| IntroductionThe aim of the research is to clarify the effects and molecular mechanisms of BTG1 overexpression on invasion and metastasis of colorectal cancer.B-cell translocation gene 1(BTG1)is a member of the BTG/transducer of Erb family.Since the identification of B-cell translocation gene 1(BTG1)as antiproliferation genes more than two decades ago,their protein products have been implicated in a variety of cellular processes including cell division,DNA repair,transcriptional regulation and messenger RNA stability.To clarify the mechanisms of tumor biomarker in carcinogenesis deletions affecting the transcriptional coregulator BTG1 are frequently observed in colorectal cancer.The human antiproliferative BTG(B-cell translocation gene)/ Transducer of Erb B2 gene family which encodes BTG protein family includes six proteins(BTG1、BTG2、BTG3、BTG4、TOB1/TOB and TOB2)and we report that Btg1 deficiency enhances the self-renewal capacity of mouse.The present study evaluated the impact of BTG1 gene expression on the clinical outcome of104-106 amino acids,which BTG domain as the characteristic of this family.Combined expression of the fusion protein and a loss of BTG1 drive upregulation of the target molecule.Compared to other family members,BTG1 and BTG2 have a same domain C box.Recent studies have uncovered novel roles for BTG1 and BTG2 in genotoxic and integrated stress responses,as well as during hematopoiesis.This review summarizes what is currently known about the roles of BTG family in these and other cellular processes.In addition,we will highlight the molecular mechanisms and biological consequences ofBTG1 deregulation during cancer progression and elaborate on the potential clinical implications of these findings.Recently,the mechanism of BTG1 anticancer effect in breast,ovary and liver cancer have been validated gradually,but reports about study in vivo and especially BTG1 expression,effects and mechanism in colorectal cancer remain less.BTG1 expression in colorectal cancer tissue,its effect on cell phenotype and relative molecular mechanisms are still elusive.We detected BTG1 m RNA and protein expression in colorectal cancer tissue and cells to finally analyze its clinical-pathological meanings.The study will offer a virtue protein target for colorectal cancer diagnosis and treatment,which has a promising prospect offering scientific basement for colon cancer three early revention.Methods1.Using plasmid infection colorectal cancer cell,BTG1 overexpression in HCT-116 cells of colorectal cancer,marked as HCT116,Clone32,Clone40.2.Analyzes the effects on adhesion of colorectal cancer cells with MTT,wound scratch assay and Transwell3.Observe the effects of BTG1 expression on lung cancer of HCT-116 cells in nude mice.Results1.The effects of BTG1 expression on adhesion,migration and invasion of colorectal cancer cellsBTG1 was overexpressed in HCT-116,evidenced by Western blot and followed geometric analysis.BTG1-overexpressing HCT-116 had a lower homogenous and heterogeneous adhesion,a weaker ability to migrate and invade by wound healing and transwell assays,observe the formation of lamellipodium by Immunofluorescence staining.2.The effects of BTG1 expression on phenotype-related molecules of colorectal cancer cellsThe phenotype-related molecules were screened by Western blot,real-time RT-PCR or ELISA.3.The effects of BTG1 expression on lung cancer of colorectal cancer cells in nude miceConclusionIt was suggested that BTG1 expression might promote HCT-116 metastasis on lung cancer not by EMT but by JNK to decreasing migration,invasion and epithelial-mesenchymal transition,need further investment of adhesion and adjustment in CEA expression. |