Upregulation of Bcl2 in NSCLC with acquired resistance to EGFR‑TKI
- Hio Teng Cheong
- Fei Xu
- Chi Tung Choy
- Connie Wun Chun Hui
- Tony Shu Kam Mok
- Chi Hang Wong
Published online on: November 9, 2017
Copyright: © Cheong et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Lung cancer has the highest incidence and mortality rate worldwide among all malignancy‑associated mortalities, of which non‑small cell lung cancer accounts for 80% of all cases. Resistance against epidermal growth factor receptor‑tyrosine kinase inhibitors (EGFR‑TKIs) develops following 8‑12 months of disease progression, and is a critical issue. HCC827 cell lines with resistance to EGFR‑TKIs were successfully screened. The half maximal inhibitory concentration values were 1,000‑fold higher than the values for the parental HCC827 cell line, thereby demonstrating cross‑resistance against the same family of TKIs. The expression of B‑cell lymphoma 2 (Bcl2) was markedly increased in the resistant clones, as well as in the patient biopsies. The phosphatase and tensin homolog phosphoinositide 3‑kinase signaling axis is a potential mechanism for acquiring resistance, and therefore targeting Bcl2 may be a useful strategy for further investigations.