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    SIX1 SIX homeobox 1 [ Homo sapiens (human) ]

    Gene ID: 6495, updated on 23-Apr-2017

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Studies strongly suggest that Six1 overexpression promotes CRC growth and metastasis and remodels tumor stroma by stimulating angiogenesis and recruiting TAM. MAPK activation may be a pivotal event in Six1-associated tumor progression.

    Six1 promotes colorectal cancer growth and metastasis by stimulating angiogenesis and recruiting tumor-associated macrophages.
    Xu H, Zhang Y, Peña MM, Pirisi L, Creek KE.

    Restoration of SIX1 was sufficient to abolish proliferation, migration and invasion induced by miR-362 overexpression in cervical cancer cells. The newly identified miR-362/SIX1 pathway provides insight into cervical cancer progression, and may represent a novel therapeutic target.

    MicroRNA-362 is downregulated in cervical cancer and inhibits cell proliferation, migration and invasion by directly targeting SIX1.
    Shi C, Zhang Z.

    study replicated the association of POAG with two SNPs at the SIX1-SIX6 locus and demonstrated that SNPs, rs10483727 and rs33912345, are significantly associated with POAG, especially with NTG in patients aged above 40 years

    Association of three single nucleotide polymorphisms at the SIX1-SIX6 locus with primary open angle glaucoma in the Chinese population.
    Sang J, Jia L, Zhao B, Wang H, Zhang N, Wang N.

    results suggest that SIX1 is a key proliferation regulator in mouse DFCs and human PDLCs, which provides novel insight into Six family gene function in mammals.

    Six1 is required for mouse dental follicle cell and human periodontal ligament-derived cell proliferation.
    Kawasaki T, Takahashi M, Yajima H, Mori Y, Kawakami K.

    miR-188 suppresses proliferation and invasion by targeting SIX1 in oral squamous cell carcinoma cells.

    microRNA-188 is downregulated in oral squamous cell carcinoma and inhibits proliferation and invasion by targeting SIX1.
    Wang L, Liu H.

    Pro-survival effects by NF-kappaB, Akt and ERK(1/2) and anti-apoptosis actions by Six1 disrupt apoptotic functions of TRAIL-Dr4/5 pathway in ovarian cancer, which may explain why up-regulated DR4 and DR5 in ovarian cancer are associated with poor prognosis and low survival ratio of the patients.

    Pro-survival effects by NF-κB, Akt and ERK(1/2) and anti-apoptosis actions by Six1 disrupt apoptotic functions of TRAIL-Dr4/5 pathway in ovarian cancer.
    Yang J, Li G, Zhang K.

    Upregulation of Six1 could downregulate miR-204-5p expression.

    MiR-204-5p/Six1 feedback loop promotes epithelial-mesenchymal transition in breast cancer.
    Zeng J, Wei M, Shi R, Cai C, Liu X, Li T, Ma W.

    Mutations of SIX1 gene underlie Wilms tumor recurrences.

    Chromosomal anomalies at 1q, 3, 16q, and mutations of SIX1 and DROSHA genes underlie Wilms tumor recurrences.
    Spreafico F, Ciceri S, Gamba B, Torri F, Terenziani M, Collini P, Macciardi F, Radice P, Perotti D., Free PMC Article

    Six1 signaling has a role in paclitaxel-dependent apoptosis in MCF-7 cell line

    The role of Six1 signaling in paclitaxel-dependent apoptosis in MCF-7 cell line.
    Armat M, Oghabi Bakhshaiesh T, Sabzichi M, Shanehbandi D, Sharifi S, Molavi O, Mohammadian J, Saeid Hejazi M, Samadi N., Free PMC Article

    Six1 mutations/gene deletion are unlikely to be a major cause of nonsyndromic CAKUT.

    SIX1 gene: absence of mutations in children with isolated congenital anomalies of kidney and urinary tract.
    Negrisolo S, Centi S, Benetti E, Ghirardo G, Della Vella M, Murer L, Artifoni L.

    Data show that the protein domain interfaces may represent therapeutic targets in homeo domain protein SIX1-positive Hodgkin lymphoma (HL) subsets.

    Aberrant expression of homeobox gene SIX1 in Hodgkin lymphoma.
    Nagel S, Meyer C, Kaufmann M, Drexler HG, MacLeod RA., Free PMC Article

    Data show that both Ezrin and SIX1 proteins are highly expressed in alpha fetoprotein-negative hepatocellular carcinoma (HCC) and significantly related with the TNM stage.

    [Clinicopathological significance of ezrin and SIX1 protein expression in alpha fetoprotein-negative hepatocellular carcinoma].
    Kong J, Zhou X, Han L, Quan C, Cui X, Lin Z.

    These data suggest differential SIX-factor regulation might have contributed to species differences in nephron progenitor programs such as the duration of nephrogenesis and the final nephron count

    Differential regulation of mouse and human nephron progenitors by the Six family of transcriptional regulators.
    O'Brien LL, Guo Q, Lee Y, Tran T, Benazet JD, Whitney PH, Valouev A, McMahon AP., Free PMC Article

    Single nucleotide polymorphism in SIX1 gene is associated with primary open angle glaucoma.

    Genetic association of SNPs near ATOH7, CARD10, CDKN2B, CDC7 and SIX1/SIX6 with the endophenotypes of primary open angle glaucoma in Indian population.
    Philomenadin FS, Asokan R, N V, George R, Lingam V, Sarangapani S., Free PMC Article

    High expression of SIX1 is an independent prognostic marker in colorectal cancer.

