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Nanophytochemicals in Cancer Therapy
Published in Parimelazhagan Thangaraj, Lucindo José Quintans Júnior, Nagamony Ponpandian, Nanophytomedicine, 2023
Madhumitha Kedhari Sundaram, Asha Inbanathan, Arif Hussain
These studies show that specific nanoformulations ensure consistent release and high tissue accumulation, and with the addition of specific ligands, targeted delivery via receptor-mediated endocytosis can lead to an increased anticarcinogenic response (Goorbandi, Mohammadi and Malekzadeh, 2020). It is seen that these formulations are more capable of eliciting a strong antiproliferative response as well as cell-cycle arrest. Further, they can initiate apoptosis through the activation of the caspase cascade as well as by modulating the expression of apoptotic regulatory genes like BCL2, BCL-xl, Bim, Bax and Bad (Senthil Kumar et al., 2020). Several nanophytochemical formulations were able to modulate the signalling pathways such as PI3K and Wnt. This is an important facet of this therapeutic as these pathways govern numerous hallmark features. Various nanoformulations were able to retain and enhance the effect on inflammation and reactive oxygen species (ROS) generation by suppressing the expression of COX-2 and modulating the NF-kB pathway amongst other molecular mechanisms (Pool et al., 2018; Tian et al., 2019; Balan et al., 2020). Lowering inflammation and modifying the redox environment in cancer cells are important steps in mediating a strong anticancer effect. Redox changes are often linked with the onset of apoptosis and further limitation of proliferation (Sundaram, Khan et al., 2020).
Death Receptor-Mediated Apoptosis and Lymphocyte Homeostasis
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Lixin Zheng, Richard M. Siegel, Jagan R. Muppidi, Felicita Hornung, Michael J. Lenardo
Lymphokine withdrawal apoptosis depends on newly synthesized proteins because it has been shown that actinomycin D and cycloheximide, inhibitors of DNA transcription and protein synthesis, respectively, can block this process.89 The molecular mechanisms of lymphokine withdrawal apoptosis are not as clear as for antigen-induced death. Experiments with mice deficient in Fas and other death receptors have not shown any role of these molecules in lymphokine withdrawal apoptosis. However, the proto-oncogene Bcl-2 family is crucially involved in regulating lymphokine deprivation death. Bcl-2 and Bcl-XL are the major anti-apoptotic members of the family. They antagonize BAX/Bcl-Xs/BAD and other pro-apoptotic proteins of the family by stabilizing mitochondrial membrane potential and membrane integrity. This prevents cytochrome C release and activation of the caspase-9 cascade that leads to apoptosis.90-92
Cell Biology for Bioprocessing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
Two anti-apoptotic proteins, Bcl-2 and Bcl-xL, counter the actions of the pro-apoptotic components. Bcl-2 is localized on the mitochondrial membrane and inhibits the release of pro-apoptotic molecules from the mitochondria by maintaining membrane integrity. Bcl-xL is localized in the cytoplasm and binds to pro-apoptosis members of the Bcl-2 family. The involvement of multiple protagonistic and antagonistic factors ensures tight control of the apoptotic event.
Formulation and evaluation of a two-stage targeted liposome coated with hyaluronic acid for improving lung cancer chemotherapy and overcoming multidrug resistance
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Xuelian Wang, Hongye Cai, Xinyu Huang, Zhuhang Lu, Luxi Zhang, Junjie Hu, Daizhi Tian, Jiyu Fu, Guizhi Zhang, Yan Meng, Guohua Zheng, Cong Chang
Apoptosis, a form of programmed cell death, is crucial for preventing cancer development, and inducing apoptosis has become a popular target for cancer treatment [42]. There are two major apoptotic pathways: the exogenous (mitochondrial pathway) and endogenous pathways (death receptor pathway), both of which aim to initiate cell death. The Bcl-2 protein family plays a key role in apoptosis regulation, including anti-apoptotic/pro-survival proteins such as BCL-2, BCL-XL, as well as pro-apoptotic proteins such as Bax and Bak. In the mitochondrial apoptosis pathway, activated Bax forms multimeric pores in the mitochondrial membrane, leading to a decrease in MMP and an increase in membrane permeability [43]. Subsequently, a series of apoptotic factors are released from mitochondria into the cytoplasm. The apoptosis initiator protease caspase-9 is then activated, followed by downstream effector caspase-3 activation, ultimately inducing apotosis. As shown in Figure 9E–F, after treatment with HA/TT LP/PTX, the expression of the anti-apoptotic protein Bcl-2 was downregulated, while the expression of Bax, cleaved caspase 3, and cleaved caspase 9 was upregulated, indicating the induction of apoptosis.
Parecoxib exhibits anti-inflammatory and neuroprotective effects in a rat model of transient global cerebral ischemia
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Shaoxing Liu, Yue’e Dai, Chen Zhou, Tao Zhu
Previously He et al. (2019) showed that apoptosis contributes to a significant proportion of neuronal death after cerebral ischemia reperfusion. Similarly, Song et al. (2019) found that apoptosis was involved in cerebral ischemia reperfusion which was accompanied by elevated gene expression of Bax associated with reduction in protein expression of Bcl-2. Shen et al. (2017) reported that the mitochondrial pathway was involved in IL-1β-induced apoptosis of nucleus pulposus cells, as evidenced by elevated expression ratio of Bax/Bcl-2. The Bcl-2 protein family members consist of pro-apoptotic (Bax, Bad) and anti-apoptotic (Bcl-2, Bcl-xl), which are major regulators of the mitochondrial apoptotic pathway after ischemia injury (Cory, Huang, and Adams 2013). It was proposed that Bcl-2/Bax ratio determines whether a cell is protected from, or progresses to, programmed cell death (Guo and Li 2018; Sekerdag, Solaroglu, and Gursoy-Ozdemir 2018). Previously Lipton (1999) showed that necrotic neurons appeared at 6–12 hr and a second peak appeared at 24–72 hr after ischemia reperfusion. In this study, the TUNEL-positive cells, apoptotic rate, and expression of both Bax and Bcl-2 were significantly increased in cortex; however, the ratio of Bcl-2/Bax decreased significantly at 72 hr after tGCI. Our findings demonstrated that parecoxib treatment significantly enhanced Bcl-2 expression accompanied by a fall in Bax expression (i.e., elevated Bcl-2/Bax ratio), attenuating neuronal apoptosis in the prefrontal cortex of tGCI rats.
Anti-cancer potential of the lipoidal and flavonoidal compounds from Pisum sativum and Vicia faba peels
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Amal M. El-Feky, Marwa M. Elbatanony, Marwa M. Mounier
Apoptosis, or programmed cell death, takes place in all living organisms. Disruption of apoptotic mechanisms could lead to the deregulation of cell proliferation. Targeting the process of apoptosis is an appropriate strategy for prevention and treatment of cancer. Based upon that apigenin effectively suppressed the growth of both colon and breast tumor cell line with LC50 on breast less than colon, changes in expression of apoptosis- (apoptosis-related genes) of apigenin over (MCF-7) were investigated. Quantitative estimation of BcL2, Bax, Bax/ Bcl2 ratio and caspase 7 were determined. Bcl-2 family members are associated with the intrinsic pathway of poptosis comprised of both pro-apoptotic (e.g. Bax, Bid) and anti-apoptotic (e.g. Bcl-2, Bcl-XL) members. Expression of the anti-apoptotic Bcl-2 in breast cancer cell line treated with apigenin was significantly decreased as compared with control “untreated breast cancer cells “as shown in Fig. 4. Apigenin resulted in an increase in Bax protein levels in MCF‐7 cells chart Fig. 5.