SNAI2 overexpression appears to be associated with poor prognosis in breast cancer, yet it remains unclear in which breast cancer subtypes this occurs SNAI2 has been implicated in diseases of melanocyte development and cancer in humans. Many malignancies arise from a rare population of cells that alone have the ability to self-renew and sustain the tumor (i.e., cancer stem cells) In our model system, phenotype change correlates with an increase in the expression of SNAIL2 and TWIST2 factors, which indicates their possible role in regulating invasive growth of thyroid cancer with the mutation of NRAS (Q61R). Related: Signal Transduction Thyroid Cancer NRAS Penolazzi L, Bonaccorsi G, Gafà R, et al Expression of SNAI2 (SLUG, SLUGH, SLUGH1, SNAIL2) in cancer tissue. The cancer tissue page shows antibody staining of the protein in 20 different cancers Therefore, we hypothesized that SNAI2 (Slug) may mediate 5FU chemotherapy resistance through inhibition of miR-145 in colorectal cancer (CRC) and thus, represents a novel therapeutic target to enhance current CRC treatment strategies
Background: Epithelial ovarian cancer (EOC) is one of the most lethal malignancies in women worldwide. Many studies showed the transcription factor SNAI2-induced Epithelial-Mesenchymal Transition (EMT) through inhibiting E-cadherin (E-cad) expression 338Background: Androgen receptor (AR) signalling is important in prostate cancer progression, and therapies that specifically target this pathway are the mainstay of treatment for advanced disease.... Loss of SNAI2 in prostate cancer and effect on patient response to androgen deprivation therapy. | Journal of Clinical Oncolog SM83 reduced the expression of Snai2, an epithelial-to-mesenchymal transition factor often associated with increased stem-like properties and metastatic potential especially in breast cancer cells Transcription factor SNAI2 plays key roles during development and has also been known to promote metastasis by inducing invasive phenotype and tumor-initiating activity of cancer cells. However, the post-translational regulation of SNAI2 is less well studied. We performed a dual-luciferase-based, ge
20583 Ensembl ENSG00000019549 ENSMUSG00000022676 UniProt O43623 P97469 RefSeq (mRNA) NM_003068 NM_011415 RefSeq (protein) NP_003059 NP_035545 Location (UCSC) Chr 8: 48.92 - 48.92 Mb Chr 16: 14.71 - 14.71 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Zinc finger protein SNAI2 is a transcription factor that in humans is encoded by the SNAI2 gene. It promotes the differentiation. Our results suggest that SNAI2 is a key regulator of the aggressive phenotype observed in endocrine-resistant breast cancer cells, an independent prognostic biomarker in ER+ advanced breast cancer treated with endocrine therapy, and may be a promising therapeutic target in combination with endocrine therapies in ER+ metastatic breast cancer exhibiting high SNAI2 levels
Complete clonal loss of SNAI2 is uncommon in prostate cancer, being reported in 0.6% of localized cases in The Cancer Genome Atlas cohort. 24 Similarly, in our analysis, SNAI2 loss was only identified subclonally, and on FISH analysis, biallelic loss was only observed in up to a maximum of 30% of cells, even in extreme responders The transcription factor Snai2, encoded by the SNAI2 gene, is an evolutionarily conserved C2H2 zinc finger protein that orchestrates biological processes critical to tissue development and tumorigenesis
SNAI2/SLUG, a metastasis-promoting transcription factor, is a labile protein that is degraded through the ubiquitin proteasome degradation system. Here, we conducted comprehensive gain- and loss-of-function screens using a human DUB cDNA library of 65 genes and an siRNA library of 98 genes, and iden A drug-resistant protein named SNAI2 helps cancers metastasize and shields cancer from both the immune system and chemotherapy. But now Princeton University's Yibin Kang (lower right) and his colleagues have found a way to use the cell's recycling system to control SNAI2, providing a new possibility for treatments A dangerous protein named SNAI2 helps cancers metastasize and shields cancer from both the immune system and chemotherapy. Worse, SNAI2 is in a family of proteins that are notoriously hard to.
