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. Author manuscript; available in PMC: 2023 Nov 1.
Published in final edited form as: Clin Cancer Res. 2023 May 1;29(9):1658–1669. doi: 10.1158/1078-0432.CCR-22-2861

Figure 2. Transcriptional regulation of A3A and A3B.

Figure 2.

A Activation of IFN signaling facilitates the recruitment of STAT2 to the promoter of A3A, while genotoxic stress promotes the recruitment of the NF-κB transcription factor complex. Transcriptional activation of A3A through genotoxic stress is inhibited by ATR.

B The PKC/ncNF-κB pathway dominates A3B transcription and recruits transcription factor complexes to the A3B promoter, intronic, and distal enhancers. In turn, the PKC/ncNF-κB pathway is activated by genotoxic stress, TNFα, IL-6, and possibly IFN signaling. Transcriptional repression is facilitated by the DREAM complex [and the upstream RB/E2F pathway] and the PRC1.6 complex. Viral oncogenes, including HPV-E6, HPV-E7, and PyV Tag can also activate A3B, although this is unlikely to contribute to A3B expression in breast cancer.