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    TGFB1I1 transforming growth factor beta 1 induced transcript 1 [ Homo sapiens (human) ]

    Gene ID: 7041, updated on 10-Dec-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    TGFB1I1 promotes cell proliferation and migration in urothelial carcinoma.

    TGFB1I1 promotes cell proliferation and migration in urothelial carcinoma.
    Liang PI, Wei YC, Chen HD, Ma YC, Ke HL, Chien CC, Chuang HW.

    03/13/2024
    Paxillin family proteins Hic-5 and LPXN promote lipid storage by regulating the ubiquitination degradation of CIDEC.

    Paxillin family proteins Hic-5 and LPXN promote lipid storage by regulating the ubiquitination degradation of CIDEC.
    Fang M, Liu X, Xu W, Wang X, Xu L, Zhao TJ, Li P, Yang H., Free PMC Article

    02/27/2024
    Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.

    Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.
    Alpha KM, Xu W, Turner CE., Free PMC Article

    08/28/2021
    Exosome-mediated Hic-5 regulates proliferation and apoptosis of osteosarcoma via Wnt/beta-catenin signal pathway.

    Exosome-mediated Hic-5 regulates proliferation and apoptosis of osteosarcoma via Wnt/β-catenin signal pathway.
    Sha L, Ma D, Chen C., Free PMC Article

    05/1/2021
    TGFbeta1I1 suppressed cell migration and invasion in colorectal cancer by inhibiting the TGF-beta pathway and EMT progress.

    TGFβ1I1 suppressed cell migration and invasion in colorectal cancer by inhibiting the TGF-β pathway and EMT progress.
    Ruan XJ, Ye BL, Zheng ZH, Li ST, Zheng XF, Zhang SZ.

    05/1/2021
    Increased expression of the transforming growth factor beta-inducible gene HIC-5 in systemic sclerosis skin and fibroblasts: a novel antifibrotic therapeutic target.

    Increased expression of the transforming growth factor β-inducible gene HIC-5 in systemic sclerosis skin and fibroblasts: a novel antifibrotic therapeutic target.
    Piera-Velazquez S, Fertala J, Huaman-Vargas G, Louneva N, Jiménez SA.

    01/23/2021
    HIC-5 in cancer-associated fibroblasts contributes to esophageal squamous cell carcinoma progression.

    HIC-5 in cancer-associated fibroblasts contributes to esophageal squamous cell carcinoma progression.
    Du X, Xu Q, Pan D, Xu D, Niu B, Hong W, Zhang R, Li X, Chen S., Free PMC Article

    09/26/2020
    Results reveal novel regulation of vimentin organization/dynamics by the FA scaffold protein Hic-5 via modulation of RhoGTPases and downstream formin activity.

    The focal adhesion scaffold protein Hic-5 regulates vimentin organization in fibroblasts.
    Vohnoutka RB, Gulvady AC, Goreczny G, Alpha K, Handelman SK, Sexton JZ, Turner CE., Free PMC Article

    06/27/2020
    The molecular mechanism involved in Hic-5-mediated invasion.

    Hic-5 in pancreatic stellate cells affects proliferation, apoptosis, migration, invasion of pancreatic cancer cells and postoperative survival time of pancreatic cancer.
    Qian B, Wei L, Yang Z, He Q, Chen H, Wang A, Yang D, Li Q, Li J, Zheng S, Fu W.

    06/6/2020
    HIC-5 regulates mitochondrial ROS production in tumor cells while requiring activated KRAS to mediate its effect on NOX4 in oncogene-induced senescence and tumor invasiveness.

    A mitochondrial ROS pathway controls matrix metalloproteinase 9 levels and invasive properties in RAS-activated cancer cells.
    Mori K, Uchida T, Yoshie T, Mizote Y, Ishikawa F, Katsuyama M, Shibanuma M., Free PMC Article

    08/10/2019
    HIC-5 regulates mitochondrial ROS production in tumor cells while requiring activated KRAS to mediate its effect on NOX4 in oncogene-induced senescence and tumor invasiveness.

    Regulation of mitochondrial ROS production by HIC-5: a common feature of oncogene-induced senescence and tumor invasiveness?
    Doppler W, Jansen-Dürr P., Free PMC Article

    08/10/2019
    Hic-5 is a crucial regulator of extracellular matrix remodeling in Cancer-associated fibroblasts by promoting fibrillar adhesion formation through a novel interaction with tensin1.

    Hic-5 regulates fibrillar adhesion formation to control tumor extracellular matrix remodeling through interaction with tensin1.
    Goreczny GJ, Forsythe IJ, Turner CE., Free PMC Article

    03/30/2019
    These results identify Hic-5 as a critical modulator of tumor cell phenotype.

    Hic-5 expression is a major indicator of cancer cell morphology, migration, and plasticity in three-dimensional matrices.
    Gulvady AC, Dubois F, Deakin NO, Goreczny GJ, Turner CE., Free PMC Article

    03/9/2019
    High HIC5 expression is associated with tumorigenesis of colorectal cancer.