PURPOSE Androgen receptor (AR) signaling is important in prostate cancer progression, and therapies that target this pathway have been the mainstay of treatment for advanced disease for over 70 years. Tumors eventually progress despite castration through a number of well-characterized mechanisms; however, little is known about what determines the magnitude of response to short-term pathway. SNAI2 controls key aspects of stem cell function in mouse and human, suggesting that similar mechanisms control normal development and cancer stem cell properties. These insights are expected to contribute significantly to the genetics of cancer and to the development of both cancer therapy and new methods for assessing treatment efficacy The transcriptional repressor SNAI2 was previously identified as a key regulator of IR sensitivity in normal and malignant stem cells through its repression of the proapoptotic BH3-only gene PUMA. Here, we demonstrate a clear correlation between SNAI2 expression levels and radiosensitivity across multiple RMS cell lines Keywords: Ovarian cancer, PDCD10, miR-222-3p, SNAI2, Migration . Introduction. Epithelial ovarian cancer (EOC), which generally presents at an advanced stage in the most lethal malignancies in women, is the most common cause of gynecological cancer death
SNAI2 is not inherently bad; it plays an important role at key stages of development. But in healthy cells, SNAI2 only turns on for very narrow windows of time, such as during wound repair, when healthy cells need to move in to close the gap. In cancer patients, SNAI2 lingers, allowing cancer cells to use it to metastasize around the body This is NOT a known cancer gene. It is not found in the Cancer Gene Census . This is NOT an expert curated gene . Mouse insertional mutagenesis experiments DO NOT support the designation of SNAI2 as a cancer causing gene. This gene does not have a cancer hallmark. You can see more information about hallmarks
Regulation of breast cancer metastasis by Runx2 and estrogen signaling: the role of SNAI2. Chimge NO (1), Baniwal SK, Little GH, Chen YB, Kahn M, Tripathy D, Borok Z, Frenkel B. INTRODUCTION: In contrast to its role in breast cancer (BCa) initiation, estrogen signaling has a protective effect in later stages, where estrogen receptor (ER)α loss. SNAI1 represses SNAI2 expression. To confirm whether the correlation was an actual causal relationship, ovarian cancer cell line with epithelia-like phenotype, OVCA429 was engineered to. The extent of treatment response observed was determined by the prevalence of cells with loss of SNAI2 in pre-treatment biopsies. Conclusions: Cell plasticity with transition to a mesenchymal phenotype defines prostate cancer cell survival to acute AR signalling inhibition. Tumour response is determined by the proportion of cells present. Breast cancer is a major cause of mortality in women. The transcription factor SNAI2 has been implicated in the pathogenesis of several types of cancer, including breast cancer of basal origin
Slug/SNAI2 regulates cell proliferation and invasiveness of metastatic prostate cancer cell lines. Tumour Biol. 2010;31:297-307 4. Wang C, Liu X, Huang H. et al. Deregulation of Snai2 is associated with metastasis and poor prognosis in tongue squamous cell carcinoma. INT J CANCER. 2012;130:2249-58 5. Uygur B, Wu WS A SNAI2-PEAK1 stromal axis drives progression and lapatinib resistance in HER2-positive breast cancer by supporting a cytokine expression profile that converges on PI3K/Akt signaling Sarkis Hamalian , Robert Güth , Farhana Runa , Justin Molnar , Eric Vickers , Megan Agajanian , Jonathan Humphries , Martin J. Humphries , Julia Tchou , Ioannis K. A SNAI2-PEAK1 stromal axis correlates with disease progression in HER2-positive breast cancer. We first examined patient survival across all breast cancer subtypes in relation to PEAK1 expression.
In human breast cancer, the expression of SNAI1 and/or the homologous SNAI2 (Slug) has been associated with E-cadherin repression, local or distant metastasis, tumor recurrence, or poor prognosis in different tumor series. However, the specific contribution of either factor to breast tumor progression is still unclear To determine the effects of SNAI2 in vivo, we used our metastatic anaplastic thyroid cancer (ATC) mouse model. To investigate the effects of LOX and SNAI2 on MMPs and TIMPs, protein arrays were used. Primary tumors from patients with metastatic, breast and colon cancer, and tissue array for thyroid cancer were assessed for SNAI2 and TIMP4.
SNAI2 overexpression appears to be associated with poor prognosis in breast cancer, yet it remains unclear in which breast cancer subtypes this occurs. Here we show that excess SNAI2 is associated with a poor prognosis of luminal B HER2+ breast cancers in which SNAI2 expression in the stroma but not the epithelium correlates with tumor proliferation Epithelial-to-mesenchymal transition (EMT) has been associated with poor treatment outcomes in various malignancies and is inversely associated with miRNA145 expression. Therefore, we hypothesized that SNAI2 (Slug) may mediate 5-fluorouracil (5FU) chemotherapy resistance through inhibition of miR145 in colorectal cancer and thus represents a novel therapeutic target to enhance current.
