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Regulation of Airway Smooth Muscle Proliferation by β2-Adrenoceptor Agonists
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
Alastair G. Stewart, Paul R. Tomlinson, Leslie Schachte
The hypophosphorylated form of Rb binds to and inhibits the activity of the transcriptional factor E2F.175–179 Phosphorylation of Rb by cyclin D-Cdk4 reduces its ability to form inhibitory complexes with E2F.173 In cells lacking functional Rb, the microinjection of antibodies or antisense plasmids to cyclin Dl does not prevent entry into S phase,154,180,181 whereas the microinjection of cyclin E antibody prevents cell cycle progression.154 These observations further support the contention that cyclin E plays a role in the signalling of cell cycle progression downstream of the point at which cyclin D has its regulatory effect.
Use of Molecular Markers of Endometrial Receptivity
Published in Botros Rizk, Yakoub Khalaf, Controversies in Assisted Reproduction, 2020
Alejandro Rincón, David Bolumar, Diana Valbuena, Carlos Simón
Different groups have described the expression of cyclin E in endometrium in relation to endometrial hyperplasia and cancer (32,33). However, from a reproductive point of view, this molecule could be an effective biomarker for endometrial receptivity. Cyclin E is expressed in the cytoplasm of glandular epithelial cells during the proliferative phase up to day 18 of the menstrual cycle, at which time its localization moves to the nuclear compartment.
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
Recently, Hao et al. (2018) showed that C-phycocyanin could significantly induce apoptosis and cell-cycle arrest, as well as suppress cell migration, proliferation, and colony formation ability of NSCLC cells through regulating multiple key genes. The pigment was also found to affect the cell phenotype by regulating the NF-κB signaling of NSCLC cells. C-phycocyanin was shown to have photodynamic effect in generating cytotoxic stress through ROS induction, which killed MDA-MB-231 breast cancer cells under 625-nm laser irradiation (Bharathiraja et al. 2016). Apoptotic cell death characteristics such as shrinking of cells, cytoplasmic condensation, nuclei cleavage and the formation of apoptotic bodies were observed in the treated cells. C-phycocyanin was also found to be effective against triple-negative MDA-MB-231 breast cancer cells (Ravi et al. 2015). Treatment of C-phycocyanin inhibited cell proliferation and reduced colony formation. It also caused G1 cell-cycle arrest, which could be attributed to decreased mRNA levels of cyclin E and CDK-2 and increased p21 levels.
Cyclin-dependent kinase inhibitors for the treatment of lung cancer
Published in Expert Opinion on Pharmacotherapy, 2020
Angel Qin, Haritha G. Reddy, Frank D. Weinberg, Gregory P. Kalemkerian
High levels of cyclin E are observed in lung tumors and over-expression in mouse models leads to dysplasia and lung carcinoma [53,54]. Cyclin E, like cyclin D1, is also over-expressed in a subset of noninvasive lung lesions, indicating potential importance in lung carcinogenesis [55]. Cyclin A, which is important for progression through S phase via interaction with CDK2, is commonly elevated in NSCLCs and a subset of bronchial pre-malignant lesions [56,57]. Finally, high expression of cyclin B1 is observed in NSCLC, especially squamous cell carcinoma, and precursor lesions, and elevated levels of cyclin B1 are associated with poor outcomes in patients with early-stage squamous cell lung cancer [58]. As previously discussed, regulation of the CDK1-cyclin B complex can occur through phosphorylation of CDK1 by WEE1. High expression of CDK1 has been reported in early-stage lung adenocarcinoma along with downregulation of WEE1 expression [59]. Patients with NSCLC whose tumor lack WEE1 have a higher recurrence rate and poorer outcomes [60].
Obacunone reduces inflammatory signalling and tumour occurrence in mice with chronic inflammation-induced colorectal cancer
Published in Pharmaceutical Biology, 2020
Xiaoping Luo, Zhilun Yu, Bei Yue, Junyu Ren, Jing Zhang, Sridhar Mani, Zhengtao Wang, Wei Dou
The cell cycle is precisely controlled by specific proteins, including P21, cyclin A2, and cyclin E1. P21, a tumour suppressor gene, is involved in the regulation of cell proliferation by inhibiting the cyclin-dependent kinase (CDK) complex (Karimian et al. 2016). Cyclin A plays a role in the rate-limiting step for entry into mitosis and its overexpression accelerates the G1 to S transition causing DNA replication (Furuno et al. 1999). Accumulation of cyclin E at the transitional period of G1-S accelerates cells entry into the S phase (Lundberg and Weinberg 1998; Ewen 2000). We, therefore, performed immunoblot analysis of the protein levels of P21, cyclin A2, and cyclin E1 in Caco2 cells. Our results showed a significant increase in the P21 protein level after obacunone treatment (Figure 8(C)). Conversely, we observed a markedly decrease in cyclin A2 and cyclin E1 protein levels in Caco2 cells. Similarly, obacunone exerted prominently suppressive effects on mRNA levels of cell proliferation-related genes (CCNA2, CCND2, CCND3, CCNE1, CCNE2, CDK2, and P21; Figure 8(D)).
Ribociclib (LEE011) suppresses cell proliferation and induces apoptosis of MDA-MB-231 by inhibiting CDK4/6-cyclin D-Rb-E2F pathway
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Tianqi Li, Yudi Xiong, Qingqing Wang, Fengxia Chen, Yangyang Zeng, Xiaoyan Yu, Yuan Wang, Fuxiang Zhou, Yunfeng Zhou
The 72-h treatment on MDA-MB-231 cells with escalating LEE011 led to a dose-dependent decrease in CDK4, CDK6, p-Rb, Rb, E2F1, CDK2 and cyclin E1 level, accompanied by synchronous rise of cyclin D1. View of their established significance in activating the Rb pathway, cyclin-CDK complexes have occupied a predominant status in cell cycle control [7,28]. And LEE011-induced alterations in CDK4/6-cyclin D-Rb-E2F1 axis supported our assumption. We incorporated cyclin E1 detected out of targeted effect, which means the inhibition on Rb-E2F pathway will decrease cyclin E1 and CDK2-cyclin E complexes level [7]. Owing to the following dysregulation in E2F downstream genes FoxM1, CCNA1, Myc [10], this impediment may facilitate G1-S cell cycle arrest and halts cell proliferation ultimately [29]. Additionally, different from what we have presumed [13,30], tiny changes occurred with P16, which could be explained as limited necessity of P16 (CDNK2A) for TNBC [31]. Disruptions upon the CDK4/6-cyclin D-P16-Rb pathway have emerged frequently in many human cancers [32,33], considering its highest negativity with TNBC group [34], we may find it not too hard to contact this two events together.