Cellular senescence in cancer: a brief review

Abstract

Certain cancer treatments cause an increase in the number of senescent cells in cancer and nonmalignant cells. Senescence which is characterized by telomere shortening, DNA damage, and improper expression of oncogenes are all examples of triggers that cause cellular senescence.  Failure to rejoin the cell cycle after mitotic stimulation, resistance to cell death, and an increased secretory phenotype are all signs of senescence. A rising number of studies point that spontaneous senescence and therapy-induced senescence (TIS) play a strong role in cancer aggressiveness. Senescent cells may have a role in oncogenesis mainly through the senescence associated secretory phenotype (SASP), which produces an immunosuppressive environment. This aids in tumor development and relapse by secreting factors such as IL-6, IL-8, CCL5, VEGF, and CXCL5 that contribute to cell proliferation, migration, invasiveness, angiogenesis, and epithelial–mesenchymal transition (EMT) as well as immune-mediated clearance.