顺铂
药理学
蛋白激酶B
细胞凋亡
癌症研究
MAPK/ERK通路
联合疗法
医学
氧化应激
激酶
DNA损伤
神经毒性
肺癌
化学
化疗
毒性
肿瘤科
内科学
生物化学
DNA
作者
Minerva,Amrita Bhat,Sonali Verma,Gresh Chander,Rajeshwer Singh Jamwal,Bhawani Shankar Sharma,Audesh Bhat,Taruna Katyal,Rakesh Kumar,Ruchi Shah
标识
DOI:10.4103/jcrt.jcrt_792_22
摘要
Cisplatin, that is, cis-diamminedichloroplatinum is a coordinate compound that is mainly preferred as prior treatment against several solid tumors and malignancies like ovaries, head and neck, testicular, and lung cancers because of its anticancer activity. Cisplatin binds at the N7 position of purine and forms adducts, leading to altered activity of DNA that triggers apoptosis. DNA damage is followed by several signaling pathways like induced oxidative stress, upregulated p53, mitogen-activated protein kinase (MAPK), and Jun N-terminal kinases (JNK) or Akt pathways along with induced apoptosis. Additionally, cisplatin treatment comes with few disadvantages such as toxic effects, that is, hepatotoxicity, cardiotoxicity, neurotoxicity, etc., and drug resistance. Furthermore, to overcome cisplatin resistance and toxicological effects, combination drug therapy has been considered. The aim of the review is to focus on the molecular mechanism of action of cisplatin and combination drug therapy to reduce the side effects in cancer therapy.
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