    Overexpression of SIX1 is an independent prognostic marker in stage I-III colorectal cancer.
    Kahlert C, Lerbs T, Pecqueux M, Herpel E, Hoffmeister M, Jansen L, Brenner H, Chang-Claude J, Bläker H, Kloor M, Roth W, Pilarsky C, Rahbari NN, Schölch S, Bork U, Reissfelder C, Weitz J, Aust D, Koch M.

    Three causative genes for BOR syndrome have been reported thus far: EYA1, SIX1, and SIX5, but the causative genes for approximately half of all BOR patients remain unknown.[review]

    Branchio-oto-renal syndrome: comprehensive review based on nationwide surveillance in Japan.
    Morisada N, Nozu K, Iijima K.

    SIX1 and EYA are often co-overexpressed in tumors, and the SIX1-EYA2 interaction has been shown to be critical for metastasis in a breast cancer model.

    The SIX1-EYA transcriptional complex as a therapeutic target in cancer.
    Blevins MA, Towers CG, Patrick AN, Zhao R, Ford HL., Free PMC Article

    Six1 plays an important role in the TIC population in luminal breast cancers and induces a TIC phenotype by enhancing both TGF-beta and ERK signaling.

    Expression of Six1 in luminal breast cancers predicts poor prognosis and promotes increases in tumor initiating cells by activation of extracellular signal-regulated kinase and transforming growth factor-beta signaling pathways.
    Iwanaga R, Wang CA, Micalizzi DS, Harrell JC, Jedlicka P, Sartorius CA, Kabos P, Farabaugh SM, Bradford AP, Ford HL., Free PMC Article

    SIX1 plays an important role in the progression ofhepatocellular carcinoma

    Overexpression of sineoculis homeobox homolog 1 predicts poor prognosis of hepatocellular carcinoma.
    Kong J, Zhou X, Liu S, Jin T, Piao Y, Liu C, Lin Z., Free PMC Article

    Recurrent mutations included a hotspot mutation (Q177R) in the homeo-domain of SIX1 and SIX2 in tumors with high proliferative potential (18.1% of blastemal cases); mutations in the DROSHA/DGCR8 microprocessor genes

    Mutations in the SIX1/2 pathway and the DROSHA/DGCR8 miRNA microprocessor complex underlie high-risk blastemal type Wilms tumors.
    Wegert J, Ishaque N, Vardapour R, Geörg C, Gu Z, Bieg M, Ziegler B, Bausenwein S, Nourkami N, Ludwig N, Keller A, Grimm C, Kneitz S, Williams RD, Chagtai T, Pritchard-Jones K, van Sluis P, Volckmann R, Koster J, Versteeg R, Acha T, O'Sullivan MJ, Bode PK, Niggli F, Tytgat GA, van Tinteren H, van den Heuvel-Eibrink MM, Meese E, Vokuhl C, Leuschner I, Graf N, Eils R, Pfister SM, Kool M, Gessler M.

    in tumors with DGCR8 E518K and DROSHA exon 29 (miRNAPG-HS) mutations ... greater prevalence of tumors with blastemal predominant histology in patients with miRNAPG-HS and/or SIX1/2 Q177R mutations

    Recurrent DGCR8, DROSHA, and SIX homeodomain mutations in favorable histology Wilms tumors.
    Walz AL, Ooms A, Gadd S, Gerhard DS, Smith MA, Guidry Auvil JM, Meerzaman D, Chen QR, Hsu CH, Yan C, Nguyen C, Hu Y, Bowlby R, Brooks D, Ma Y, Mungall AJ, Moore RA, Schein J, Marra MA, Huff V, Dome JS, Chi YY, Mullighan CG, Ma J, Wheeler DA, Hampton OA, Jafari N, Ross N, Gastier-Foster JM, Perlman EJ., Free PMC Article

    Six1 overexpression in HPV16-immortalized keratinocytes increased cell proliferation and promoted cell migration and invasion by inducing epithelial-mesenchymal transition.

    Six1 overexpression at early stages of HPV16-mediated transformation of human keratinocytes promotes differentiation resistance and EMT.
    Xu H, Pirisi L, Creek KE., Free PMC Article

    HDAC5 promoted the Six1 expression.

    HDAC5 promotes cell proliferation in human hepatocellular carcinoma by up-regulating Six1 expression.
    Feng GW, Dong LD, Shang WJ, Pang XL, Li JF, Liu L, Wang Y.

    tumor cells that expressed high levels of SIX1 could promote lymphangiogenesis and counteract the negative effects of TGFbeta on lymphangiogenesis by increasing the expression of VEGF-C

    SIX1 promotes tumor lymphangiogenesis by coordinating TGFβ signals that increase expression of VEGF-C.
    Liu D, Li L, Zhang XX, Wan DY, Xi BX, Hu Z, Ding WC, Zhu D, Wang XL, Wang W, Feng ZH, Wang H, Ma D, Gao QL.

    Results suggest that the increase of SIX1 expression could promote tumorigenesis, progression and invasive growth of cervical cancer by promoting DNA replication.

    Sine oculis homeobox homolog 1 promotes DNA replication and cell proliferation in cervical cancer.
    Liu D, Zhang XX, Xi BX, Wan DY, Li L, Zhou J, Wang W, Ma D, Wang H, Gao QL.

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