Evidence map›Paper›PMID 29449642›Full record

ArticleCell death & disease2018

NIT1 suppresses tumour proliferation by activating the TGFβ1-Smad2/3 signalling pathway in colorectal cancer.

Chun Lin, Jianming Zhang, Yanxia Lu, Xiaomin Li, Wenjuan Zhang, Wei Zhang, Weihao Lin, Lin Zheng, Xuenong Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Chun LinDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Jianming ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yanxia LuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xiaomin LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Wenjuan ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Wei ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Weihao LinDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Lin ZhengDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xuenong LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. nfydlxn@126.com.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NIT1 protein has been reported to be a potential tumour suppressor in tumour progression. However, little is known about the specific role of NIT1 in tumour development and progression. In this study, we confirmed the specific effects of NIT1 in the regulation of colorectal carcinoma cell proliferation. Here, we showed that NIT1 was significantly downregulated in colorectal cancer tissues compared with that in adjacent normal tissues. The decreased expression of NIT1 was significantly correlated with poor differentiation and more serosal invasion. Functional experiments showed that NIT1 inhibited CRC cell growth both in vitro and in vivo. NIT1 induced cell cycle arrest and apoptosis. Furthermore, NIT1 recruited Smad2/3 to the TGFβ receptor and activated the TGFβ-Smad2/3 pathway by interacting with SARA and SMAD2/3 in CRC. Further study has shown that SMAD3 directly binds to the promoter regions of NIT1 and enhances the transcription of NIT1. Together, our findings indicate that NIT1 suppresses CRC proliferation through a positive feedback loop between NIT1 and activation of the TGFβ-Smad signalling pathway. This study might provide a new promising strategy for CRC.

Indexed as

Cell ProliferationAminohydrolasesAnimalsApoptosisBinding SitesCaco-2 CellsCell Cycle CheckpointsColorectal NeoplasmsFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHCT116 CellsHEK293 CellsHT29 CellsHumansMaleAminohydrolasesnitrilaseSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID29449642
PMCPMC5833788
OpenAlexW2791343031

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.