Evidence map›Paper›PMID 31728150›Full record

ArticleCellular & molecular biology letters2019

PAK4, a target of miR-9-5p, promotes cell proliferation and inhibits apoptosis in colorectal cancer.

Meihua Wang, Qianqian Gao, Yufang Chen, Ziyan Li, Lingping Yue, Yun Cao

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cellular & molecular biology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

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  12. LncRNA IGFL2-AS1 as a ceRNA Promotes HCT116 Cell Malignant Proliferation via the miR-433-3p/PAK4 Axis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
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  13. Targeting p21-activated kinase 4 (PAK4) with pyrazolo[3,4-Journal of enzyme inhibition and medicinal chemistry · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Meihua WangDepartment of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, 68 Honghe Road Changzhou, Changzhou, 213032 Jiangsu China.
Qianqian GaoDepartment of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, 68 Honghe Road Changzhou, Changzhou, 213032 Jiangsu China.
Yufang ChenDepartment of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, 68 Honghe Road Changzhou, Changzhou, 213032 Jiangsu China.
Ziyan LiDepartment of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, 68 Honghe Road Changzhou, Changzhou, 213032 Jiangsu China.
Lingping YueDepartment of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, 68 Honghe Road Changzhou, Changzhou, 213032 Jiangsu China.
Yun CaoDepartment of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, 68 Honghe Road Changzhou, Changzhou, 213032 Jiangsu China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is a leading cause of cancer-related death worldwide. P21-activated kinase 4 (PAK4) and miR-9-5p have emerged as attractive therapeutic targets in several tumor types, but in CRC, the regulation of their biological function and their target association remain unclear.

methodsThe expression of PAK4 in CRC tissues was determined using quantitative real-time PCR and immunohistochemistry analyses. The targeted regulation between miR-9-5p and PAK4 was predicted and confirmed with bioinformatics analysis and the dual-luciferase reporter assay. Functional experiments, including the MTT assay and flow cytometry, were performed to investigate the impact of PAK4 knockdown and miR-9-5p overexpression on cell proliferation and apoptosis in CRC cells.

resultsWe found that the expression of PAK4 was upregulated in CRC tissues. PAK4 knockdown significantly suppressed cell proliferation and promoted apoptosis in cells of the CRC cell lines HCT116 and SW1116. We also found that miR-9-5p directly targeted the 3'-UTR of PAK4 mRNA and negatively regulated its expression. The degree of downregulation of miR-9-5p inversely correlated with PAK4 expression. Intriguingly, enforced expression of miR-9-5p suppressed cell proliferation and promoted apoptosis. This could be partially reversed by PAK4 overexpression.

conclusionThese results suggest that miR-9-5p targeting of PAK4 could have therapeutic potential for CRC treatment.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdultAgedApoptosisCell ProliferationColorectal NeoplasmsHCT116 CellsHumansMicroRNAsMiddle Agedp21-Activated Kinases3' Untranslated RegionsMicroRNAsMIRN92 microRNA, humanp21-Activated KinasesPAK4 protein, humanApoptosisColorectal cancermiR-9-5pPAK4Proliferation

Identifiers

PMID31728150
PMCPMC6842216
OpenAlexW2985571854

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.