Evidence map›Paper›PMID 29953500›Full record

ArticlePloS one2018

Potential role of HIF-1-responsive microRNA210/HIF3 axis on gemcitabine resistance in cholangiocarcinoma cells.

Runglawan Silakit, Yingpinyapat Kitirat, Suyanee Thongchot, Watcharin Loilome, Anchalee Techasen, Piti Ungarreevittaya, Narong Khuntikeo, Puangrat Yongvanit, Ji Hye Yang, Nam Hee Kim and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  8. Extracellular vesicles in pancreatic cancer: a new era in precision medicine.Translational gastroenterology and hepatology · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
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  17. The Role of microRNAs in Cholangiocarcinoma.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
  20. Article
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

12 authors at 2 institutions in 2 countries.

Runglawan SilakitDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Yingpinyapat KitiratDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Suyanee ThongchotDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Watcharin LoilomeDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Anchalee TechasenCholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, Thailand.
Piti UngarreevittayaCholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, Thailand.
Narong KhuntikeoCholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, Thailand.
Puangrat YongvanitCholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, Thailand.
Ji Hye YangDepartment of Oral Pathology, Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea.
Nam Hee KimDepartment of Oral Pathology, Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea.
Jong In YookDepartment of Oral Pathology, Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea.
Nisana NamwatDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.ORCID 0000-0002-6743-5047
Khon Kaen University · THYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-210 (miR-210) is a robust target for hypoxia-inducible factor, and its overexpression has been detected in a variety of solid tumors. However, the role of miR-210 in the development, progression and response to therapy in cholangiocarcinoma (CCA) remains undefined. We report here that high miR-210 expression was significantly correlated with the shorter survival of CCA patients. Overexpression of miR-210 inhibited CCA cell proliferation at the G2/M phase and reduced the gemcitabine sensitivity in CCA cells under CoCl2-induced pseudohypoxia. Concomitantly, inhibition of endogenous miR-210 activity using miRNA sponges increased cell proliferation under CoCl2-induced pseudohypoxia, resulting in an increase in gemcitabine sensitivity in CCA cells. We showed that HIF-3α, a negative controller of HIF-1α, was a target of miR-210 constituting a feed-forward hypoxic regulatory loop. Our data suggest an important role of miR-210 in sustaining HIF-1α activity via the suppression of HIF-3α, regulating cell growth and chemotherapeutic drug resistance in CCA.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticSignal TransductionTumor HypoxiaApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsBile Duct NeoplasmsCell Line, TumorCholangiocarcinomaCobaltFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMicroRNAsNeoplasm ProteinsApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsCobaltcobaltous chlorideHIF1A protein, humanHIF3A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN210 microRNA, humanNeoplasm ProteinsRepressor ProteinsRNA, Neoplasm

Identifiers

PMID29953500
PMCPMC6023215
OpenAlexW2811365993

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.