Nikhil Kumar, Shah Kavita
Department of Chemistry, Purdue University Institute for Cancer Research, 560 Oval Drive, West Lafayette, IN, 47907, USA.
School of Biotechnology, Kalinga Institute of Industrial Technology, Bhubaneswar, 751024, India.
Biomark Res. 2024 Sep 27;12(1):109. doi: 10.1186/s40364-024-00651-4.
AURKA is predominantly famous as an essential mitotic kinase. Recent findings have also established its critical role in a plethora of other biological processes including ciliogenesis, mitochondrial dynamics, neuronal outgrowth, DNA replication and cell cycle progression. AURKA overexpression in numerous cancers is strongly associated with poor prognosis and survival. Still no AURKA-targeted drug has been approved yet, partially because of the associated collateral toxicity and partly due to its limited efficacy as a single agent in a wide range of tumors. Mechanistically, AURKA overexpression allows it to phosphorylate numerous pathological substrates promoting highly aggressive oncogenic phenotypes. Our review examines the most recent advances in AURKA regulation and focuses on 33 such direct cancer-specific targets of AURKA and their associated oncogenic signaling cascades. One of the common themes that emerge is that AURKA is often involved in a feedback loop with its substrates, which could be the decisive factor causing its sustained upregulation and hyperactivation in cancer cells, an Achilles heel not exploited before. This dynamic interplay between AURKA and its substrates offers potential opportunities for targeted therapeutic interventions. By targeting these substrates, it may be possible to disrupt this feedback loop to effectively reverse AURKA levels, thereby providing a promising avenue for developing safer AURKA-targeted therapeutics. Additionally, exploring the synergistic effects of AURKA inhibition with its other oncogenic and/or tumor-suppressor targets could provide further opportunities for developing effective combination therapies against AURKA-driven cancers, thereby maximizing its potential as a critical drug target.
极光激酶A(AURKA)主要作为一种重要的有丝分裂激酶而闻名。最近的研究发现还证实了它在众多其他生物学过程中发挥着关键作用,包括纤毛发生、线粒体动力学、神经元生长、DNA复制和细胞周期进程。在多种癌症中,AURKA的过表达与预后不良和生存率低密切相关。然而,目前尚无针对AURKA的药物获批,部分原因是相关的附带毒性,部分原因是其作为单一药物在多种肿瘤中的疗效有限。从机制上讲,AURKA的过表达使其能够磷酸化众多病理底物,从而促进高度侵袭性的致癌表型。我们的综述探讨了AURKA调控方面的最新进展,并聚焦于AURKA的33个此类直接癌症特异性靶点及其相关的致癌信号级联反应。其中一个共同的主题是,AURKA常常与其底物形成反馈回路,这可能是导致其在癌细胞中持续上调和过度激活的决定性因素,而这是一个此前未被利用的致命弱点。AURKA与其底物之间的这种动态相互作用为靶向治疗干预提供了潜在机会。通过靶向这些底物,有可能破坏这种反馈回路,从而有效逆转AURKA的水平,进而为开发更安全的AURKA靶向疗法提供一条有前景的途径。此外,探索AURKA抑制与其其他致癌和/或肿瘤抑制靶点的协同效应,可为开发针对AURKA驱动的癌症的有效联合疗法提供更多机会,从而最大限度地发挥其作为关键药物靶点的潜力。