Evidence map›Paper›PMID 27509128›Full record

ArticlePloS one2016

miR-6734 Up-Regulates p21 Gene Expression and Induces Cell Cycle Arrest and Apoptosis in Colon Cancer Cells.

Moo Rim Kang, Ki Hwan Park, Jeong-Ook Yang, Chang Woo Lee, Soo Jin Oh, Jieun Yun, Myeong Youl Lee, Sang-Bae Han, Jong Soon Kang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 13% 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, 46 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Moo Rim KangBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Ki Hwan ParkBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Jeong-Ook YangBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Chang Woo LeeBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Soo Jin OhBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Jieun YunBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Myeong Youl LeeBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Sang-Bae HanCollege of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea.
Jong Soon KangBio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.
Korea Research Institute of Bioscience and Biotechnology · KRChungbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, microRNAs have been implicated in the regulation of gene expression in terms of both gene silencing and gene activation. Here, we investigated the effects of miR-6734, which has a sequence homology with a specific region of p21WAF1/CIP1 (p21) promoter, on cancer cell growth and the mechanisms involved in this effect. miR-6734 up-regulated p21 expression at both mRNA and protein levels and chromatin immunoprecipitation analysis using biotin-labeled miR-6734 confirmed the association of miR-6734 with p21 promoter. Moreover, miR-6734 inhibited cancer cell growth and induced cell cycle arrest and apoptosis in HCT-116 cells, which was abolished by knockdown of p21. The phosphorylation of Rb and the cleavage of caspase 3 and PARP were suppressed by miR-6734 transfection in HCT-116 cells and these effects were also reversed by p21 knockdown. In addition, miR-6734 transfection caused prolonged induction of p21 gene and modification of histones in p21 promoter, which are typical aspects of a phenomenon referred to as RNA activation (RNAa). Collectively, our results demonstrated that miR-6734 inhibits the growth of colon cancer cells by up-regulating p21 gene expression and subsequent induction of cell cycle arrest and apoptosis, suggesting its role as an important endogenous regulator of cancer cell proliferation and survival.

Indexed as

ApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticHCT116 CellsHistonesHumansMembrane ProteinsMicroRNAsMitochondrial ProteinsPromoter Regions, GeneticCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21HistonesMembrane ProteinsMicroRNAsMIRN6734 microRNA, humanMitochondrial Proteins

Identifiers

PMID27509128
PMCPMC4979902
OpenAlexW2489832387

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.