Evidence map›Paper›PMID 31616518›Full record

ArticleExperimental and therapeutic medicine2019

MicroRNA-139-5p regulates chronic inflammation by suppressing nuclear factor-κB activity to inhibit cell proliferation and invasion in colorectal cancer.

Mingming Zhu, Wen Zhang, Jun Ma, Youguo Dai, Qi Zhang, Qin Liu, Burong Yang, Gang Li

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

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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.

Mingming ZhuDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Wen ZhangDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Jun MaDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Youguo DaiDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Qi ZhangDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Qin LiuDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Burong YangDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.
Gang LiDepartment of Abdominal Tumor Surgery, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inflammatory microenvironment, which mediates the initiation and malignant development of tumors, has been reported to be associated with microRNA (miRNA) dysregulation. In the present study, the expression of miR-139-5p was analyzed in colorectal cancer (CRC) cell lines SW480, HT29, HCT-8, LoVo and HCT116, aiming to investigate the function and mechanism of miR-139-5p in the regulation of the malignant phenotypes of CRC. miR-139-5p expression was found to be considerably downregulated in CRC cell lines compared with the human normal colon mucosal epithelial cell line NCM460. Subsequently, it was demonstrated that overexpression of miR-139-5p in colon cancer cell lines significantly suppressed the cell proliferation

Indexed as

chronic inflammationcolorectal cancerinvasionmicroRNA-139-5pproliferation

Identifiers

PMID31616518
PMCPMC6781828

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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.