Evidence map›Paper›PMID 35729324›Full record

ArticleExperimental & molecular medicine2022

hnRNPC induces isoform shifts in miR-21-5p leading to cancer development.

Seokju Park, Hee Doo Yang, Jwa-Won Seo, Jin-Wu Nam, Suk Woo Nam

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  5. IsomiR stoichiometry changes as disease biomarkers.Molecular therapy. Nucleic acids · 2025
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  10. IsomiRome analysis reveals dysregulation of 5' isomiRs during SARS-CoV-2 infection.Computational and structural biotechnology journal · 2025
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  12. Oncofetal IGF2BP3-mediated control of microRNA structural diversity in the malignancy of early-stage lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

5 authors at 3 institutions in 2 countries.

Seokju Park *Department of Life Science, College of Natural Sciences, Hanyang University, Wangsimni-ro 222, Seongdong-gu, Seoul, 04763, Republic of Korea.
Hee Doo Yang *Department of Pathology, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 06591, Republic of Korea.
Jwa-Won SeoDepartment of Information Systems, University of Maryland, Baltimore County, MD, 20742, USA.
Jin-Wu NamDepartment of Life Science, College of Natural Sciences, Hanyang University, Wangsimni-ro 222, Seongdong-gu, Seoul, 04763, Republic of Korea. jwnam@hanyang.ac.kr.ORCID http://orcid.org/0000-0003-0047-3687
Suk Woo NamDepartment of Pathology, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 06591, Republic of Korea. swnam@catholic.ac.kr.
Catholic University of Korea · KRHanyang University · KRUniversity of Maryland, Baltimore County · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miRNA) processing is a critical step in mature miRNA production. Its dysregulation leads to an increase in miRNA isoforms with heterogenous 5'-ends (isomiRs), which can recognize distinct target sites because of their shifted seed sequence. Although some miRNA genes display productive expression of their 5'-isomiRs in cancers, how their production is controlled and how 5'-isomiRs affect tumor progression have yet to be explored. In this study, based on integrative analyses of high-throughput sequencing data produced by our group and publicly available data, we demonstrate that primary miR-21 (pri-miR-21) is processed into the cancer-specific isomiR isomiR-21-5p | ±1, which suppresses growth hormone receptor (GHR) in liver cancer. Treatment with antagomirs against isomiR-21-5p | ±1 inhibited the in vitro tumorigenesis of liver cancer cells and allowed the recovery of GHR, whereas the introduction of isomiR-21-5p | ±1 mimics attenuated these effects. These effects were validated in a mouse model of spontaneous liver cancer. Heterogeneous nuclear ribonucleoprotein C and U2 small nuclear RNA auxiliary factor 2 were predicted to bind upstream of pre-miR-21 via a poly-(U) motif and influence Drosha processing to induce the production of isomiR-21-5p | ±1. Our findings suggest an oncogenic function for the non-canonical isomiR-21-5p | ±1 in liver cancer, and its production was shown to be regulated by hnRNPC.

Indexed as

Heterogeneous-Nuclear Ribonucleoprotein Group CMicroRNAsAnimalsHigh-Throughput Nucleotide SequencingLiver Neoplasms, ExperimentalMiceProtein IsoformsRNA Processing, Post-TranscriptionalHeterogeneous-Nuclear Ribonucleoprotein Group CMicroRNAsMIRN21 microRNA, mouseProtein Isoforms

Identifiers

PMID35729324
PMCPMC9256715
OpenAlexW4283314012

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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.