ArticleJournal of cancer research and clinical oncology2011
Molecular analysis of oncogenicity of the transcription factor, BRN3A, in cervical cancer cells.
Article in Journal of cancer research and clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- BRN3A, a transcription factor, regulates the expression of genes involved in biological processes shaping the HPV induced cervical cancer.Genes & genomics · 2025Article
- Novel Variant Identified in the Enhancer Region of Host Transcription Factor, BRN3A, is a Significant Risk Factor for HPV-Induced Uterine Cervix Cancer.International journal of molecular and cellular medicine · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe host cellular transcription factor, BRN3A, has been observed to play a vital role in cancer of the uterine cervix. BRN3A possesses multipartite functions, which include transcription of the genes of the high-risk HPVs and mediation of cellular changes in the host. In this study, we made an effort to decipher the regulation of BRN3A in cervical cancer cells by studying its interaction with different components of the cell.
methodsIn cervical cancer cells, the endogenous HIPK2 was induced through cisplatin treatment, and then, its subsequent effect on BRN3A was primarily investigated through co-immunostaining and western blotting as HIPK2 has been observed to act as a co-repressor of Brn3a. The physical interaction of the two proteins was analyzed through co-immunoprecipitation. We resorted to chromatin immunoprecipitation in order to testify the autoregulatory pathway of BRN3A in cervical cancer cells. Interaction of BRN3A with cellular components, p73 and active form of JNK, was also studied through co-immunostaining.
resultsWe observed that BRN3A is independent of the regulative activity of HIPK2 and undergoes positive autoregulation in cervical cancer cells. Interestingly, during the study, it was revealed that BRN3A is unaffected by the treatment of cisplatin. Interaction of BRN3A with p73 and phosphorylated JNK in cervical cancer cells, observed in the present study, would help in understanding the molecular mechanism directed by BRN3A.
conclusionsBRN3A possesses anti-apoptotic property, and considering the above results, it may be regarded as the key component in promoting tumorigenic growth in the uterine cervical cells.
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