Malignant transformation depends on robust mechanisms to override DNA damage response signaling to preserve their proliferation speed despite the genotoxic abrasions. According to the article, “AATF suppresses apoptosis, promotes proliferation and is critical for Kras-driven lung cancer,” tumor cells rely on the effective suppression of p53-mediated induction of apoptosis regardless of their genomic instability either through TP53-inactivating mutations or through counteracting signaling molecules. In addition, it has also been known that lower levels of AATF protein expression correlate with higher expression rates of p53, Puma, and cleaved Caspase-3. This is all after genotoxic stress. AATF is also referred to as Che-1 and from “The anti-apoptotic factor Che-1/AATF links transcriptional regulation, cell cycle control, and DNA damage response,” article it states, that its phosphorylated by ATM and Chk2 and this leads to the stabilization of AAATF. As a result, it increases p53 and p21 expression contributing to stopping cell growth in response to DNA damage.
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