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MiR‐590‐3p regulates cardiomyocyte P19CL6 proliferation, apoptosis and differentiation in vitro by targeting PTPN1 via JNK/STAT/NF‐kB pathway
Author(s) -
Wang Fanshun,
Zhang Hongqiang,
Wang Chunsheng
Publication year - 2020
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/iep.12377
Subject(s) - microbiology and biotechnology , apoptosis , signal transduction , cell growth , gene knockdown , cellular differentiation , biology , stat , hedgehog signaling pathway , chemistry , biochemistry , stat3 , gene
Cardiomyocyte differentiation is a multi‐step process which involves a number of signalling pathways. microRNAs exhibit regulatory functions in various diseases and are involved in the signalling pathways in multiple physiological processes, but the specific functions of particular mRNAs is often not fully understood. of an example of this is that the role of miR‐590‐3p in the differentiation of cardiomyocytes remains unclear. In the current study, RT‐qPCR was used to determine the expression of miR‐590‐3p in cardiomyocytes differentiated from the embryonic carcinoma cell line P19CL6. MTT, EdU, caspase‐3 activity and flow cytometry assays were performed to examine the influence of miR‐590‐3p on cell behaviour. A luciferase assay was used to confirm binding between miR‐590‐3p and PTPN1. Western blotting was used to determine the relationship between the JNK/STAT/NF‐kB pathway and PTPN1. The results inferred that miR‐590‐3p became heavily expressed in differentiated P19CL6. Knockdown miR‐590‐3p suppressed the cell proliferation while at the same time, accelerated apoptosis. Moreover, PTPN1 was identified as the target of miR‐590‐3p. More importantly, PTPN1 overexpression activated the JNK/STAT/NF‐kB pathway and limited the differentiation of P19CL6. Thus the conclusions from this study are that miR‐590‐3p has the potential to regulate the proliferation, apoptosis and differentiation of cardiomyocyte P19CL6 in vitro by targeting PTPN1 via the JNK/STAT/NF‐kB pathway.