![]() JNK c-Jun N-terminal kinase cancer cell survival chemoresistance tumor development. We highlight recent advances in our knowledge of the roles of JNK in cancer cell survival, which may provide insight into the distinct functions of JNK in cancer and its potential for cancer therapy. There is a focus on the specific "Yin and Yang" functions of JNK1 and JNK2 in the regulation of cancer cell survival. The present review focuses on recent advances in understanding the prosurvival function of JNK and its role in tumor development and chemoresistance, including a comprehensive analysis of the molecular mechanisms underlying JNK-mediated cancer cell survival. The identified JNK1-c-Jun-Notch1 axis strongly inhibited. Mechanistically, light specifically activated JNK1 to phosphorylate c-Jun, which in turn induced Notch1 transcription. c-Jun N-terminal kinases (JNKs) are among the most crucial mitogen-activated protein kinases (MAPKs) and regulate various cellular processes, including cell proliferation, apoptosis, autophagy, and inflammation. The prosurvival effect of JNK may involve an immune evasion mechanism mediated by transforming growth factor-β, toll-like receptors, interferon-γ, and autophagy, as well as compensatory JNK-dependent cell proliferation. Intriguingly, Notch1, a well-established negative regulator of photoreceptor genesis, was significantly attenuated in Jnk1 knockout (KO) mice compared to wild-type mice. 30 June 2004 accepted 24 August 2004 Jun Turnover Is Controlled Through JNK-Dependent Phosphorylation of the E3 Ligase Itch Min Gao,1 Tord Labuda,1,2 Ying Xia,1 Ewen Gallagher,1 Deyu Fang,3. JNK positively regulates autophagy to counteract apoptosis, and its effect on autophagy is related to the development of chemotherapeutic resistance. JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. ![]() C-Jun N-terminal kinase (JNK) is involved in cancer cell apoptosis however, emerging evidence indicates that this Janus signaling promotes cancer cell survival. ![]()
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