Department of Biological Sciences and Bioengineering (BSBE), Indian Institute of Technology, Kanpur, Uttar Pradesh 208016, India.
Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Sydney, NSW 2007, Australia; Faculty of Health, Australian Research Centre in Complementary and Integrative Medicine, University of Technology Sydney, Ultimo, Australia.
Ageing Res Rev. 2024 Jun;97:102315. doi: 10.1016/j.arr.2024.102315. Epub 2024 Apr 26.
Lung cancer stands as the primary contributor to cancer-related fatalities worldwide, affecting both genders. Two primary types exist where non-small cell lung cancer (NSCLC), accounts for 80-85% and SCLC accounts for 10-15% of cases. NSCLC subtypes include adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. Smoking, second-hand smoke, radon gas, asbestos, and other pollutants, genetic predisposition, and COPD are lung cancer risk factors. On the other hand, stresses such as DNA damage, telomere shortening, and oncogene activation cause a prolonged cell cycle halt, known as senescence. Despite its initial role as a tumor-suppressing mechanism that slows cell growth, excessive or improper control of this process can cause age-related diseases, including cancer. Cellular senescence has two purposes in lung cancer. Researchers report that senescence slows tumor growth by constraining multiplication of impaired cells. However, senescent cells also demonstrate the pro-inflammatory senescence-associated secretory phenotype (SASP), which is widely reported to promote cancer. This review will look at the role of cellular senescence in lung cancer, describe its diagnostic markers, ask about current treatments to control it, look at case studies and clinical trials that show how senescence-targeting therapies can be used in lung cancer, and talk about problems currently being faced, and possible solutions for the same in the future.
肺癌是全球癌症相关死亡的主要原因，影响男女两性。肺癌主要有两种类型，其中非小细胞肺癌（NSCLC）占 80-85%，小细胞肺癌（SCLC）占 10-15%。NSCLC 亚型包括腺癌、鳞状细胞癌和大细胞癌。吸烟、二手烟、氡气、石棉和其他污染物、遗传易感性和 COPD 是肺癌的风险因素。另一方面，如 DNA 损伤、端粒缩短和癌基因激活等应激因素会导致细胞周期延长停滞，即衰老。尽管衰老最初是一种抑制肿瘤的机制，可减缓细胞生长，但如果这一过程过度或控制不当，可能会导致与年龄相关的疾病，包括癌症。细胞衰老在肺癌中有两个作用。研究人员报告称，衰老通过限制受损细胞的增殖来减缓肿瘤生长。然而，衰老细胞还表现出促炎的衰老相关分泌表型（SASP），这被广泛报道可促进癌症。本综述将探讨细胞衰老在肺癌中的作用，描述其诊断标志物，探讨目前控制衰老的治疗方法，研究表明衰老靶向疗法如何用于肺癌的病例研究和临床试验，并讨论目前面临的问题以及未来可能的解决方案。
