research
biology.protein
Signal transduction
Carcinogenesis
Signal Transduction
medicine.drug
Subjects
Details
- ISSN :
- 1165158X and 01455680
- Volume :
- 64
- Database :
- OpenAIRE
- Journal :
- Cellular and Molecular Biology
- Accession number :
- edsair.doi.dedup.....0d6844f83a08fed2dc5dc9d2e32e88de
- Full Text :
- https://doi.org/10.14715/cmb/2018.64.4.2