Keywords: SNAI2, Stromal fibroblast, Reprogram, Stiffness, Ovarian cancer Background High grade serous ovarian cancer (OC) remains a devas-tating gynecological malignancy hallmarked by a high degree of heterogeneity [1]. Conventional classification scheme based on histopathological evaluation failed t Prostate Cancer (PCa)-related deaths are mostly due to metastasization of poorly differentiated adenocarcinomas often endowed with neuroendocrine differentiation (NED) areas. The SNAI2/Slug gene is a major regulator of cell migration and tumor metastasization. We here assessed its biological significance in NED, and metastatic potential of PCa Loss of TOX3 was verified to be correlated with advanced clinical stage and adverse prognosis of ccRCC. Downregulation of TOX3 could accelerate the EMT by decreasing transcriptional repression of SNAI1 and SNAI2. These data support a novel cancer suppressor role of TOX3 and provide new insights into the progression of ccRCC. 2. Materials and.
This may cause by a lower or loss of miR-1271 expression in other subtypes of breast cancer. SNAI2 (also known as Slug), a member of the SNAIL family, is a C2H2-type zinc finger transcription factor involved in the regulation of cell differentiation fate and determination . SNAI2 plays an essential role in development and cancer-associated EMT Targeting the SNAI2 through it's recycling enzyme is ground-breaking. SNAI2 is notoriously difficult to get rid of because it's difficult to target with medications. It also has a few tricks up its sleeves to help cancer cells - SNAI2 makes cancer cells invisible to the immune system and resistant to chemotherapy Keywords: Breast cancer, Transforming growth factor-β, Epithelial to mesenchymal transition, miR-1271, SNAI2, ERα Introduction Breast cancer is the most frequently diagnosed malig-nancy in women worldwide [1]. It is the most common malignant tumor, and the third largest cause o SNAI2 promotes breast cancer cell proliferation, colony formation, migration, and invasion To evaluate the effects of SNAI2 on breast cancer cells, we suppressed SNAI2 by shRNA ( Fig. 4A ). Compared to the negative controls, cell proliferation, colony formation, migration, and invasion were significantly suppressed when cells were treated with.
Epithelial-mesenchymal transition is an important mechanism of epithelial tumor progression, local invasion and metastasis. The E-cadherin (CDH1) repressor SLUG (SNAI2) and the basic helix. It is generally accepted that the SLUG (SNAI2) transcription factor, encoded by the SNAI2 gene, induces EMT, initiating cancer dissemination processes. This fact was supported by a previous study, in which the higher expression levels of the SLUG protein and SLUG mRNA were observed in the tumours of patients with metastatic BC or disease. invasiveness, which could be abolished by SNAI2 silencing. Furthermore, an immunohistochemical analysis of SNAI2 in archived primary prostate cancer specimens revealed a correlation with the RUNX2 histoscore, and simultaneous strong staining for SNAI2, RUNX2, and AR (but not any pair alone) was associated with diseas SNAI2 also suppresses the expression of a muscle differentiation program modulated by MYOG, MEF2, and CDKN1A. Further, RAS/MEK-signaling modulates SNAI2 levels and binding to chromatin, suggesting that the differentiation blockade by oncogenic RAS is mediated in part by SNAI2. Greehey Children's Cancer Research Institute's (Greehey CCRI.
Epithelial-mesenchymal transition (EMT) is involved in important malignant features of cancer cells, like invasion, metastatic potential, anti-apoptotic and stem-cell like phenotypes. Among several transcription factors, SNAI2/SLUG is supposed to play an essential role for EMT. Paraffin embedded tumor samples from 63 patients with metastatic non-small cell lung cancer, enrolled in a randomized. In breast cancer patients, primary tumors often spread to vital organs such as the lungs, driven by pro-metastatic genes such as Snai2. Shown here is a histologic section of a mouse lung bearing a metastatic lesion derived from primary mammary tumor. The metastatic lesion in the lung appears as a dense tumor cell cluster. Image courtesy of. SNAI2 (snail family zinc finger 2), a member of the SNAIL family, is a C2H2-type zinc finger transcription factor involved in the regulation of cell differentiation fate and determination . SNAI2 plays an essential role in development and cancer-associated EMT SNAI2 in-frame with the Firefly Luciferase coding se-quence to produce lentiviruses containing this fusion gene (SNAI2-Luc). Breast cancer cell line SUM159 was then transduced with SNAI2-Luc lentiviruses and with retroviruses constitutively expressing renilla luciferase to generate a dual-luciferase reporter stable cell line. I cancer cell lines, EMT score and log 10 trans-formed gene expression data were analyzed for correlation. B-E) SPHK1 expression is strongly correlated with the expression of SNAI2 (B, C), but not SNAI1 (D, E), in 2 independent data sets of breast cancer patient samples, GSE3893 Schuetz and GSE6532 Loi Breast. Gray marker
