Hypothetical model. Illustrating that HN1L overexpression confers carboplatin resistance via NF-κB activation in OC (IMAGE)
Caption
In classical NF-κB pathway, in response to cytokine like IL-1β, NF-κB inhibitor (IκBα) will be phosphorylated and degraded. Thus, NF-κB is liberated, and translocated into nucleus to bind to the κB consensus sequence and activate its target genes transcription. In OC cells with significant higher HN1L expression, HN1L would further augment the activation of NF-κB, thus, inducing NF-κB target genes, like cytokines, growth factors, antiapoptotic genes, DNA repair genes, drug resistance genes, antioxidative genes, oncogenic genes, etc. Together, these genes would collectively function to further promote OC tumor phenotype, and lead to carboplatin (Carbo) resistance in OC. Additionally, it is possible that HN1L is further induced by activated NF-κB, thus, forming a feedback loop, to further enhance the Carbo resistance phenotype. Finally, it is also possible that, in addition to NF-κB pathway, HN1L may also regulate NF-κB-independent pathway(s) to contribute to Carbo resistance. These interesting aspects warrant further exploration in the future.
Credit
Han Wei, Aishat Motolani, Kenneth P. Nephew, Guanglong Jiang, Faranak Alipourgivi, Steven Sun, Xiumei Huang, Mateusz Opyrchal, George Sandusky, Yunlong Liu, Tao Lu
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CC BY-NC-ND