NDLI: HDAC3 deteriorates colorectal cancer progression via microRNA-296-3p/TGIF1/TGFβ axis

Content Provider	Springer Nature : BioMed Central
Author	Li, Jinxiao Hu, Man Liu, Na Li, Huarong Yu, Zhaomin Yan, Qian Zhou, Minfeng Wang, Yayuan Song, Yanjuan Pan, Guangtao Liang, Fengxia Chen, Rui
Abstract	Background The mechanism of histone deacetylase 3 (HDAC3) in colorectal cancer (CRC) has already been discussed. However, the feedback loop of HDAC3/microRNA (miR)-296-3p and transforming growth factor β-induced factor 1 (TGIF1) in CRC has not been explained clearly. Thus, the mainstay of this study is to delve out the mechanism of this axis in CRC. Methods To demonstrate that HDAC3 regulates the miR-296-3p/TGIF1/TGFβ axis and is involved in CRC progression, a series of cell biological, molecular and biochemical approaches were conducted from the clinical research level, in vitro experiments and in vivo experiments. These methods included RT-qPCR, Western blot assay, cell transfection, MTT assay, EdU assay, flow cytometry, scratch test, Transwell assay, dual luciferase reporter gene assay, chromatin immunoprecipitation, nude mouse xenograft, H&E staining and TUNEL staining. Results Higher HDAC3 and TGIF1 and lower miR-296-3p expression levels were found in CRC tissues. HDAC3 was negatively connected with miR-296-3p while positively correlated with TGIF1, and miR-296-3p was negatively connected with TGIF1. Depleted HDAC3 elevated miR-296-3p expression and reduced TGIF1 expression, decreased TGFβ pathway-related proteins, inhibited CRC proliferation, invasion, and migration in vitro and slowed down tumor growth and induction of apoptosis in vivo, which were reversed by miR-296-3p knockdown. Restored miR-296-3p suppressed TGIF1 and reduced TGFβ pathway-related proteins, inhibited CRC proliferation, invasion, and migration in vitro and slowed down tumor growth and induction of apoptosis in vivo, which were reversed by TGIF1 overexpression. Conclusion This study illustrates that down-regulation of HDAC3 or TGIF1 or up-regulation of miR-296-3p discourages CRC cell progression and slows down tumor growth, which guides towards a novel direction of CRC treatment.
Related Links	https://jeccr.biomedcentral.com/counter/pdf/10.1186/s13046-020-01720-w.pdf
Ending Page	13
Page Count	13
Starting Page	1
File Format	HTM / HTML
ISSN	17569966
DOI	10.1186/s13046-020-01720-w
Journal	Journal of Experimental & Clinical Cancer Research
Issue Number	1
Volume Number	39
Language	English
Publisher	BioMed Central
Publisher Date	2020-11-17
Access Restriction	Open
Subject Keyword	Cancer Research Immunology Apoptosis Oncology Colorectal cancer Histone deacetylase 3 MicroRNA-296-3p Thymine-guanine-interacting factor 1 Transforming growth factor β signaling pathway Invasion Migration
Content Type	Text
Resource Type	Article
Subject	Oncology Cancer Research
Journal Impact Factor	11.4/2023
5-Year Journal Impact Factor	11.4/2023

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Correction to: HDAC3 deteriorates colorectal cancer progression via microRNA-296-3p/TGIF1/TGFβ axis

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Correction to: HDAC3 deteriorates colorectal cancer progression via microRNA-296-3p/TGIF1/TGFβ axis

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