Evidence map›Paper›PMID 34147083›Full record

ArticleBMC cancer2021

The mechanisms of colorectal cancer cell mesenchymal-epithelial transition induced by hepatocyte exosome-derived miR-203a-3p.

Heyang Xu, Qiusheng Lan, Yongliang Huang, Yang Zhang, Yujie Zeng, Pengwei Su, Ziqiang Chu, Wei Lai, Zhonghua Chu

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 24 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 4 institutions in 1 country.

Heyang Xu *Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Qiusheng Lan *Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Yongliang HuangDepartment of General Surgery, Foshan Maternal and Child Health Hospital, Southern Medical University, Foshan, China.
Yang ZhangGuangzhou Blood Center, Guangzhou, Guangdong Province, China.
Yujie ZengGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Pengwei SuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Ziqiang ChuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Wei LaiGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. Weilaiv2001@126.com.
Zhonghua ChuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastrointestinal Surgery Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. sumschuzhonghua@hotmail.com.
Sun Yat-sen Memorial Hospital · CNSun Yat-sen University · CNFoshan Maternity and Child Health Care Hospital · CNGuangzhou Blood Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver metastasis is the most common cause of death in patients with colorectal cancer (CRC). Phosphatase of regenerating liver-3 induces CRC metastasis by epithelial-to-mesenchymal transition, which promotes CRC cell liver metastasis. Mesenchymal-to-epithelial transition (MET), the opposite of epithelial-to-mesenchymal transition, has been proposed as a mechanism for the establishment of metastatic neoplasms. However, the molecular mechanism of MET remains unclear.

methodsUsing Immunohistochemistry, western blotting, invasion assays, real-time quantitative PCR, chromatin immunoprecipitation, luciferase reporter assays, human miRNA arrays, and xenograft mouse model, we determined the role of hepatocyte exosome-derived miR-203a-3p in CRC MET.

resultsIn our study, we found that miR-203a-3p derived from hepatocyte exosomes increased colorectal cancer cells E-cadherin expression, inhibited Src expression, and reduced activity. In this way miR-203a-3p induced the decreased invasion rate of CRC cells. COCLUSION: MiR-203a-3p derived from hepatocyte exosomes plays an important role of CRC cells to colonize in liver.

Indexed as

AnimalsCell ProliferationColorectal NeoplasmsCongenital HypothyroidismDisease Models, AnimalEpithelial-Mesenchymal TransitionExosomesHumansMiceMice, NudeMicroRNAsThyroid DysgenesisMicroRNAsMIRN203 microRNA, humanColorectal cancerExosomeMesenchymal-to-epithelial transitionmiR-203a-3p

Identifiers

PMID34147083
PMCPMC8214778
OpenAlexW3175671292

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Registered trials

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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.