ArticleAmerican journal of translational research2019
HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
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- Partial-Methylated HeyL Promoter Predicts the Severe Illness in Egyptian COVID-19 Patients.Disease markers · 2022Article
- Pseudogene ACTBP2 increases blood-brain barrier permeability by promoting KHDRBS2 transcription through recruitment of KMT2D/WDR5 in AβCell death discovery · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
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Abstract
The HEY2 (hairy and enhancer of split-related with YRPW motif 2) is reported to play potential roles in tumorigenesis. However, the underlying mechanism in tumorigenesis is remain elusive. The present study aims to investigate the molecular mechanism of biological function of HEY2 in hepatocellular carcinoma (HCC). Dysfunction of the transforming growth factor-beta (TGF-β) pathway plays a critical role in HCC pathogenesis. Here, we identified HEY2 as a suppressor for TGF-β biological response. We demonstrated that HEY2 protein in tumor cytoplasm was up-regulated in HCC. Further, HEY2 overexpression inhibited TGF-β-induced growth arrest of HCC cells and inhibited TGF-β-induced downregulation of c-Myc, both in mRNA and in protein levels. While knockdown of HEY2, by small interfering RNA, was shown to enhance the TGF-β-mediated biological response of HCC cells. Moreover, HEY2 could form complexes with Smad3 and Smad4 and repress Smad3/Smad4 transcriptional activity. In conclusion, our findings indicate a novel role of HEY2 in mediating the TGF-β/Smad signaling pathway in HCC tumorigenesis.
Indexed as
Identifiers
31396342PMC6684919W2997749950What OpenQuestion holds
Registered trials
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