    The impact of stromal Hic-5 on the tumorigenesis of colorectal cancer through lysyl oxidase induction and stromal remodeling.
    Omoto T, Kim-Kaneyama JR, Lei XF, Orimo A, Ohnishi K, Yoshihara K, Miyauchi A, Li S, Gao L, Umemoto T, Tanaka J, Nakahara K, Takeya M, Ishida F, Kudo SE, Haraguchi S, Miyazaki T, Miyazaki A.

    03/9/2019
    this paper shows that IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5

    IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5.
    Paul J, Singh AK, Kathania M, Elviche TL, Zeng M, Basrur V, Theiss AL, Venuprasad K.

    12/22/2018
    Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5.

    Different chromatin and DNA sequence characteristics define glucocorticoid receptor binding sites that are blocked or not blocked by coregulator Hic-5.
    Lee BH, Stallcup MR., Free PMC Article

    08/4/2018
    Isolated Hic-5(-/-);PyMT CAFs were defective in stress fiber organization and exhibited reduced contractility. These cells also failed to efficiently deposit and organize the ECM in two and three dimensions. This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior

    Hic-5 remodeling of the stromal matrix promotes breast tumor progression.
    Goreczny GJ, Ouderkirk-Pecone JL, Olson EC, Krendel M, Turner CE., Free PMC Article

    09/9/2017
    Hic-5 regulates GR binding site selection by a novel mechanism, exploiting gene-specific requirements for chromatin remodeling enzymes to selectively influence DNA occupancy and gene regulation by a transcription factor.

    Glucocorticoid receptor binding to chromatin is selectively controlled by the coregulator Hic-5 and chromatin remodeling enzymes.
    Lee BH, Stallcup MR., Free PMC Article

    06/10/2017
    As aging increased, more ARA55 were expressed in PZ stromal cells, leading to more sensitive androgen/androgen receptor (AR) signal pathway, then constituting a more feasible environment to cancer cells.

    Aging up-regulates ARA55 in stromal cells, inducing androgen-mediated prostate cancer cell proliferation and migration.
    Zou Q, Cui D, Liang S, Xia S, Jing Y, Han B.

    02/18/2017
    Hic-5 appears to enhance complex formation between MT1-MMP and FAK in activated endothelial cells, which likely coordinates matrix proteolysis and cell motility.

    Hic-5 mediates the initiation of endothelial sprouting by regulating a key surface metalloproteinase.
    Dave JM, Abbey CA, Duran CL, Seo H, Johnson GA, Bayless KJ., Free PMC Article

    12/17/2016
    Hic-5 plays a central role in the positive feedback ROS-JNK signaling cascade that regulates hepatocellular carcinoma progression.

    Hydrogen peroxide inducible clone-5 mediates reactive oxygen species signaling for hepatocellular carcinoma progression.
    Wu JR, Hu CT, You RI, Pan SM, Cheng CC, Lee MC, Wu CC, Chang YJ, Lin SC, Chen CS, Lin TY, Wu WS., Free PMC Article

    08/13/2016
    Hic-5 influences the genomic occupancy of multiple steroid receptors and thereby blocks some aspects of hormonal regulation.

    Selective coregulator function and restriction of steroid receptor chromatin occupancy by Hic-5.
    Chodankar R, Wu DY, Gerke DS, Stallcup MR., Free PMC Article

    04/2/2016
    Endothelial Hic-5 plays an important role in the formation of microvilli-like structures and in the interaction between ECs and monocytes, leading to monocyte recruitment and subsequent development of atherosclerosis.

    Role of Hic-5 in the formation of microvilli-like structures and the monocyte-endothelial interaction that accelerates atherosclerosis.
    Arita-Okubo S, Kim-Kaneyama JR, Lei XF, Fu WG, Ohnishi K, Takeya M, Miyauchi A, Honda H, Itabe H, Miyazaki T, Miyazaki A.

    12/5/2015
    Studies in vitro and in vivo using TGF-beta1 and TGFB1I1 shRNA demonstrated that TGFB1I1 is required for TGF-beta stimulated EMT that contributes to malignant progression of astrocytomas.

    Multidimensional analysis of gene expression reveals TGFB1I1-induced EMT contributes to malignant progression of astrocytomas.
    Liu Y, Hu H, Wang K, Zhang C, Wang Y, Yao K, Yang P, Han L, Kang C, Zhang W, Jiang T., Free PMC Article

    11/14/2015
    Hic-5 siRNA also suppressed TGF-beta2-induced fibrogenic activity and dexamethasone-induced myocilin expression in HTM cells.

    Hic-5 Regulates Actin Cytoskeletal Reorganization and Expression of Fibrogenic Markers and Myocilin in Trabecular Meshwork Cells.
    Pattabiraman PP, Rao PV., Free PMC Article

    10/31/2015
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