Evidence map›Paper›PMID 36158660›Full record

ReviewFrontiers in oncology2022

The role of miR-200 family in the regulation of hallmarks of cancer.

Klaudia Klicka, Tomasz M Grzywa, Aleksandra Mielniczuk, Alicja Klinke, Paweł K Włodarski

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

79 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  16. MicroRNA Crossroads in PCOS and Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026
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19 more citing papers are in PubMed but not listed here.

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

5 authors.

Klaudia KlickaDepartment of Methodology, Medical University of Warsaw, Warsaw, Poland.
Tomasz M GrzywaDepartment of Methodology, Medical University of Warsaw, Warsaw, Poland.
Aleksandra MielniczukDepartment of Methodology, Medical University of Warsaw, Warsaw, Poland.
Alicja KlinkeDepartment of Methodology, Medical University of Warsaw, Warsaw, Poland.
Paweł K WłodarskiDepartment of Methodology, Medical University of Warsaw, Warsaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiRNAs are short non-coding RNAs that regulate gene expression post-transcriptionally contributing to the development of different diseases including cancer. The miR-200 family consists of five members, miR-200a, miR-200b, miR-200c, miR-141, and miR-429. Their expression is dysregulated in cancer tissue and their level is altered in the body fluids of cancer patients. Moreover, the levels of miR-200 family members correlate with clinical parameters such as cancer patients' survival which makes them potentially useful as diagnostic and prognostic biomarkers. MiRNAs can act as either oncomiRs or tumor suppressor miRNAs depending on the target genes and their role in the regulation of key oncogenic signaling pathways. In most types of cancer, the miR-200 family acts as tumor suppressor miRNA and regulates all features of cancer. In this review, we summarized the expression pattern of the miR-200 family in different types of cancer and their potential utility as biomarkers. Moreover, we comprehensively described the role of miR-200 family members in the regulation of all hallmarks of cancer proposed by Hanahan and Weinberg with the focus on the epithelial-mesenchymal transition, invasiveness, and metastasis of tumor cells.

Indexed as

hallmarks of cancerinvasivenessmetastasismiR-200miR-200 familymiRNAtumor progression

Identifiers

PMID36158660
PMCPMC9492973

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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.