The correlation between the tumor versus normal ratio (T:N) of SNAI2 RNA expression and that of VDR in samples from colon cancer patients was studied using the Spearman correlation coefficient. Since SNAI1 RNA was not detected in any normal tissue, the T:N cannot be calculated and its expression was evaluated as presence or absence in tumor tissue Purpose: We assessed the relevance of Slug (SNAI2) for apoptosis resistance and invasion potential of neuroblastoma cells in vitro and in vivo . Experimental Design: We evaluated the effect of imatinib mesylate on invasion and analyzed the genes modulated by imatinib mesylate treatment in neuroblastoma cells. Slug expression, inhibited by imatinib mesylate treatment, was knocked down in. <p>SNAI2/SLUG, a metastasis-promoting transcription factor, is a labile protein that is degraded through the ubiquitin proteasome degradation system. Here, we conducted comprehensive gain- and loss-of-function screens using a human DUB cDNA library of 65 genes and an siRNA library of 98 genes, and identified USP20 as a deubiquitinase (DUB) that. AR modulates EMT via upregulation of SLUG-encoding gene, SNAI2. In the context of prostate cancer, the AR has been shown to play a crucial role in cell migration and invasion through modulating expression of EMT effector proteins . However, the precise role that AR plays in HCC development remains poorly understood SNAI2 (also known as SLUG), one of the three members in the SNAIL family transcription factors, has been reported to promote cancer metastasis by enhancing cell mobility and invasion (Shih and Yang 2011), promoting the survival of metastatic cells (Kim et al. 2014), and enhancing the activities of breast cancer stem cells (Guo et al. 2012)
Purpose: To examine the effects of curcumin on epithelial-mesenchymal transition (EMT) via regulation of miR-206 and SNAI2 in colorectal cancer (CRC) cells. Relationship between SNAI2 and miR-206 and the effects of curcumin on related mechanisms were also identified. Methods: Transwell assays were used to analyze cellular migration and invasion moting metastasis and invasion in human cancer [2]. Among these is Slug, an oncogenic transcriptional repressor that acts as a master regulator of cell migration in many tissues [3]. Slug is the product of the SNAI2 gene and is overexpressed in numerous cancers, including leu-kemia [4,5], esophageal cancer [6], lung cancer [7], breas cells (cancer stem cells versus tumor initiating cells) is still a matter of debate [7-9]. Several studies implicate a subset of human breast cancer cells with an enhanced ability to form tumors in immunocompromised mice [10,11]. This subpopulation of cells also demonstrated the capacity for self-renewal and generation of hetero-geneous progeny
Ginkgoic acid impedes gastric cancer cell proliferation, migration and EMT through inhibiting the SUMOylation of IGF-1R. Furthermore, the co-transfection of SUMO1, UBC9 and IGF-1R vectors or the overexpression of SNAI2 reversed the inhibitory effects of GA on cell proliferation, migration and EMT Stromal SNAI2 expression enhances the tumorigenicity of luminal B HER2 + breast cancers and can identify a subset of patients with poor prognosis, making SNAI2 a potential therapeutic target for this disease
Abstract. SNAI2/SLUG, a metastasis-promoting transcription factor, is a labile protein that is degraded through the ubiquitin proteasome degradation system. Here, we conducted comprehensive gain- and loss-of-function screens using a human DUB cDNA library of 65 genes and an siRNA library of 98 genes, and identified USP20 as a deubiquitinase. stimulated prostate cancer cell invasiveness, which could be abolished by SNAI2 silencing. Furthermore, an immunohistochemical analysis of SNAI2 in archived primary prostate cancer specimens revealed a correlation with the RUNX2 histoscore, and simultaneou SNAI2 upregulation is associated with an aggressive phenotype in fulvestrant-resistant breast cancer cells and is an indicator of poor response to endocrine therapy in estrogen receptor-positive metastatic breast cancer
