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MicroRNAs in Human Cancers and Therapeutic Applications
Published in Peixuan Guo, Kirill A. Afonin, RNA Nanotechnology and Therapeutics, 2022
Ji Young Yoo, Balveen Kaur, Tae Jin Lee, Peixuan Guo
In contrast to the downregulated tumor suppressive miRNAs, certain miRNAs are found to be significantly upregulated in cancers. First putative oncogenic miRNA (onco-miRs), miR-155, was shown to be highly overexpressed in a variety of cancers, including human B-cell lymphoma, pediatric Burkitt’s lymphoma, Hodgkin’s disease, primary mediastinal non-Hodgkin’s lymphoma, CLL, AML, lung cancer, and breast cancer (Jurkovicova et al., 2014). Later studies found that miR-155 directly targeted Src homology 2 domain-containing inositol-5-phosphatase (SHIP) and CCAAT enhancer-binding protein beta (C/EBPbeta), both of which are involved in the interleukin-6 (IL-6) signaling pathway (Costinean et al., 2009). MiR-155 is also found in high levels in nonalcoholic steatohepatitis (NASH) and can lead to the development of HCC (Wang et al., 2009). MiR-17-92 is a cluster of six onco-miRs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92-1. This cluster is frequently amplified in follicular lymphoma and diffuses large B cell lymphoma and is also highly expressed in a variety of other cancers such as breast, colon, lung, pancreas, prostate, and stomach cancer (Olive et al., 2013). They promote tumor proliferation and angiogenesis while controlling E2F1 expression (He et al., 2005; O’Donnell et al., 2005; Xiao et al., 2008). Both E2F1 and E2F3 are involved in a regulatory loop with the miR-17-92 cluster (Sylvestre et al., 2007). Downregulation of these onco-miR expressions in cancerous tissue has been shown to induce apoptosis, cell cycle arrest and reduce metastatic ability, which makes them potential therapeutic targets.
Combination treatment with auranofin and nutlin-3a induces synergistic cytotoxicity in breast cancer cells
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Dong-Jin Ye, Yeo-Jung Kwon, Hyoung-Seok Baek, Eunah Cho, Tae-Uk Kwon, Young-Jin Chun
Nutlin-3a as illustrated in Figure 1a is a small-molecule inhibitor which inhibits p53-MDM2 interaction, thereby preventing MDM2-mediated p53 degradation with a consequent demonstration of cytotoxic efficacy against cancer cells expressing wild-type p53 (Turner et al. 2013). In addition, nutlin-3a also inhibits the interaction between MDM2 and p73α (an isoform of p73) (Lau et al. 2008). p73 is a member of the p53 family and similar to p53 induces expression of pro-apoptotic genes in response to intracellular stress signals (Jost, Marin, and Kaelin 1997; Melino et al. 2004). Lau et al. (2008) found that nutlin-3a induced p73-mediated apoptosis in p53-mutant as well as p53-deficient cells. Unlike p53, Dotsch et al. (2010) reported that p73 mutation is rarely observed in tumors. Therefore, evidence indicates that nutlin-3a may induce cell death in diverse types of cancer cells irrespective of p53 mutations. Several investigators employed the principle that nutlin-3a inhibits the interaction between MDM2 and many tumor suppressors such as p53, p73α, and E2F1. In addition, studies examining the efficiency of combination therapy using nutlin-3a with DNA damaging drugs such as cisplatin and carboplatin were also conducted (Ambrosini et al. 2007; Tonsing-Carter et al. 2015).
The effects of ambient particulate matter on human adipose tissue
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Lior Hassan, Tal Pecht, Nir Goldstein, Yulia Haim, Itai Kloog, Shaked Yarza, Batia Sarov, Victor Novack
Chronic exposure to PM10. In comparison to the higher % leucocytes in response to acute exposure to PM10, a negative association was noted between chronic exposure to PM10 and % leucocytes as evidenced from the total non-adipocytes fraction of the tissue (Leuco%/OM/FACS). Further, chronic PM10 exposure was associated with a significant decrease in SC E2F1 protein levels. Similar to the intermediate exposure, chronic PM10 exposure was correlated with smaller sized OM adipocytes. Overall, these results indicated that chronic exposure to PM10 was associated with reduced adipocyte hypertrophy in OM tissue as well as a fall in the presence of OM adipose tissue macrophages which may be indicative of attenuated inflammation in the tissue.