Evidence map›Paper›PMID 29749476›Full record

ArticleMolecular medicine reports2018

miR‑23a suppresses pancreatic cancer cell progression by inhibiting PLK‑1 expression.

Bin Chen, Akao Zhu, Lei Tian, Ying Xin, Xinchun Liu, Yunpeng Peng, Jingjing Zhang, Yi Miao, Jishu Wei

RetractedErratum issuedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2018. 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 It has been retracted, and should not be counted.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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

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  12. miR-557 inhibits the proliferation and invasion of pancreatic cancer cells by targeting EGFR.International journal of clinical and experimental pathology · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Bin ChenHepatopancreatobiliary Surgery Department, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Akao ZhuHepatopancreatobiliary Surgery Department, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Lei TianThe Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Ying XinThyroid Breast Surgery Department, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Xinchun LiuThe Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yunpeng PengThe Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jingjing ZhangThe Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yi MiaoThe Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jishu WeiThe Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jiangsu Province Hospital · CNNanjing Medical University · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to explore the effects and underlying mechanisms of microRNA (miR)‑23a on pancreatic cancer (PC) cells progression. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were used to detect the mRNA and protein miR‑23a and PLK‑1 level. Cell viability, cell cycle, migration and invasion assasy, and in vivo tumorigenicity assay were used to investigate the effects of miR‑204. Further luciferase reporter assay was used to explore the mechanisms contributing to miR‑204 effects. It was observed that miR‑23a expression was upregulated and negatively associated with polo‑like kinase‑1 (PLK‑1) expression in human PC tissues. PLK‑1 was a direct target of miR‑23a in PC cells. Functional analysis demonstrated that miR‑23a overexpression suppressed cell proliferation, inhibited cell migration and invasion and promoted cell apoptosis in vitro. When PC cells were transfected with has‑miR‑23a PLK‑1 was downregulated and its downstream molecules were deregulated, including decreased expression of B‑cell lymphoma‑2, cyclin B1 and vimentin, and increased expression of Bax and E‑cadherin. The inhibitory effect of miR‑23a on PC cell progression was observed in vivo tumor xenografts. The results of the study suggest that miR‑23a inhibits PC cell progression by directly targeting PLK‑1‑associated signaling and promoting miR‑23a expression may be a potential method for treating patients with PC.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAnimalsApoptosisCell Cycle ProteinsFemaleHumansMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsPancreatic NeoplasmsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsCell Cycle ProteinsMicroRNAsMIRN23a microRNA, humanPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRNA, Neoplasm

Identifiers

PMID29749476
PMCPMC6059658
OpenAlexW2802099638

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.