SNAI2 (Snail Family Transcriptional Repressor 2) is a Protein Coding gene. Diseases associated with SNAI2 include Waardenburg Syndrome, Type 2D and Piebald Trait.Among its related pathways are TGF-B Signaling in Thyroid Cells for Epithelial-Mesenchymal Transition and CDK-mediated phosphorylation and removal of Cdc6 Translating today's discoveries in childhood cancer research into tomorrow's treatments. One of only two institutes in the United States dedicated solely to pediatric cancer research, the Greehey Children's Cancer Research Institute, with its 18 laboratories, focuses its strengths in cancer genomics, DNA repair, RNA biology, and drug development to find new and less toxic treatments for. Ovarian cancer (OvCa) is one of the most lethal malignancies in women. as an EMT inhibitor in OvCa by targeting SNAI2. Nanoparticle delivery of miR-506 can suppress EMT and reduce tumor growth in orthotopic mouse models of OvCa, suggesting miR-506 may serve as a potential therapeutic tool for patients with OvCa. Introduction
SNAI2 is a neurogenic transcription factor belonging to the SNAIL family implicated in the epithelial-mesenchymal transition and cell survival, in important morphogenetic processes during embryo development and in tumor metastasis. The gene has 3 exons (243bp, 546bp,1299bp). Transcription. Transcript length: 2.2Kb The restoration of miR-203 in highly metastatic breast cancer cells inhibited tumor cell invasion in vitro and lung metastatic colonization in vivo by repressing SNAI2. Taken together, our results suggest that the SNAI2 and miR-203 regulatory loop plays important roles in EMT and tumor metastasis
Snai2, which is the most important member of the Snail family, can enhance tumor cell proliferation and invasiveness [28, 29], whereas Twist1 can mediate EMT during cancer progression, particularly in the acquisition of metastatic potential . Notably, Snai2 appears the most strongly expressed and the most commonly activated EMT marker in both. breast cancer (EMT8 signature). The EMT8 signature was designed based on a previously described 5-gene signature (CDH1, CTNNB1, CTNNA2, CDH2, CDH3) [31], which we extended with KRT19, an established marker for breast cancer cells, and SNAI2 and TWIST due to their role as determinants of EMT in breast can-cer metastasis and invasion
To test this directly, SNAI2 expression was monitored on LEF1 knockdown in HEK293 cells (Figure 5H and Supplementary Figure S3G). As expected and previously reported for breast cancer-derived tumor cells, LEF1 depletion resulted in decreased steady state SNAI2 protein as well as mRNA levels Transcriptional repressor that modulates both activator-dependent and basal transcription. Involved in the generation and migration of neural crest cells. Plays a role in mediating RAF1-induced transcriptional repression of the TJ protein, occludin (OCLN) and subsequent oncogenic transformation of epithelial cells (By similarity). Represses BRCA2 expression by binding to its E2-box-containing.
Furthermore, an immunohistochemical analysis of SNAI2 in archived primary prostate cancer specimens revealed a correlation with the RUNX2 histoscore, and simultaneous strong staining for SNAI2, RUNX2, and AR (but not any pair alone) was associated with disease recurrence MicroRNA-33a (miR-33a) upregulation and siRNA-mediated Snail family transcriptional repressor 2 (SNAI2) silencing suppressed gastric cancer (GC) cell invasion ability (×200). A: cells passing through the basolateral chamber were stained with crystal violet in the MKN-45 cell line Previous studies have reported that BACH1 can directly bind to the promoters of the EMT markers, including SNAI2 in ovarian cancer 15 and FOXA1 in pancreatic cancer. 17 The ChIP-seq dataset targeting BACH1 in the hTFtarget database was investigated to determine whether BACH1 binds to the promoters of other EMT markers in ESCC cells
In breast cancers, SNAI2 expression is enriched in the triple-negative subtype, and tumors with lymph-node meatastsis and high grade 1. Experimental model systems also support a role for SNAI2 in breast cancer cell stemness, basal phenotype, and metastasis 18, 21. Thus, inhibition of SNAI2 expression by C/EBPδ may contribute to the development. El estudio, llevado a cabo en un modelo de ratón y publicado en la revista 'Cancer Research', demuestra que la ausencia del gen SNAI2 en el estroma tumoral provoca que este tenga más complicado.
Introduction. Epithelial-mesenchymal transition (EMT), a reversible dynamic process by which epithelial cells acquire characteristics of mesenchymal cells, is involved in the initiation of metastasis during cancer progression (Kalluri and Weinberg, 2009).Among other things, cancer cells undergoing EMT gain migratory and invasive properties and acquire stem cell traits (Ye and Weinberg, 2015) Introduction. In female cancer patients, 4% of all diagnoses are for uterine cancer. As such, it is the sixth most common cancer in women around the world.1 Uterine carcinosarcoma (UCS) is a rare subtype of uterine cancer that constitutes less than 5% of all uterine cancers.2 3 UCS is highly aggressive and shows a high prevalence of chemo-resistance and a very poor prognosis compared with.
