Evidence map›Paper›PMID 32749639›Full record

ArticleDigestive diseases and sciences2021

MiR-137-3p Inhibits Colorectal Cancer Cell Migration by Regulating a KDM1A-Dependent Epithelial-Mesenchymal Transition.

Xiaoling Ding, Jie Zhang, Ziqin Feng, Qianru Tang, Xiaorong Zhou

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In one paragraph

Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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  7. miR-137: a potential therapeutic target for lung cancer.Frontiers in cell and developmental biology · 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 1 institution in 1 country.

Xiaoling DingDepartment of Gastroenterology, The Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, Jiangsu, 226001, China.
Jie ZhangDepartment of Immunology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong, 226019, Jiangsu, China.
Ziqin FengSchool of Medicine, Nantong University, Nantong, 226019, Jiangsu, China.
Qianru TangSchool of Medicine, Nantong University, Nantong, 226019, Jiangsu, China.
Xiaorong ZhouDepartment of Immunology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong, 226019, Jiangsu, China. zhouxiaorong@ntu.edu.cn.ORCID 0000-0002-6120-7318
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn colorectal cancer (CRC), miR-137-3p downregulation is associated with disease progression, but the mechanism is not fully understood. KDM1A, also known as LSD1, is upregulated in various cancer and promotes tumor metastasis. Interestingly, miR-137-3p is downregulated by hypoxia, which plays critical roles in tumor metastasis, and KDM1A is a miR-137-3p target gene in brain tumors.

aimsTo study if CRC metastasis is regulated by a hypoxia/miR-137-3p/KDM1A axis and if the epithelial-mesenchymal transition (EMT) process is involved.

methodsWe measured the levels of miR-137-3p, KDM1A, and some EMT markers in CRC biopsy tissues and cell lines. We also investigated the regulation of KDM1A by miR-137-3p and the effects of KDM1A inhibition on the EMT process and cell migration.

resultsWe verified the low miR-137-3p and high KDM1A levels in CRC tumors. Inhibiting miR-137-3p upregulated KDM1A expression and promoted the invasiveness of CRC cells. KDM1A knockdown, or treatment with tranylcypromine, a specific KDM1A inhibitor, reduced the migration and invasion of CRC cells by inhibiting the EMT process. CRC cells cultured under hypoxic conditions expressed less miR-137-3p but more KDM1A than cells cultured under normal conditions, implying the involvement of miR-137-3p and KDM1A in hypoxia-induced tumor metastasis.

conclusionsWe conclude that MiR-137-3p inhibits CRC cell migration by regulating a KDM1A-dependent EMT process. Our study suggests that restoring the expression of miR-137-3p or targeting KDM1A might be potential therapeutic strategies for CRC.

Indexed as

AgedCell AdhesionCell Line, TumorCell MovementColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistone DemethylasesHumansMaleMicroRNAsMiddle AgedUp-RegulationHistone DemethylasesKDM1A protein, humanMicroRNAsMIRN137 microRNA, humanColorectal neoplasmsEpithelial–mesenchymal transitionHistone lysine demethylasesMicroRNAsNeoplasm metastasis

Identifiers

PMID32749639
OpenAlexW3047563167

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.