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Nuclear Receptor Coactivators: Mechanism and Therapeutic Targeting in Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Andrew Cannon, Christopher Thompson, Rakesh Bhatia, Sushil Kumar
In breast cancer, studies have revealed several mechanisms by which NCOA1 contributes to disease progression, and therapy resistance/failure. The formation of new tumor vasculature is critical for both sustaining the high metabolic demands of rapidly growing tumors as well as for the initiation of the invasion/metastasis cascade. In several mouse models, the expression of NCOA1 was associated with microvessel density (MVD) as assessed by CD31 staining and qRT-PCR expression of CD31 [12]. Knockout and overexpression of NCOA1 in these models resulted in decrease and increase in MVD, respectively [12]. NCOA1 mediated this effect by enhancing transcription of HIF-1alpha and AP-1 gene target, VEGFa. In patient samples, the association of NCOA1 expression with MVD was validated and high NCOA1 expression and high MVD was associated with decreased overall survival (OS) [12]. Consistent with these findings of more aggressive disease in patients expressing high levels of NCOA1, a second study found increased numbers of circulating tumor cells as well as increased involvement of the lung by metastatic lesions (normalized to primary tumor volume) in a Tg(Neu x hNCOA1) mouse model [13]. As in the previous study, NCOA1 acted as a coactivator of AP-1 transcriptional complex to augment CSF-1 expression [13]. Subsequent knockdown of CSF-1 abrogated lung colonization confirming the involvement of this cytokine in the metastatic process [13]. The combined effect of high NCOA1 and high CSF-1 expression resulted in a statistically significant decrease in OS of breast cancer patients compared to the low NCOA1 low CSF-1 expression cohort [13]. Additional studies of the role of NCOA1 in the breast cancer metastasis showed that knockdown of NCOA1 in mouse-derived breast cancer cells lines attenuated the migratory capacity of breast cancer cells through downregulation of AP-1-mediated expression of integrin A5 and disruption of focal adhesion kinase signaling [14].
Suspended cell lines for inactivated virus vaccine production
Published in Expert Review of Vaccines, 2023
Jiayou Zhang, Zhenyu Qiu, Siya Wang, Zhenbin Liu, Ziling Qiao, Jiamin Wang, Kai Duan, Xuanxuan Nian, Zhongren Ma, Xiaoming Yang
The Src family, also known as the P160 steroid receptor coactivator family, contains three members: Src-1, Src-2, and Src-3. The lack of Src-1 (also known as NCOA1) in human breast cancer cells has been shown to significantly prolong the time of adhesion plaque disassembly and reassembly and reduce the cell adhesion and migration ability on fibronectin [100]. In MCF-7 breast cancer cells, Src-2 knockdown reduced estrogen-induced cell proliferation and target gene expression [114]. Paxillin is a plaque-associated protein involved in regulating integrin signaling and organizing the actin cytoskeleton. Paxillin is associated with many signaling molecules, including adaptor molecules (p130Cas and CRK), kinases (FAK, Pyk2, PAK, and Src), tyrosine phosphatases (PTP – PEST), ARF – GAP proteins (p95pkl and PAG3), and papillomavirus E6 oncoproteins [115]. Paxillin knockout cells have defects in adhesion remodeling [102]; furthermore, loss of Paxillin leads to impaired activation of its downstream target FAK, which is an outward signaling marker of integrin [103].
Effect of titanium dioxide nanoparticles on histone modifications and histone modifying enzymes expression in human cell lines
Published in Nanotoxicology, 2022
Marta Pogribna, Beverly Word, Beverly Lyn-Cook, George Hammons
KMT2E (MLL5), a H3K4me3-specific methyltransferase, has been reported to play a key role in diverse biological processes, including cell cycle progression, genomic stability maintenance, adult hematopoiesis, and spermatogenesis (Zhang et al. 2017). KMT2E dysfunction is associated with several human diseases, including cancers, neurological orders, atherosclerosis, and coronary artery disease. KMT2E gene expression profiles show upregulation in a variety of cancers, including large intestine and stomach, for examples. Analysis of several datasets revealed that NCOA1 was upregulated in gastric cancer; lower NCOA1 expression was associated with better overall survival of gastric cancer patients (Meng et al. 2019). Suppression of NCOA1 expression was found to decrease the invasiveness of human colon cancer cells (Meerson and Yehuda 2016). SETDB2 (KMT1F), a H3K9me3-specific methyltransferase, is involved in chromosome segregation (Falandry et al. 2010). SETDB2 is highly expressed in primary human gastric cancer tissues; overexpression was significantly associated with the late stage of gastric cancers and poor prognosis of gastric cancer patients (Nishikawaji et al. 2016). High expression levels are also observed in acute myeloid leukemia (Mu & Chen 2020). UBE2B (RAD6B) is involved in DNA repair. UBE2B is highly expressed in rectal cancer and significantly correlates with tumor regression grade (Huang et al. 2020). USP16 is involved in various biological processes (Xu et al. 2021). USP16 expression was found to be elevated in prostate cancer (Ge et al. 2021) and USP16 functions as an oncogenic factor in lung tumorigenesis in mice (Xu et al. 2021).