Evidence map›Paper›PMID 33300054›Full record

ArticleMolecular medicine reports2021

miR‑576‑5p promotes epithelial‑to‑mesenchymal transition in colorectal cancer by targeting the Wnt5a‑mediated Wnt/β‑catenin signaling pathway.

Jialin Luo, Luying Liu, Jinwen Shen, Ning Zhou, Yanru Feng, Na Zhang, Quanquan Sun, Yuan Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Unleashing Wnts: Wnt Ligands Fuel Cancer Spread.Journal of cancer biology · 2025
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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

8 authors at 3 institutions in 1 country.

Jialin LuoInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Luying LiuInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Jinwen ShenInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Ning ZhouInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Yanru FengInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Na ZhangInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Quanquan SunInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
Yuan ZhuInstitute of Cancer and Basic Medicine of Chinese Academy of Sciences; Department of Radiation Oncology, Cancer Hospital of The University of Chinese Academy of Sciences; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
University of Chinese Academy of Sciences · CNZhejiang Cancer Hospital · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the most common types of malignancy and the third most commonly diagnosed form of cancer worldwide, ranking as the fourth leading cause of cancer‑associated mortality. MicroRNA (miR)‑576‑5p has been reported to be highly expressed in patients with CRC; however, its biological role remains unclear. The present study aimed therefore to investigate the biological role and underlying mechanism of miR‑576‑5p in CRC cell line SW480. The viability of SW480 cells following transfection with miR‑576‑5p mimic or inhibitor was analyzed using MTT assay. Wound healing and Transwell assays were performed to determine the cell migratory and invasive abilities, respectively. A dual luciferase reporter assay was used to verify the predicted binding site between miR‑576‑5p and Wnt5a. Reverse transcription‑quantitative PCR and western blotting were used to analyze the expression levels of miR‑576‑5p, E‑cadherin, N‑cadherin, vimentin, Snail1, Wnt5a, β‑catenin, c‑myc, cyclin D1 and p/t‑c‑Jun. Using bioinformatics analysis, high expression of miR‑576‑5p was found not only in tumor tissues, compared with the normal tissue, but also in CRC cells, compared with NCM460 cells. Furthermore, the inhibition of miR‑576‑5p expression significantly decreased the cell viability and the migratory and invasive abilities of SW480 cells, and suppressed the epithelial‑to‑mesenchymal transition (EMT). In addition, miR‑576‑5p could interact with Wnt5a and regulate the expression level of Wnt5a in order to influence the activity of Wnt/β‑catenin signaling. The results from rescue experiments further demonstrated that the effect of miR‑576‑5p overexpression on cell metastasis and EMT was reversed by Wnt5a overexpression or treatment with XAV‑939, which is an inhibitor of the Wnt/β‑catenin signaling pathway. In conclusion, the findings from the present study suggested that inhibition of miR‑576‑5p may suppress SW480 cell metastasis and EMT by targeting Wnt5a and regulating the Wnt5a‑mediated Wnt/β‑catenin signaling pathway, providing a potential therapeutic target for the treatment of CRC.

Indexed as

Epithelial-Mesenchymal TransitionWnt Signaling PathwayColorectal NeoplasmsHCT116 CellsHumansMicroRNAsRNA, NeoplasmWnt-5a ProteinMicroRNAsMIRN576 microRNA, humanRNA, NeoplasmWnt-5a ProteinWNT5A protein, humancolorectal cancerepithelial‑to‑mesenchymal transitionmiR‑576‑5pWnt5aWnt/β‑catenin signaling

Identifiers

PMID33300054
PMCPMC7723166
OpenAlexW3110562497

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.