Post-Transcriptional Regulation of Cardiac Sarcomere Protein Titin Through 3’ Untranslated Regions

Shrout, Tara

doi:10.15695/vurj.v9i0.3772

Cited by 1 publication

(1 citation statement)

References 19 publications

(18 reference statements)

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“…We have investigated that truncated p16 mRNAs that do not include the miR‐141 binding site are frequently expressed in CMT cells and may be a common aspect of the breast cancer phenotype. A number of reports have suggested that 3′‐UTR length variability may be the result of a mechanism to remove miRNA target sites from key mRNAs in proliferating cells [Sandberg et al, ; Shrout, ]. Surprisingly, the longer 3′‐UTR sequence of the p16/INK4A gene was found to be expressed in CMT28.…”

Section: Discussionmentioning

confidence: 99%

Altered microRNA Expression Profiles and Regulation of INK4A/CDKN2A Tumor Suppressor Genes in Canine Breast Cancer Models

Kabir

DeInnocentes

Bird

2015

J of Cellular Biochemistry

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microRNA (miRNA) expression profiling of cancer versus normal cells may reveal the characteristic regulatory features that can be correlated to altered gene expression in both human and animal models of cancers. In this study, the comprehensive expression profiles of the 277 highly characterized miRNAs from the canine genome were evaluated in spontaneous canine mammary tumor (CMT) models harboring defects in a group of cell cycle regulatory and potent tumor suppressor genes of INK4/CDKN2 family including p16/INK4A, p14ARF, and p15/INK4B. A large number of differentially expressed miRNAs were identified in three CMT cell lines to potentially target oncogenes, tumor suppressor genes and cancer biomarkers. A group of the altered miRNAs were identified by miRNA target prediction tools for regulation of the INK4/CDKN2 family tumor suppressor genes. miRNA-141 was experimentally validated for INK4A 3'-UTR target binding in the CMT cell lines providing an essential mechanism for the post-transcriptional regulation of the INK4A tumor suppressor gene in CMT models. A well-recognized group of miRNAs including miR-21, miR-155, miR-9, miR-34a, miR-143/145, and miR-31 were found to be altered in both CMTs and human breast cancer. These altered miRNAs might serve as potential targets for advancing the development of future therapeutic reagents. These findings further strengthen the validity and use of canine breast cancers as appropriate models for the study of human breast cancers.

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Section: Discussionmentioning

confidence: 99%