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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
Transcriptional activation of the nuclear coactivator four-and-a-half LIM protein 2 (FLH2) demonstrates promiscuous nuclear binding partners and has been linked to an array of cellular responses. However, the extent of FLH2 expression and function in hormone-insensitive cancers has been understudied, with the exception of CRC. Its expression in CRC cells has been linked to Sp1 [134] and KLF8 expression resulting in increased tumorigenesis, invasion, and metastasis [135]. Further, others have used reciprocal co-immunoprecipitation assays and shown that it interacts with Snail1 in CRC [136], Smad2/3/4 to activate p21 [137], FOXK1 [138], and β-catenin [139, 140]. In CRC, FHL2 mediates upregulation of several genes such as vimentin, Snail, MMP2, MMP9, and E-cadherin [138, 141], suggesting that FHL2 is likely important for EMT in cancer cells. The FHL2 KD in PC cells resulted in decreased proliferation and survival, abrogation of radiotherapy resistance, and induction of MEK/ERK signaling and expression of cyclin D1, cyclin E, cyclin A, and cyclin B1 [142]. MEK inhibition in the same PC cells yielded similar results, suggesting that MEK activation may likely contribute to the signaling cascade upstream of FHL2; however, this relationship was not confirmed.
Gene networks associated with non-syndromic intellectual disability
Published in Journal of Neurogenetics, 2018
Soohyun Lee, Stephen Rudd, Jacob Gratten, Peter M. Visscher, Johannes B. Prins, Paul A. Dawson
The outcomes of our searches resulted in a list of 245 genes, including 171 autosomal and 74 X-chromosomal genes (Supplementary Table 1). The chromosomal distribution of the genes collated in this study shows a bias to the X-chromosome (Figure 1) that likely reflects the earlier research focus on X-linked ID. In recent years, the proportion of NS-ID associated genes located on the autosomes has expanded, indicating the significance of both the X-chromosome and autosomes to NS-ID. Approximately, one-quarter of NS-ID genes (N=57) map to one of six gene clusters located at 19p13 (CC2D1A, MAST1, NACC1, TECR, TRMT1, ZNF700), Xq22 (ACSL4, AMMECR1, BEX4, DCX, DRP2, GPRASP1, GUCY2F, KCNE5, PAK3, RIPPLY1, TMEM164), Xq26 (MAP7D3, SAGE1, SLC9A6, ZDHHC9), Xq28 (AFF2, FLNA, FMR3, GD11, MECP2, NAA10, SLC6A8), Xp22 (AP1S2, ARSF, ATXN3L, CDKL5, CNKSR2, MAP3K15, NLGN4X, PTCHD1, RPL9P7), and Xp11 (CASK, DDX3X, FAAH2, FGD1, FTSJ1, GSPT2, HUWE1, IQSEC2, KDM5C, KLF8, PQBP1, SHROOM4, SLC38A5, SMC1A, SSX6, SYP, TSPAN7, USP9X, WDR13, WDR45). These gene clusters are relevant when considering deletions at 19p13 and Xq22, and duplications at Xp22, Xp11, Xq26 and Xq28, which have been associated with ID (Fukushi et al., 2014; Li et al., 2010; Møller et al., 2014; Nizon et al., 2015; Peddibhotla et al., 2013; Yamamoto et al., 2014).