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Microalgae and Cyanobacteria as a Potential Source of Anticancer Compounds
Published in Gokare A. Ravishankar, Ranga Rao Ambati, Handbook of Algal Technologies and Phytochemicals, 2019
In another study, Kim et al. (2008) demonstrated that PTX-2 induced its anticancer effects against leukemia cells through suppression of constitutive NF-κB activity. The study found that treatment of PTX-2 down-regulated NF-κB dependent expression of Cox2, IAP-1, IAP-2 and XIAP genes at the transcriptional and translational levels. In addition, the compound induced apoptosis by activating caspase-3 activity. In a separate study, Whitton et al. (2016) found that PTX-2 inhibited telomerase activity with down-regulation of hTERT expression in human leukemia cells. Treatment with PTX-2 also reduced c-Myc and Sp1 gene expression and DNA binding activity of the leukemia cells.
Mitochondrial Stress and Cellular Senescence
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Irene L. Tan, Michael C. Velarde
Despite the permanent state of cell cycle arrest, senescent cells still remain metabolically active (James et al. 2016). They often acquire resistance to apoptosis (Crecenzi, Palumbo, and Brady 2003; Marcotte, Lacelle, and Wang 2004). Hence, it is not surprising that these cells persist in culture and in vivo (Sanders et al. 2013). Indeed, the number of senescent cells tends to increase with age (López-Otín et al. 2013). The mechanisms by which senescent cells resist apoptosis are not fully understood. One hypothesis is through down regulation of caspase-3, an important mediator of apoptosis (Marcotte, Lacelle, and Wang 2004).
Peptide Receptor Radionuclide Therapy: Preclinical Findings
Published in Marco Chinol, Giovanni Paganelli, Radionuclide Peptide Cancer Therapy, 2016
Astrid Capello, Wouter A. P. Breeman, Bert Bernard, Marion de Jong, Eric P. Krenning
In addition, several procaspases also contain potential RGD-binding motifs near the site necessary for activation to the mature caspase. Caspases are proteases that are critical in programmed cell death (78). Buckley and coworkers (79) demonstrated that RGD peptides are able to directly activate caspase-3 and thereby induce apoptosis. Other work has shown that molecules specific for GPIIb/IIIa integrins can also stimulate caspase-3 activity (80). Since caspase-3 is one of the key executioner proteases (81) in the apoptosis pathway, it seems likely that this enzyme will be an important site of action for targeted therapeutics that are designed to selectively induce cell death.
Design, synthesis, apoptotic, and antiproliferative effects of 5-chloro-3- (2-methoxyvinyl)-indole-2-carboxamides and pyrido[3,4-b]indol-1-ones as potent EGFRWT/EGFRT790M inhibitors
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Lamya H. Al-Wahaibi, Anber F. Mohammed, Fatema El-Zahraa S. Abdel Rahman, Mostafa H. Abdelrahman, Xuyuan Gu, Laurent Trembleau, Bahaa G. M. Youssif
Caspases have an important role in the induction and completion of apoptosis33. Among caspases, caspase-3 is an important caspase that cleaves various proteins in cells, resulting to apoptosis34. Compounds 5f and 5 g, the most potent derivatives, were tested as caspase-3 activators against pancreatic cancer cell line (Panc-1)32, and the results are shown in Table 3. Compounds 5f and 5 g demonstrated excellent caspase-3 protein overexpression levels of 560.2 ± 5.0 and 542.5 ± 5.0 pg/mL, respectively. They increased the protein caspase-3 in the Panc-1 human pancreatic cancer cell line by approximately 8 times when compared to control untreated cells, and they were even more active than the reference staurosporine (503.2 ± 4.0 pg/mL). These results indicate that the tested compounds act as caspase-3 activators and can therefore be regarded as apoptotic inducer agents.
FGFR2 modulates the Akt/Nrf2/ARE signaling pathway to improve angiotensin II-induced hypertension-related endothelial dysfunction
Published in Clinical and Experimental Hypertension, 2023
Kun Jiao, Ping Su, Yongling Li
Furthermore, to uncover the effects of FGFR2 on the apoptosis of Ang II-induced HUVECs, flow cytometry analysis was applied. On the contrary, it turned out that the apoptosis of HUVECs was increased by Ang II induction and FGFR2 overexpression suppressed the apoptosis of Ang II-induced HUVECs (Figure 3A), as displayed by the quantification (Figure 3B). To further confirm the effects of FGFR2 on cell apoptosis, the expression of apoptosis-related proteins was analyzed by western blot. It was discovered that the expression of Bax and cleaved PARP were upregulated and Bcl-2 expression was downregulated in Ang II-induced HUVECs, which were reversed by FGFR2 overexpression (Figure 3C). Caspase 3 is a prominent mediator of apoptosis. As expected, Ang II-enhanced caspase 3 activity in HUVECs was also depleted by FGFR2 up-regulation (Figure 3D). In summary, FGFR2 might protect against Ang II-stimulated HUVECs apoptosis.
Effects of Carvacrol in an Experimentally Induced Esophageal Burn Model: Expression of VEGF and Caspase-3 Proteins
Published in Journal of Investigative Surgery, 2021
Hikmet Zeytun, Ebru Gökalp Özkorkmaz
In the control group, caspase-3 expression was negative in epithelial, connective tissue, and muscle cells (Figure 3A). In contrast, in the burn group, caspase-3 expression was positive in degenerated epithelial cells, apoptotic cells within the connective tissue, and cells that had migrated to the muscle layer. Caspase-3 activity was significantly increased in inflammatory cells surrounding blood vessels (Figure 3B). In the burn and carvacrol group, some apoptotic cells within the epithelial layer showed caspase-3 expression and activity. Caspase-3 was positively expressed in connective tissue and in a small number of degenerated cells between the muscle layers (Figure 3C). In the control group, VEGF protein expression was observed in vascular endothelial cells and some connective tissue macrophage cells (Figure 3D). In the burn group, VEGF expression was significantly increased in connective tissue inflammatory cells, degenerated and congested vascular endothelial cells, and inflammatory cells of the muscle layer (Figure 3E). In the burn and carvacrol group, VEGF expression was positive in a small number of inflammatory cells in the papillary region of the epithelium, dilated vascular endothelial cells, and some connective tissue macrophage cells (Figure 3F).