Evidence map›Paper›PMID 35814269›Full record

ArticleOxidative medicine and cellular longevity2022

Exosomal miR-224-5p from Colorectal Cancer Cells Promotes Malignant Transformation of Human Normal Colon Epithelial Cells by Promoting Cell Proliferation through Downregulation of CMTM4.

Feng Wu, Jiani Yang, Guoyin Shang, Zhijia Zhang, Sijia Niu, Yang Liu, Hongru Liu, Jing Jing, Yu Fang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Research progress ofFrontiers in immunology · 2026
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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 1 institution in 1 country.

Feng WuDepartment of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Jiani YangDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150081, China.
Guoyin ShangDepartment of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Zhijia ZhangDepartment of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Sijia NiuDepartment of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Yang LiuPharmacy Intravenous Admixture Services, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Hongru LiuDepartment of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Jing JingDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, Heilongjiang 150000, China.
Yu FangDepartment of Phase I Clinical Trial Ward, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, Heilongjiang 150081, China.ORCID https://orcid.org/0000-0002-6653-6962
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Interactions between malignant cells and neighboring normal cells are important for carcinogenesis. In addition, cancer cell-derived exosomes have been shown to promote the malignant transformation of recipient cells, but the mechanisms remain unclear. Methods: The level of miR-224-5p in CRC cell-derived exosomes was determined by RT-qPCR assay. In addition, PKH26 dye-labeled exosomes were used to assess the efficacy of the transfer of exosomes between SW620 and normal colon epithelial cell line CCD 841 CoN. Results: In this study, we found that overexpression of miR-224-5p significantly promoted the proliferation, migration, and invasion and inhibited the oxidative stress of SW620 cells. In addition, miR-224-5p can be transferred from SW620 cells to CCD 841 CoN cells via exosomes. SW620 cell-derived exosomal miR-224-5p markedly promoted proliferation, migration, and invasion of CCD 841 CoN cells. Meanwhile, SW620 cell-derived exosomal miR-224-5p notably decreased the expression of CMTM4 in CCD 841 CoN cells. Furthermore, SW620 cell-derived exosomal miR-224-5p significantly promoted tumor growth in a xenograft model Conclusion: These findings suggested that SW620 cell-derived exosomal miR-224-5p could promote malignant transformation and tumorigenesis

Indexed as

Colorectal NeoplasmsMicroRNAsCarcinogenesisCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticDown-RegulationEpithelial CellsHumansMARVEL Domain-Containing ProteinsCMTM4 protein, humanMARVEL Domain-Containing ProteinsMicroRNAsMIRN224 microRNA, human

Identifiers

PMID35814269
PMCPMC9262543
OpenAlexW4283742704

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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.