AdMETase/SeMET therapy was effective against Bcl-2-overproducing A549 lung cancer cells, which were resistant to staurosporine-induced apoptosis, with a strong bystander effect.
Additionally, TRIM32 overexpression promoted lung cancer cell proliferation and motility and mediated the expression of Bax, Bcl-2, cleaved caspase-3, matrix metalloproteinase-2 (MMP-2) and MMP-9 were inhibited by JAK2/STAT3 signaling inhibitor (AG490).
In addition, SOX9 was identified as a transcription factor of FOXA1 in lung cancer and involved in affecting the expression of FOXA1 targeted genes-Bcl2, CDKN1B, RPRM and NKX2.
Result from the present study demonstrated that treatment with pemetrexed suppressed lung cancer cell proliferation, inhibited mRNA and protein expression levels of anti‑apoptotic Bcl2, and increased the mRNA and the protein expression levels of pro‑apoptotic p53 and apoptosis regulator BAX.
Heat shock protein family A member 12B (HSPA12B) protein was negatively regulated by uc.454 at the posttranscriptional level by dual-luciferase reporter assay and affected the expressions of Bcl-2 family members, which finally induced LC apoptosis.
These results demonstrated that TMPZ could suppress carcinogenesis of lung cancer cells through blocking cell cycle and inducing mitochondria-dependent apoptosis by regulating Caspase-3 and Bax/Bcl-2, suggesting that TMPZ may be a promising drug to treat lung cancer.
The objective of this study is to determine whether ferulenol has an anticancer effect by regulation the Bcl2 protein expression in lung cancer induced by benzo[a]pyrene in Wistar rats.
The present study concluded that baicalein combined with cisplatin induced cytotoxicity and apoptosis of A549 cells, and such activity may be associated with the regulation of Bcl-2, Bax and caspase-3, indicating a promising alternative method for lung cancer.
Differentiating responses of lung cancer cell lines to Doxorubicin exposure: in vitro Raman micro spectroscopy, oxidative stress and bcl-2 protein expression.
Further, western blot analysis was performed for proapoptotic protein Bax and antiapoptotic protein Bcl-2 and the results demonstrated that there was up regulation of Bax and down regulation of Bcl-2 suggesting that these compounds induced apoptosis in human lung cancer cells, A549.
Furthermore, knockdown of PHP14 in lung cancer cells correlated with decreased expression of a subset of NF-κB-regulated genes, such as BCL-2, COX-2, MCP-1, MMP9 and VEGF-C, which play an important role in tumor progression.
Conversely, up-regulation of c-Met and Bcl2 were confirmed in tissue samples of human lung cancer, with its level inversely correlated with miR-206 expression.
Further, we transfected microRNA-449a mimic and inhibitor in lung cancer cell line A549, and used western blot to determine the expression level of apoptosis-related molecules Bcl-2 and p53.
Thus, PIAS3 may represent a promising lung cancer therapeutic target because of its p53-independent efficacy and its potential to synergize with Bcl-2 targeted inhibitors.