Our study indicates that the ratio of Bcl-2/Bim could be a SCLC response predictor to cisplatin, and ABT-263 addition could be an effective strategy to improve the activity of chemo- or radio-therapy in SCLC.
In this study, the anti-infective drug nitroxoline (NXQ) was screened out to effectively inhibit cell survival of small-cell lung cancer (SCLC) cells, and induce SCLC cell apoptosis by suppressing antiapoptotic proteins (such as Bcl-2 and MCL1) and upregulating proapoptotic protein Bim.
Mechanistically, we uncover a novel role for gene methylation that helped discriminate high BCL-2-expressing SCLCs.<b>Conclusions:</b> Altogether, our findings identify venetoclax as a promising new therapy for high BCL-2-expressing SCLCs.<i></i>.
In conclusion, our study showed that combination of BCL2 inhibitor with HSP90 inhibitor increased activity in in vitro and in vivo study in only BCL-2 expressing SCLC compared to either single BCL2 inhibitor or HSP inhibitor.
Co-delivery of VP-16 and Bcl-2-targeted antisense on PEG-grafted oMWCNTs for synergistic in vitro anti-cancer effects in non-small and small cell lung cancer.
In this study, we demonstrated for the first time that co-targeting of N-Myc and Bcl-2 resulted in marked synergistic antitumor effects in <i>MYCN</i>-amplified SCLC.
As doxorubicin and dinaciclib also reduced BCL-X<sub>L</sub>, the combinations of BCL-2 inhibitor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic strategies for SCLC.
Our results indicate that the BCL-2rs2279115 genetic variant was associated with SCLC risk in Chinese populations and support the hypothesis that SNPs in regulatory regions of oncogenes might contribute to cancer susceptibility.
Further, increased neuroendocrine marker and decreased EGFR expression as well as greater sensitivity to BCL2 family inhibition are observed in resistant SCLC transformed cancers compared with resistant NSCLCs.
These data underline the possibility of combining IR and Bcl-2/Bcl-XL inhibition in the treatment of SCLC as they underscore the importance of administering conventional and targeted therapies in an optimal sequence.
The anti-apoptotic BCL2 gene was significantly overexpressed in six SCLC cell lines and the BCL2 inhibitor ABT-737 increased apoptosis in all three cell lines tested.
Overexpression of the PI3K isoforms p110-α and p110-β and the antiapoptotic protein Bcl-2 was shown by immunohistochemistry in primary SCLC tissue samples.
We identified the expression of Bcl-2 family genes that correlated best with sensitivity to ABT-263 in a panel of 36 SCLC and 31 leukemia/lymphoma cell lines.
The aim of this study was to investigate whether Etk is involved in the chemoresistance of small cell lung cancer (SCLC) and to correlate the drug resistance associated proteins such as bcl-2, bcl-X(L) and p53.
It was found that high expression of Etk occurs in 74.6% of SCLC cases, but only in 40% of NSCLC cases, and there is marked difference in the expression levels of Bcl-2, Bcl-X(L) and p53 between Etk-positive and Etk-negative SCLC cases.
Inhibition of BCL-2 in small cell lung cancer cell lines with oblimersen, an antisense BCL-2 oligodeoxynucleotide (ODN): in vitro and in vivo enhancement of radiation response.
Several novel therapeutics, including high-potency small molecule inhibitors of Bcl-2 and the Hedgehog signaling pathway, and a recently discovered replication-competent picornavirus, have shown remarkable activity against SCLC in preclinical models and are currently in simultaneous phase I clinical development.