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- Title
Expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins in human retinoblastoma.
- Authors
Singh, Lata; Pushker, Neelam; Saini, Neeru; Sen, Seema; Sharma, Anjana; Bakhshi, Sameer; Chawla, Bhavna; Kashyap, Seema
- Abstract
Background Regulation of apoptosis is a complex process that involves a number of genes, including Bcl-2, Bcl-x, Bax and other Bcl-2 family members. The aim of the present study is to assess the expression of Bcl- 2 and Bax in retinoblastoma, and correlate them with clinical and histopathological parameters. Methods The expression of Bcl-2 and Bax proteins were examined using immunohistochemistry, Western blotting and reverse transcriptase-polymerase chain reaction in a series of 60 prospective cases of primary retinoblastoma tissues. Results Immunohistochemistry showed expression of Bcl-2 in 40/60 (66.6%), whereas Bax expression was found only in 18/60 (30%) cases, and these correlated with mRNA expression. The Western blotting results also correlated well with the immunohistochemical expression of Bcl-2 (25 kDa) and Bax (21 kDa) proteins. Bcl-2 was expressed in 96% (24/25) of invasive tumours and in 45.7% (16/35) of non-invasive tumours. Expression of Bcl-2 significantly correlated with tumour invasiveness ( P = 0.0274) and poor differentiation ( P = 0.0163), whereas loss of Bax correlated with massive choroidal invasion and Pathological Tumor-Node-Metastasis ( pTNM) ( P = 0.0341). However, no correlation was found between Bax and Bcl-2 expression. Conclusions Our findings suggest that these apoptotic regulatory proteins may serve as poor prognostic markers and can be used as a therapeutic target for the treatment of invasive retinoblastoma. Further functional studies are required to explore the role of Bax and Bcl-2 in retinoblastoma.
- Subjects
BAX protein; APOPTOSIS; RETINOBLASTOMA; IMMUNOHISTOCHEMISTRY; WESTERN immunoblotting; REVERSE transcriptase polymerase chain reaction; MESSENGER RNA
- Publication
Clinical & Experimental Ophthalmology, 2015, Vol 43, Issue 3, p259
- ISSN
1442-6404
- Publication type
Article
- DOI
10.1111/ceo.12397