Cell Survival and Apoptosis Signaling as Therapeutic Target for Cancer: Marine Bioactive Compounds

Abstract

Inhibition of apoptosis leads to activation of cell survival factors (e.g., AKT) causes continuous cell proliferation in cancer. Apoptosis, the major form of cellular suicide, is central to various physiological processes and the maintenance of homeostasis in multicellular organisms. A number of discoveries have clarified the molecular mechanism of apoptosis, thus clarifying the link between apoptosis and cell survival factors, which has a therapeutic outcome. Induction of apoptosis and inhibition of cell survival by anticancer agents has been shown to correlate with tumor response. Cellular damage induces growth arrest and tumor suppression by inducing apoptosis, necrosis and senescence; the mechanism of cell death depends on the magnitude of DNA damage following exposure to various anticancer agents. Apoptosis is mainly regulated by cell survival and proliferating signaling molecules. As a new therapeutic strategy, alternative types of cell death might be exploited to control and eradicate cancer cells. This review discusses the signaling of apoptosis and cell survival, as well as the potential contribution of marine bioactive compounds, suggesting that new therapeutic strategies might follow.

Autophagy and senescence in fibrosing cholangiopathies

“…Autophagy maintains cellular viability during periods of various stresses [30][31][32]40,52,53]. During cellular stress, autophagy is activated and organelles are sequestered in autophagosomes and digested through fusion with lysosomes.…”

“…Lastly, we will discuss the inappropriate Cells respond to various stresses by means of adaptation, autophagy, and recovery, or they either commit to irreversible cell-cycle exit (senescence) or are eliminated through programmed cell death (apoptosis) [24]. While cellular senescence, autophagy and apoptosis are distinct cellular responses to stress, they are correlating with each other, and signaling pathways involved are often overlapping each other [25][26][27][28][29][30][31][32]. For example, autophagy is considered a survival mechanism when faced with cellular insults, however extensive autophagy can also lead to senescence or apoptosis ( Fig.…”

“…For example, autophagy is considered a survival mechanism when faced with cellular insults, however extensive autophagy can also lead to senescence or apoptosis ( Fig. 1) [30][31][32][33][34][35][36].…”

Galangin Alleviates Liver Ischemia-Reperfusion Injury in a Rat Model by Mediating the PI3K/AKT Pathway

“…Specific morphological characteristics and energy-dependent biochemical mechanisms have been associated with programmed cell death or apoptosis [9], and apoptotic pathways are often induced by upstream activators including PI3K/AKT/mTOR signaling, proapoptotic proteins in the Bcl-2 family, cellular stress stimuli, and hypoxia [10]. PI3K/AKT signaling is a classic anti-apoptosis pathway and its involvement in the process of liver I/R injury has been reported [11][12][13].…”

Kurkumin Menurunkan Ekspresi Tumor Necrosis Factor (TNF)-α Kompleks Oosit-Kumulus Sapi pada Kultur dengan Zalir Peritoneum Penderita Infertil Terkait Endometriosis

“…Pembentukan DISC ini (death inducing signaling complex) menghasilkan aktivasi caspase-8/10, yang kemudian mengaktifkan caspase-3 sebagai eksekutor. 19,20,21,22 Sel-sel yang diaktifkan oleh sitokin mungkin memproduksi dan mensekresikan sitokin yang sama sebagai sinyal parakrin atau untuk meningkatkan dan menstabilkan sinyal dalam sel yang mensekresi melalui regulasi autokrin. Mekanisme autokrin atau parakrin produksi TNF-α melibatkan beberapa protein, diantaranya NF-κB, penghambat IκBα dan A20, penghantar sinyal kinase IKK dan IKKK, sitokin TNF-α dan reseptornya TNFR1.…”