Evidence map›Paper›PMID 27534652›Full record

ArticleJournal of physiology and biochemistry2016

Inhibition of microRNA-181a may suppress proliferation and invasion and promote apoptosis of cervical cancer cells through the PTEN/Akt/FOXO1 pathway.

Hongmei Xu, Jihong Zhu, Cong Hu, Hua Song, Yiyang Li

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Let-7 Family as a Mediator of Exercise on Alzheimer's Disease.Cellular and molecular neurobiology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Role of miR‑181a‑5p in cancer (Review).International journal of oncology · 2023
    Review
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  10. Review
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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.

Hongmei XuDepartment of Obstetrics, the First Hospital of Jilin University, Changchun, 130021, China.
Jihong ZhuSection I, Department of General Gynecology, the First Hospital of Jilin University, No. 71, Xinmin Street, Changchun, 130021, China.
Cong HuReproductive Center, the First Hospital of Jilin University, Changchun, 130021, China.
Hua SongDepartment of Gynecology and Obstetrics, Qianwei Hospital of Jilin Province, Changchun, 130012, China.
Yiyang LiSection I, Department of General Gynecology, the First Hospital of Jilin University, No. 71, Xinmin Street, Changchun, 130021, China. yyl_med@126.com.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are endogenous, non-coding, small RNAs, which play a critical role in regulating varieties of the biological and pathologic processes. miR-181a has been reported to participate in tumorigenic progression. However, the roles of miR-181a in cervical cancer (CC) are still unknown. The aim of this research was to explore the effects and molecular mechanism of miR-181a in CC cells. In this paper, the levels of miR-181a in CC cell lines were determined by real-time PCR. We found that the levels of miR-181a were evidently enhanced in CC cell lines compared with normal cervical epithelium cells. Then, the miR-181a inhibitor was transiently transfected into HeLa and CaSKi cells using Lipofectamine 2000 reagent. Subsequently, the Cell Counting Kit-8 (CCK-8) and BrdU-ELISA results showed that down-regulation of miR-181a inhibited the cell viability and proliferation. Our data also demonstrated that miR-181a inhibitor arrested cell cycle progression of HeLa and CaSKi cells by up-regulation of p21 and p27 expressions. In addition, inhibition of miR-181a promoted apoptosis of HeLa and CaSKi cells due to increasing Bax expression and decreasing Bcl-2 expression. Ultimately, the effect of miR-181a inhibitor on the PTEN/Akt/FOXO1 signaling pathway was investigated by Western blot. From our results, down-regulation of miR-181a increased the expression of PTEN and decreased phosphorylation of Akt and FOXO1. Altogether, miR-181a might be an oncogene in CC cells. The potential mechanism was that inhibition of miR-181a might suppress proliferation and invasion and promote apoptosis of HeLa and CaSKi cells by modulating the PTEN/Akt/FOXO1 signaling pathway.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisbcl-2-Associated X ProteinCell CycleCell LineCell Line, TumorCell MovementCell ProliferationCervix UteriCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Epithelial CellsFemaleForkhead Box Protein O1HumansMicroRNAsBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Forkhead Box Protein O1FOXO1 protein, humanMicroRNAsMIrn181 microRNA, humanOligoribonucleotidesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2PTEN PhosphohydrolasePTEN protein, humanApoptosisCervical cancerInvasionMicroRNA-181aPTEN/Akt/FOXO1 signaling pathway

Identifiers

PMID27534652
OpenAlexW2512135817

What OpenQuestion holds

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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.