Evidence map›Paper›PMID 28427207›Full record

ArticleOncotarget2017

miR-205 inhibits cell growth by targeting AKT-mTOR signaling in progesterone-resistant endometrial cancer Ishikawa cells.

Zhihong Zhuo, Huimin Yu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. MiR-205-5p and MiR-222-3p as Potential Biomarkers of Endometrial Cancer.International journal of molecular sciences · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. The Two-Faced Role of Autophagy in Endometrial Cancer.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Article
  12. Non-Coding RNAs as Prognostic Markers for Endometrial Cancer.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Modeling Endometrial Cancer: Past, Present, and Future.International journal of molecular sciences · 2018
    Review
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

2 authors at 1 institution in 1 country.

Zhihong ZhuoNingbo No. 2 Hospital, 315010 Ningbo, People's Republic of China.
Huimin YuNingbo No. 2 Hospital, 315010 Ningbo, People's Republic of China.
Ningbo No. 2 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposemiR-205 is significantly up-regulated in endometrioid adenocarcinoma. In this study, the significant anticancer effect of a miR-205 inhibitor was investigated in both endometrial carcinoma and progesterone-resistant endometrial carcinoma cells.

resultsCompared with Ishikawa endometrial cancer cells, miR-205 was expressed at higher levels in a progesterone-resistant (PR) sub-cell line. Inhibition of miR-205 suppressed the growth of cancer cells in a dose- and time-dependent manner. Moreover, the miR-205 inhibitor induced a marked increase in the percentage of Ishikawa-PR cells in G2/M phases and a decrease in the percentage of cells in G0/G1 and S phases. In addition, miR-205 inhibitor-treated tumor cells exhibited increased apoptosis. Moreover, miR-205 was found to negatively regulate PTEN expression and lead to autophagy and activation of the AKT/mTOR pathway in PR cells, and PTEN protein levels significantly decreased with development of progesterone resistance in endometrial cancer cells. Western blot assay showed up-regulated autophagy, as indicated by expression of LC3-II/LC3-I and beclin1, in Ishikawa cells; in particular, autophagy was markedly induced in PR cells treated with the miR-205 inhibitor. MATERIALS AND

methodsWe measured and analyzed cell growth curves with and without miR-205 inhibition with the MTT assay, miR-205 expression by qRT-PCR, cell cycle and apoptosis using annexin V/propidium iodide staining and flow cytometry, and autophagy, apoptosis, and AKT-mTOR signaling by western blotting.

conclusionsInhibition of miR-205, which targets the AKT-mTOR pathway, in endometrial cancer cells provides a potential, new treatment for PR endometrial carcinoma.

Indexed as

Signal TransductionUterine DiseasesApoptosisAutophagyCell CycleCell Line, TumorEndometrial NeoplasmsEndometriumFemaleGene ExpressionHumansMicroRNAsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTOR Serine-Threonine KinasesMicroRNAsMIR205, humanMTOR protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine Kinasesautophagyendometrial carcinomamicroRNAprogesterone resistance

Identifiers

PMID28427207
PMCPMC5438629
OpenAlexW2593997208

What OpenQuestion holds

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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.