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Nutraceuticals as Supplements for Cancer Prevention
Published in Sheeba Varghese Gupta, Yashwant V. Pathak, Advances in Nutraceutical Applications in Cancer, 2019
Nicholas Micciche, Brianna Choyce, Yashwant V. Pathak
The mechanism of cannabinoids in cancer prevention is predominantly attributed to the inhibition of cancer cell proliferation and the induction of apoptosis. Agonism of CB1 and CB2 receptors cause apoptosis by stimulating ceramide synthesis. Increases in ceramide concentration causes activation of the endoplasmic reticulum (ER) stress-related signaling pathway, an evolutionarily conserved response, termed the unfolded protein response (UPR). This pathway, when activated, causes increased expression of the highly mobile transcriptional regulation factor, p8. The p8 is a key player in the cellular stress response [80]. The expression of p8 mediates early cancer development by stopping the translation of cancer cells and degrading mutated proteins. Activation of p8 results in activation of downstream targets including activating transcription factor 4 (ATF4), C/EBP homologous protein (CHOP), and tribbles homologue 3 (TRIB3). Activation of TRIB3 specifically causes inhibition of Akt, subsequent inhibition of mTORC1, and finally autophagy [70,81] (Figure 2.5).
Maturation, Barrier Function, Aging, and Breakdown of the Blood–Brain Barrier
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Elizabeth de Lange, Ágnes Bajza, Péter Imre, Attila Csorba, László Dénes, Franciska Erdő
It is known that PD is characterized by the progressive loss of select neuronal populations, but prodeath genes mediating the neurodegenerative processes is a novel proposed concept by Aimé et al. (2015). They have proposed a pathway involving tribbles pseudokinase (Trib3), which is a stress-induced gene with proapoptotic activity, to have a role in neuronal death associated with PD (Aimé et al. 2015). For PD, furthermore, Michel et al. (2016) have provided an overview of cell-autonomous mechanisms that are likely to participate in dopamine (DA) cell death in both sporadic and inherited forms of PD. Damage to vulnerable DA neurons may arise from cellular disturbances produced by protein misfolding and aggregation, disruption of autophagic catabolism (a conserved catabolic process that degrades cytoplasmic constituents and organelles in the lysosome), endoplasmic reticulum stress, mitochondrial dysfunction, or loss of calcium homeostasis and where pertinent show how these mechanisms may mutually cooperate to promote neuronal death (Michel et al. 2016).
Role and molecular mechanism of stem cells in colorectal cancer initiation
Published in Journal of Drug Targeting, 2020
Meng-Yan Wang, Yu-Han Qiu, Mei-Lian Cai, Cong-Hui Zhang, Xiao-Wei Wang, Hong Liu, Yi- Chen, Wu-Li Zhao, Jing-Bo Liu, Rong-Guang Shao
Tribbles homologue 3 (TRIB3) is a kind of pseudo-kinase that acts as a stress sensor in chronic inflammatory and malignant diseases [60] and has been proven to be an oncoprotein in both solid tumours and leukaemia. TRIB3 expression is correlated with a negative prognosis for patients with colorectal cancer [61].