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• W3188237376 abstract "Abstract Background Cardiac troponin I (cTnI), encoded by TNNI3, is an inhibitory subunit of troponin complex expressed in cardiac muscle and is well known for its central role in the regulation of cardiac contraction. Although its aberrant expression has been reported in non-small cell lung cancer tissues and human carcinoma cells, its roles in cancers are still largely unknown. Methods In this work, the mRNA expression profiles of 289 Kidney renal papillary cell carcinoma (KIRP) samples were obtained from The Cancer Genome Atlas (TCGA) database. The tumor samples were classified into TNNI3-low and TNNI3-high groups. A total of 361 differentially expressed genes (DEgenes) were found correlated with TNNI3 expression. Univariate Cox analysis, log-rank test and the least absolute shrinkage and selection operator analysis were used to identify the candidate prognostic genes. The regulatory role of TNNI3 on Wnt signaling pathway was detected by western blot, wound healing assay and cell counting kit-8 assay. Results Multivariable Cox regression analysis was performed to establish a prognostic risk formula including genes PTPRH, LGR5 and DMRT3. The low-risk group had a better overall survival than the high-risk group ( p < 0.0001), and the areas under the receiver operating characteristic curve for 3- and 5-year overall survival were 0.75 and 0.74, respectively. We thereafter constructed an target gene network to explore the potential functions of the three genes. The Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis identified their involvement with canonical Wnt signaling and several cancer-related pathways. In wound healing assay, the wound was closed obviously faster in the TNNI3 over-expression group as compared to control and blank groups. Significant increase in cell proliferation was seen at 72 h after transfection with TNNI3 as compared to the control and blank groups.The expressions of LGR5 and β-catenin increased in the TNNI3 over-expression group as compared to control and blank groups. Conclusion Collectively, our data provide evidence that TNNI3 could enhance cell migration and proliferation in 786-O cells and the three-gene signature related to TNNI3 could serve as an independent prognostic biomarker for KIRP. Insights are indeed provided into the potential oncogenic functions of TNNI3 in cancer research." @default.
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• W3188237376 date "2021-08-03" @default.
• W3188237376 modified "2023-09-25" @default.
• W3188237376 title "Cardiac-Specific Gene TNNI3 as a Potential Oncogene for Kidney Cancer and Its Involvement in Wnt Signaling Pathway" @default.
• W3188237376 doi "https://doi.org/10.21203/rs.3.rs-754351/v1" @default.
• W3188237376 hasPublicationYear "2021" @default.
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