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The Role of Mitochondrial Dysfunction in Mitophagy and Apoptosis and Its Relevance to Cancer
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
In addition to direct MOMP effectors, another class of pro-apoptotic factors is comprised of proteins, that harbor only one BH domain (BH3) in their primary sequence, known as the BH3-only protein sub-family [60]. BH3-only proteins such as Bcl-2-associated death promoter (Bad), Bcl-2 interacting killer (Bik), Bcl-2 modifying factor (Bmf), harakiri (Hrk), and Noxa sensitize cells to apoptosis by sequestering the pro-survival proteins from interaction with Bax or Bak. Hence, BH3-only proteins are in general referred to as apoptotic sensitizers. In addition, a sub-group of so-called direct activators has been identified among the BH3-only proteins. Apart from acting as sensitizers, proteins such as truncated BH3-interacting domain death agonist (tBid), Bcl-2-like protein 11 (Bim), p53 upregulated modulator of apoptosis (Puma), and Noxa, can directly bind to and activate the MOMP effectors Bax and Bak.
Nutraceutical’s Role in Proliferation and Prevention of Colorectal Cancer
Published in Sheeba Varghese Gupta, Yashwant V. Pathak, Advances in Nutraceutical Applications in Cancer, 2019
Mayur M. Patel, Shruti U. Rawal, Jayvadan K. Patel
Amino acids like methionine, arginine, and glutamine, and microelements like calcium, selenium, potassium, copper, and zinc are vital in the development and progression of CRC [98]. Besides these, vitamins like B6, B12, folic acid, ascorbic acid, A, D, and E have also been researched to possess anticolorectal cancer activity by several research groups [99,100]. Selenium is a trace element that is found in many foods including sea food, lean meats, pork, beef, turkey, chicken, fish, shellfish, eggs, legumes (beans and peas), nuts, and seeds. The North Carolina Colon Cancer Study has depicted significant reduction in colorectal cancer development with higher selenium and folate consumption. A strong association of calcium administration and vitamin D has been highlighted in many of the in vitro studies [101]. Calcium and vitamin D consumption has been found to reduce the fatty acids and secondary bile acid concentrations, thereby lowering their cytotoxicity in vitro. A blinded study has also proved their protective effect in subjects with higher risks of FAP, thereby reducing the recurrence of adenomatous polyps. Ascorbic acid (vitamin C) is an important dietary supplement that plays several pharmacological actions including anticancer and apoptotic actions. The anticancer role of ascorbic acid was made evident in the study by Kim et al., wherein it was found to induce apoptosis in HCT-8 colon cancer cell line through enhanced translocation of Bcl-2-associated death promoter protein (BAD) to mitochondria, increased Bcl-2-associated X protein (BAX) expression, and calcium influx in endoplasmic reticulum [102].
2-(Naphthalene-2-thio)-5,8-dimethoxy-1,4-naphthoquinone induces apoptosis via ROS-mediated MAPK, AKT, and STAT3 signaling pathways in HepG2 human hepatocellular carcinoma cells
Published in Drug and Chemical Toxicology, 2022
Yang Liu, Ying-Hua Luo, Shu-Mei Li, Gui-Nan Shen, Jia-Ru Wang, Yi Zhang, Yu-Chao Feng, Wan-Ting Xu, Yu Zhang, Tong Zhang, Hui Xue, Hong-Xing Wang, Yang Cui, Ying Wang, Cheng-Hao Jin
Apoptosis is the best therapeutic way to kill cancerous cells, as it occurs in certain physiological or pathological conditions by genes that closely regulate cell death, such as B-cell lymphoma 2 (Bcl-2) and caspase family members (Liu et al. 2009, Jin et al. 2017). The Bcl-2 family is divided into two categories: anti-apoptotic proteins, such as Bcl-2, that inhibit apoptosis, and pro-apoptotic proteins, such as Bcl-2-associated death promoter (Bad), that promote apoptosis (Zhang et al. 2015). Caspase-3 is the most important terminal shearing enzyme in the process of apoptosis, and an important part of the cell death mechanism (Liu et al. 2018). In addition, some signaling pathways are active in apoptotic cells, such as mitogen-activated protein kinase (MAPK), AKT, and signal transducer and activator of transcription 3 (STAT3) (Yang et al. 2010, Pan et al. 2015a, Gross, 2016).
Isochamanetin is a Selective Inhibitor for CyclinD1 in SKOV3 Cell Lines
Published in Nutrition and Cancer, 2019
Y. Swarnalatha, V. G. Vidhya, Annapoorni Murugan
Bcl-2 and Bax are the intrinsic and extrinsic pathways and antiapoptotic and proapoptotic factors of the members of Bcl-2 family of proteins. Our results indicated that isochamanetin acts by significantly downregulating Bcl-2 while upregulating Bax. However, Bax can release cytochrome C with the Bax/Bak hetero-oligomer formation, whereas Bcl-2 can interact with activator molecules or Bax/Bak, thus binding to these proteins. The cell death induced by Bax and Bcl-2-associated death promoter (Bad) can directly regulate the release of mitochondrial cytochrome factors involved in apoptosis. The suppressed levels of Bcl-2 can decrease the levels of mitochondrial cytochrome C with isochamanetin. The reduction in cytochrome C levels indicates that the oxygen-freeradicals produced promote apoptosis in cancer cells.
Reg3β: A Potential Therapeutic Target for Tissue Injury and Inflammation-Associated Disorders
Published in International Reviews of Immunology, 2022
Yuwen Cao, Yu Tian, Yueqin Liu, Zhaoliang Su
The physiological role of Reg3β remains unclear, but several functions have been suggested, such as anti-inflammation, differentiation-induction, pro-proliferation, anti-apoptosis, and bactericide. Reg3β participates in the pathophysiology of inflammatory diseases such as pancreatitis [58]. The anti-inflammatory responses of Reg3β are similar to those of IL-10. Reg3β ameliorates inflammation by inhibiting the infiltration of neutrophils and macrophages, and the production of IL-6 and TNF-α [50]. Additionally, Reg3β completely inhibited the nuclear translocation of p65 in response to TNF-α in macrophages and acinar cells, and thus suppressed NF-κB activation [50, 51]. TNF-α and IL-6 are two regulators in the priming of liver generation, which increases after partial hematectomy in mice. They sensitize hepatocytes to growth factors and drive the hepatocytes into G1 phase to initiate proliferation [59]. Reg3β mediated the positive effect of TNF-ɑ/IL-6 by exerting negative feedback on STAT3/IL-6 activation during hepatocyte proliferation [56]. In addition, Reg3β-dependent PKA activation induced the phosphorylation of Bcl-xL/Bcl-2-associated death promoter (Bad) at Ser-112 [57]. Bad is a pro-apoptotic member of the Bcl-2 family, which can interact with Bcl-2 and Bcl-xl. Phosphorylated Bad failed to bind Bcl-2 or Bcl-xl proteins, but combined with 14-3-3, forming a complex that is stable in the cytoplasm and exerts an anti-apoptotic effect [60, 61]. Additionally, Reg3β can alleviate acetaminophen-induced hepatic protein nitration. During hepatic protein nitration, the transcriptional factor AP-1 binds to the gene promoter of Scly in the liver tissue, which upregulates Scly activity. As a result, hepatic glutathione peroxidase-1 activity increases and leads to an accelerated depletion of GSH. Reg3β impaired AP-1 and finally enhanced GSH levels [62].