Hsu Wen-Li, Noda Mami, Yoshioka Tohru, Ito Etsuro
Department of Dermatology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80145, Taiwan.
Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Explor Target Antitumor Ther. 2021;2(5):401-415. doi: 10.37349/etat.2021.00053. Epub 2021 Oct 31.
Cancer is an aging-associated disease and caused by genomic instability that is driven by the accumulation of mutations and epimutations in the aging process. Although Ca signaling, reactive oxygen species (ROS) accumulation, DNA damage response (DDR) and senescence inflammation response (SIR) are processed during genomic instability, the underlying mechanism for the cause of genomic instability and cancer development is still poorly understood and needs to be investigated. Nociceptive transient receptor potential (TRP) channels, which firstly respond to environmental stimuli, such as microbes, chemicals or physical injuries, potentiate regulation of the aging process by Ca signaling. In this review, the authors provide an explanation of the dual role of nociceptive TRP channels in regulating cancer progression, initiating cancer progression by aging-induced genomic instability, and promoting malignancy by epigenetic regulation. Thus, therapeutically targeting nociceptive TRP channels seems to be a novel strategy for treating cancers.
癌症是一种与衰老相关的疾病，由基因组不稳定引起，而基因组不稳定是由衰老过程中突变和表观突变的积累所驱动的。尽管在基因组不稳定过程中会发生钙信号传导、活性氧（ROS）积累、DNA损伤反应（DDR）和衰老炎症反应（SIR），但基因组不稳定和癌症发展的潜在机制仍知之甚少，需要进一步研究。伤害性瞬时受体电位（TRP）通道首先对环境刺激作出反应，如微生物、化学物质或物理损伤，通过钙信号增强对衰老过程的调节。在这篇综述中，作者解释了伤害性TRP通道在调节癌症进展中的双重作用，即通过衰老诱导的基因组不稳定引发癌症进展，并通过表观遗传调控促进恶性肿瘤发展。因此，以伤害性TRP通道为治疗靶点似乎是一种治疗癌症的新策略。
