China
Africa
Explore chapters and articles related to this topic
Dopamine and Tumorigenesis in Reproductive Tissues
Published in Nira Ben-Jonathan, Dopamine, 2020
Subsequent studies revealed that PTTG is overexpressed in other tumors, including thyroid, breast and ovarian carcinomas. The PTTG protein, also known as human securin, induces cellular transformation, is involved in cell cycle regulation, and controls the segregation of sister chromatids during mitosis [10]. PTTG is an anaphase inhibitor that prevents premature chromosome separation through inhibition of separase activity; hence, its degradation is required to start anaphase. Through this important function, PTTG participates in several key cellular events such as mitosis, cell cycle progression, DNA repair, and apoptosis. Another putative oncogene, gsp (Gαs subunit) was overexpressed in ~40% of hormonally active pituitary adenomas [7]. Both cAMP [11] and cGMP [12] signaling cascades also appear to be involved in pituitary tumors.
Targeting Major Signaling Pathways of Bladder Cancer with Phytochemicals: A Review
Published in Nutrition and Cancer, 2021
Connor Chestnut, Dharmalingam Subramaniam, Prasad Dandawate, Subhash Padhye, John Taylor, Scott Weir, Shrikant Anant
Baicalein is a flavone derived from the herb Huang Qin, which is used in traditional Chinese medicine as an anti-inflammatory (188). Baicalein has been examined both In Vitro and In Vivo for treatment of bladder, prostate, and hepatocellular cancer (188). Wu demonstrated In Vivo that baicalein inhibits bladder cancer proliferation and migration in a dose-dependent manner via reduction of phosphorylated NF-κB and MMP-2/9 expression (189). In Vitro studies pointed reduction in securin and AKT/γ‐H2AX survival pathways, increased ROS production, and reduced expression of the anti-apoptotic factors Bcl-xL, XIAP, and survivin (190–192). Baicalein has been shown to induce G0/G1 phase arrest through PI3K/AKT phosphorylation and increased Bax/Bcl-2 ratio, and G2/M phase arrest through induction of p38 MAPK and inhibition of CDC2 Kinase (193–195).
Cancer-Associated Fibroblasts Induce Epithelial-Mesenchymal Transition in Endometrial Cancer Cells by Regulating Pituitary Tumor Transforming Gene
Published in Cancer Investigation, 2019
Xiaoyun Wang, Xiwen Sun, Lin Mu, Wei Chen
Pituitary tumor transforming gene (PTTG), also known as securin, encodes a multifunctional protein that regulates sister chromatid separation during mitosis, maintains chromosomal stability, and responds to DNA damage under normal physiological conditions (17–19). High levels of PTTG expression have been described in a variety of human tumors, including thyroid, ovarian, breast, liver and lung cancer, and various tumor cell lines (20–22). The introduction of oncogenic PTTG results in an increase in cell proliferation, induction of cellular transformation, and promotion of tumor development in nude mice (23). However, the underlying mechanisms of CAFs and PTTG in regulating endometrial cancer are still not fully understood. In this study, we demonstrated that CAFs induce EMT in endometrial cancer cells by regulating PTTG.
Artificial oocyte activation: physiological, pathophysiological and ethical aspects
Published in Systems Biology in Reproductive Medicine, 2019
George Anifandis, Alexandros Michopoulos, Alexandros Daponte, Katerina Chatzimeletiou, Mara Simopoulou, Christina I. Messini, Nikolas P. Polyzos, Katerina Vassiou, Konstantinos Dafopoulos, Dimitrios G. Goulis
It has repeatedly been demonstrated that the Ca+2 increase during fertilization is necessary and sufficient for restarting cell cycle events in almost all kind of oocytes (Kline and Kline 1992a, 1992b; Minamikawa and Morisawa 1996; Nomura and Nemoto 1998; Yamamoto and Okada 1999). The Ca+2 increase provokes ascidian and vertebrate oocytes to enter anaphase and complete meiosis and to undergo DNA synthesis, respectively (Shilling et al. 1990). Specifically, in ascidians, the release from the meiotic arrest requires the activity of the phosphatase PP2A and calcineurin (Levasseur et al. 2013). The events mentioned above have been experimentally tested by causing an elevation in Ca+2 stores in oocytes and conversely, by injecting oocytes with Ca+2 buffers to prevent the Ca+2 elevation. Although the mechanisms underlying the Ca+2 increases with the completion of meiosis are not fully elucidated, it seems that involve a calmodulin-dependent protein kinase, which, in turn, results to the proteolysis of securin, cyclin and cohesin that hold the chromosomes together (Lorca 1993; Kawahara and Yokosawa 1994; Aizawa et al. 1996; Johnson 1998; Stemmann et al. 2001). The inactivation of mitogen-activated protein (MAP)-kinase seems to be responsible for the increase of DNA synthesis in echinoderm oocytes (Tachibana et al. 1997). In mammals, the sperm factor PLCζ causes a series of Ca+2 oscillations, playing therefore fundamental role during fertilization (Kashir et al. 2014).