Even less than a decade since the discovery of TSLC1, overwhelming evidence demonstrates that the loss of TSLC1 expression by methylation-mediated epigenetic silencing or LOH is crucially implicated in various processes during tumorigenesis. Here, we summarize TSLC1 function, highlighting the concept that TSLC1 mediates the formation of tumor suppressor network via its multidomain structure and bridges extracellular adhesive activity with intracellular signaling. Next, we focus on the histopathology of TSLC1 in various cancers and the association with clinicopathological characteristics. On the basis of these, we propose that TSLC1 represents a promising biomarker for cancer diagnosis and a potential target for cancer therapy.
IntroductionTo explore the effect of tumor suppressor in lung cancer 1 (TSLC1) on proliferation and apoptosis in esophageal cancer Eca109 cells.Material and methodsEca109 cells were divided into three groups: TSLC1 transfected group (TTG), mock group (MG) and untransfected group (UTG). The TTG and MG were transfected transiently with the pIRES2-EGFP-TSLC1 eukaryotic expression vector and pIRES2-EGFP vector respectively. The UTG was a blank control. The TSLC1 expression in TTG was analyzed with the fluorogram and RT-PCR method. Cell proliferation was measured with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium (MTT) assay. Cell cycle was measured by flow cytometry (FCM). Cell apoptosis was detected by Annexin-V/PI double staining FCM.ResultsGreen color was found in TTG and MG. The band of TSLC1 mRNA of TTG was located at about 1400 bp by RT-PCR and agarose gel electrophoresis assay. The TSLC1 inhibited cell proliferation significantly in MTT assay, and the cell proliferation was slower in TTG than MG and UTG. After TSLC1 transfection, cell numbers increased in G0/G1 phase and decreased in S phase. Forty-eight hours after transfection, the apoptosis rate and death rate of TTG were higher than MG and UTG. Thus TSLC1 induced Eca109 cells to apoptosis.ConclusionsThe TSLC1 gene had a potent effect on cell proliferation inhibition, G1/S cell cycle arrest and induction of cell apoptosis in Eca109 cells.
IntroductionTo construct a eukaryotic expression vector of the tumour suppressor in lung cancer 1 (TSLC1) gene, so as to explore the mechanisms of tumour suppression of the gene theoretically.Material and methodsThe open reading frame (ORF) of TSLC1 gene was amplified with RT-PCR from normal human foreskin acrobystia, and cloned to pMD19-T simple vector (TA Clone method). The resultant plasmid was transformed into Escherichia coli JM109 for amplification. The TA Clone recombinant was digested by double restriction enzyme (Bgl II/EcoR I) and analysed with agarose gel electrophoresis. The positive one was sequenced. The inserted DNA fragment was recovered, and then it was mounted into the eukaryotic expression vector pIRES2-EGFP, transformed into E. coli JM109 for amplification. A positive recombinant plasmid named pIRES2-EGFP-TSLC1 was confirmed by Bgl II/EcoR I double-enzyme digestion analysis.ResultsRT-PCR amplified the ORF of the TSLC1 gene. It was approximately 1400 base pairs. The obtained DNA was confirmed a high degree of homology with the sequence of TSLC1 cDNA sequence (AY358334) stored at GenBank.ConclusionsConstruction of a TSLC1 eukaryotic expression vector was successful, and it has established a solid foundation for further study.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.