Matches in SemOpenAlex for { <https://semopenalex.org/work/W4220789512> ?p ?o ?g. }
- W4220789512 endingPage "114989" @default.
- W4220789512 startingPage "114989" @default.
- W4220789512 abstract "Senescence is a special state of tumor suppression induced by cell cycle arrest. However, releasing senescence-associated secretory phenotypes by senescent cells could provide tumorigenic conditions and epigenetic changes in neighboring cells. The conventional anticancer drugs activate therapy-induced senescence by several mechanisms which include an increase in mitochondrial biogenesis and reactive oxygen species, up-regulation of tumor suppressor proteins (e.g., p53, p21, p38, and p16) and modulation of dysregulated signaling mediators, including senescence-associated β-galactosidase, ataxia-telangiectasia mutated/ATM and Rad3-related, checkpoint kinase1/2, phosphatidylinositol 3-kinases/Akt, Ras/Raf pathway, and extracellular signal-regulated kinase/mitogen-activated protein kinase. On the other hand, conventional anticancer agents induce the secretion of procarcinogenic molecules, including inflammatory mediators, such as nuclear factor-κB, tumor necrosis factor-α, and interleukins, and angiogenic mediators, namely vascular endothelial growth factor, in the tumor microenvironment. This condition urges the need for finding novel alternative therapies, novel senolytics, senescence inducers and combination therapies in the regulation of senescence towards the regulation of multiple tumorigenic conditions. This comprehensive review highlights the therapeutic targets and signaling pathways in the senescence of tumor cells. The critical roles of anticancer drug-induced senescence, senolytics, and associated combined administrations are evaluated in the attenuation of cellular senescence pathways to achieve cancer prevention and efficient treatment. Current challenges/pitfalls, limitations, and future research are also discussed." @default.
- W4220789512 created "2022-04-03" @default.
- W4220789512 creator A5009718831 @default.
- W4220789512 creator A5016520541 @default.
- W4220789512 creator A5019852381 @default.
- W4220789512 creator A5066795509 @default.
- W4220789512 date "2022-05-01" @default.
- W4220789512 modified "2023-10-09" @default.
- W4220789512 title "Cellular senescence signaling in cancer: A novel therapeutic target to combat human malignancies" @default.
- W4220789512 cites W1033197108 @default.
- W4220789512 cites W1511173728 @default.
- W4220789512 cites W1524549603 @default.
- W4220789512 cites W1592707856 @default.
- W4220789512 cites W1632349675 @default.
- W4220789512 cites W1813023439 @default.
- W4220789512 cites W1829914012 @default.
- W4220789512 cites W1851430442 @default.
- W4220789512 cites W1898081212 @default.
- W4220789512 cites W1932046626 @default.
- W4220789512 cites W1941036222 @default.
- W4220789512 cites W1964781873 @default.
- W4220789512 cites W1965124005 @default.
- W4220789512 cites W1965391084 @default.
- W4220789512 cites W1965688832 @default.
- W4220789512 cites W1966453709 @default.
- W4220789512 cites W1966514102 @default.
- W4220789512 cites W1966537207 @default.
- W4220789512 cites W1968931043 @default.
- W4220789512 cites W1970891016 @default.
- W4220789512 cites W1971250890 @default.
- W4220789512 cites W1971458298 @default.
- W4220789512 cites W1973300568 @default.
- W4220789512 cites W1976348818 @default.
- W4220789512 cites W1977400158 @default.
- W4220789512 cites W1978818809 @default.
- W4220789512 cites W1980878904 @default.
- W4220789512 cites W1981033124 @default.
- W4220789512 cites W1981518660 @default.
- W4220789512 cites W1982361636 @default.
- W4220789512 cites W1982481909 @default.
- W4220789512 cites W1982865433 @default.
- W4220789512 cites W1982998217 @default.
- W4220789512 cites W1984054872 @default.
- W4220789512 cites W1985180051 @default.
- W4220789512 cites W1987142903 @default.
- W4220789512 cites W1988354925 @default.
- W4220789512 cites W1988936955 @default.
- W4220789512 cites W1989479849 @default.
- W4220789512 cites W1990336255 @default.
- W4220789512 cites W1991037989 @default.
- W4220789512 cites W1992017365 @default.
- W4220789512 cites W1993152072 @default.
- W4220789512 cites W2001353514 @default.
- W4220789512 cites W2001733842 @default.
- W4220789512 cites W2002698073 @default.
- W4220789512 cites W2003274859 @default.
- W4220789512 cites W2003500892 @default.
- W4220789512 cites W2004196283 @default.
- W4220789512 cites W2004273407 @default.
- W4220789512 cites W2005219717 @default.
- W4220789512 cites W2005250235 @default.
- W4220789512 cites W2006096547 @default.
- W4220789512 cites W2006307101 @default.
- W4220789512 cites W2006803641 @default.
- W4220789512 cites W2007150397 @default.
- W4220789512 cites W2010417927 @default.
- W4220789512 cites W2011886148 @default.
- W4220789512 cites W2011997876 @default.
- W4220789512 cites W2012753735 @default.
- W4220789512 cites W2017906301 @default.
- W4220789512 cites W2019276374 @default.
- W4220789512 cites W2020043044 @default.
- W4220789512 cites W2021188633 @default.
- W4220789512 cites W2021503856 @default.
- W4220789512 cites W2022301078 @default.
- W4220789512 cites W2022861507 @default.
- W4220789512 cites W2024271246 @default.
- W4220789512 cites W2025675946 @default.
- W4220789512 cites W2025772032 @default.
- W4220789512 cites W2026435213 @default.
- W4220789512 cites W2026890342 @default.
- W4220789512 cites W2030523067 @default.
- W4220789512 cites W2031644195 @default.
- W4220789512 cites W2031683541 @default.
- W4220789512 cites W2033397406 @default.
- W4220789512 cites W2039210293 @default.
- W4220789512 cites W2041156660 @default.
- W4220789512 cites W2042140414 @default.
- W4220789512 cites W2048433654 @default.
- W4220789512 cites W2049523663 @default.
- W4220789512 cites W2050541542 @default.
- W4220789512 cites W2054824587 @default.
- W4220789512 cites W2055255896 @default.
- W4220789512 cites W2058816108 @default.
- W4220789512 cites W2060036335 @default.
- W4220789512 cites W2061135112 @default.
- W4220789512 cites W2061765285 @default.
- W4220789512 cites W2062107951 @default.