The results revealed that GA inhibited the proliferation and induced the apoptosis of NSCLC A549 cells in dose‑ and time‑dependent manners, which was associated with upregulated B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax) and downregulated Bcl‑2.
<b>Conclusion:</b> HEATR1 inhibition activated p53 by reducing ribosome biogenesis, which subsequently led to NSCLC cell apoptosis and reduced cell survival through the p53-PUMA-BAX/BCL2 axis.
Furthermore, western blot analysis revealed that in NSCLC cell lines, the combined treatment with gefitinib and ginsenoside Rg3 increased protein expression levels of pro-apoptotic proteins Bax and cleaved-caspase-3, whilst the expression level of anti-apoptotic protein Bcl-2 decreased.
Overexpression of CD 133 and BCL-2 in non-small cell lung cancer with neuroendocrine differentiation after transformation in ALK rearrangement-positive adenocarcinoma.
Kaplan-Meier and Cox regression analysis indicated that low miR-630, high Bcl-2, and a combination of both may independently predict poor overall survival and short relapse-free survival in patients with NSCLC.
In the present study the anti-cancer mechanism of pyrazole, was examined by the expression level of proteins Epidermal growth factor receptor (EGFR), Bcl-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2) and Cyclin-dependent kinase-2 (CDK-2) which are commonly associated with the cell signaling pathways that control cell survival and apoptosis, that could facilitate to develop a novel target and effective treatment approach for patients with NSCLC.
Thus, inhibition of anti-apoptotic BCL-2 family proteins has been proposed as a possible antineoplastic strategy, and BCL-2 inhibitors are currently being clinically trailed in patients with leukemia, lymphoma or non-small cell lung cancer.
Herein, we showed the p53-independent apoptosis by decrease the expression of phosphorylated Akt-mediated suppression of NF-κB that is also substantiated with the downregulation of anti-apoptotic factors Bcl-2 and Bcl-xl in NSCLC, resulting in an attenuation of TRAIL resistance in combined treatment.
The present study aimed to determine the possible anticancer effects of berberine hydrochloride treatment on human non-small cell lung cancer (NSCLC) cell proliferation and apoptosis via the matrix metalloproteinase 2 (MMP-2) and the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) signaling pathway.
Compared with adjacent normal tissues, the expression of miR-183 and the mRNA and protein expression of E-cadherin and Bax were decreased in NSCLC tissues, while mRNA and protein expression of MTA1, Vimentin, snail, PCNA and Bcl-2 were increased.
Mechanistically, EGFR mutations promoted NSCLC cell apoptosis in response to X-ray irradiation through the upregulation of proapoptotic protein Bax and downregulation of anti-apoptotic proteins such as Bcl-2 and DNA-dependent protein kinase catalytic subunit.
Previous studies have suggested that the B‑cell lymphoma 2 (Bcl‑2) inhibitor, TW37, may induce apoptosis of the non‑small cell lung cancer cell line, H1975/epidermal growth factor receptor‑tyrosine kinase inhibitor (EGFR‑TKI), which exhibits secondary resistance to EGFR‑TKI.
All these experiments were designed to investigate whether lncRNA MEG3 participated in the pathogenesis of NSCLC through inhibiting the expression of BRCA1 and Bcl-2 and promoting Bax expression.
Additionally, a flow cytometry assay and Western blotting showed that melittin induced NSCLC NCI-H441 cell apoptosis along with significant elevation of caspase-2 and Bax, which are regulators of cell apoptosis, and reduced Bcl-2 protein expression compared with dimethyl sulfoxide control.
Indeed, the same MCL1 stabilization system was also observed in several NSCLC cell lines; in these cells, their specific molecular-targeted drug or ABT-263 (Navitoclax), the specific inhibitor of BCL-2 and BCL-X<sub>L</sub>, but not of MCL1, effectively induced apoptosis in combination with CMA inhibition.
We assessed the biological activity (STR, mitochondrial membrane potential, expression level of Bcl-2 family proteins) of gefitinib on NSCLCs at different cell densities.