Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role of bcl-2 (an apoptosis suppressing oncogene) and bax (an apoptosis accelerating oncogene) in the development of TCC. We investigated bcl-2 and bax expression by means of immunohistochemical technique in 34 cases of TCC and in 9 cases of normal bladder tissue. Bcl-2 was positive in 44.44% of normal bladder tissue and in 82.35% of TCC. Bcl-2 staining intensity was significantly stronger in TCC than that in normal bladder tissue. Intensity and positivity of bcl-2 also increased with increasing grades of TCC. Bax was positive in 88.89% of normal bladder tissue and in 52.94% of TCC. Bax staining intensity was significantly weaker in TCC than that in the normal bladder tissue. These results suggested that increased expression of bcl-2 and decreased expression of bax in TCC play an important role in the development of TCC.
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PMID:[Expression of the bcl-2 and bax oncoprotein in TCC and its clinical significances]. 1067 49

We examined the effect of a newly synthesized DNA-binding ligand, quinacrine-netropsin hybrid molecule (QN), on cytotoxicity, apoptosis, and DNA strand breaks induced by an enediyne antitumor antibiotic, C1027. QN significantly enhanced C1027-induced cellular DNA strand breaks, caspase-3 activation, and DNA ladder formation, characteristic of apoptosis, in human HL-60 cells. Flow cytometry revealed that C1027-induced intracellular H(2)O(2) generation was enhanced by QN, suggesting that QN enhances C1027-induced cytotoxic effect through H(2)O(2)-mediated apoptosis. QN also significantly enhanced C1027-induced apoptosis in BJAB cells, and the inhibition of apoptosis was observed in BJAB cells transfected with Bcl-2 gene. The experiment using (32)P-labeled DNA fragments showed that the addition of QN enhanced C1027-induced double-stranded DNA cleavage at the 5'-AGG-3'/3'-TCC-5' sequence (cutting sites are underlined). These results suggest that QN enhances C1027-induced antitumor effect via DNA cleavage and apoptosis. The present study shows a novel approach to the potentially effective anticancer therapy.
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PMID:Amplification of C1027-induced DNA cleavage and apoptosis by a quinacrine-netropsin hybrid molecule in tumor cell lines. 1563 22