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    Home > Active Ingredient News > Antitumor Therapy > Br J Cancer: SLFN5 regulates epithelial interstitial transformation process affects breast cancer metastasis

    Br J Cancer: SLFN5 regulates epithelial interstitial transformation process affects breast cancer metastasis

    • Last Update: 2020-06-16
    • Source: Internet
    • Author: User
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    Previous studies have found that the Slfn family of mice is involved in a variety of physiological or pathological processes, including T-cell activation, thymus cell maturation, fibroblast splinter and tumor cell proliferation, however, the function of the human SLFN family needs further researchCurrently, researchers have found that SLFN5 can inhibit or promote the aggressiveability of tumor cells according to different sources of tumorsIn melanoma and renal cell carcinoma, SLFN5 is low in expression and inhibits tumor attack, while in glioblastoma, SLFN5 is positively correlated with the malignancy of tumorIn five types of cancer, including lung cancer, colorectal cancer, fibrosar, renal transparent cell carcinoma and breast cancer, it can inhibit tumor aggression by inhibiting the expression of MT1-MMPHowever, in breast cancer (BRCA), the role of SLFN5 has yet to be further studiedThe researchers analyzed gene differences in clinical samples and related cell lines through the Tumor Genome Map (TCGA) database and found that the expression level of SLFN5 was negatively correlated with BRCA's metastasisBy slow virus knocking down or overexpressing SLFN5 to detect changes in cell morphology, molecular markers, and cell aggression, it was found that knocking low expression levels of SLFN5 can induce the epithelial-interstitial transformation (EMT) process of BRCA cell lines and enhance the cell's aggressive ability;Further studies have found that SLFN5 inhibits the expression of ZEB1 without affecting the expression levels of ZEB2, SNAI1, SNAI2, TWIST1 and TWIST2The use of low-key and overexpression of ZEB1 confirms that SLFN5 affects cell phenotype and invasive ability by regulating ZEB1Chromain Isoplasine Immunoprecipitation Experiment (ChIP-Seq) and luciferase report ingons genetic experiments further clarify that SLFN5 can bind directly to and inhibit the transcription level of ZEB1 by binding directly with the SLFN5 module on the ZEB1 promoter region, while the C-side structurally missing SLFN5 mutants cannot bind and lose inhibitionThe results show that SLFN5 can regulate the reversible epithelial-interstitial transformation process and inhibit breast cancer metastasis by inhibiting ZEB1 transcription, suggesting that SLFN5 may be a potential target for breast cancer treatment
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