Evidence map›Paper›PMID 30379969›Full record

ArticlePloS one2018

Suppression of miR-22, a tumor suppressor in cervical cancer, by human papillomavirus 16 E6 via a p53/miR-22/HDAC6 pathway.

Weerayut Wongjampa, Tipaya Ekalaksananan, Peechanika Chopjitt, Jureeporn Chuerduangphui, Pilaiwan Kleebkaow, Natcha Patarapadungkit, Chamsai Pientong

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-weighted citation impact, top 5% 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, 51 citations in OpenAlex.

  1. Review
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  10. The Preventive Role of the Vitamin D Endocrine System in Cervical Cancer.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Article
  18. Article
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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

7 authors at 1 institution in 1 country.

Weerayut WongjampaDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Tipaya EkalaksanananDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Peechanika ChopjittHPV & EBV and Carcinogenesis Research Group, Khon Kaen University, Khon Kaen, Thailand.
Jureeporn ChuerduangphuiDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Pilaiwan KleebkaowHPV & EBV and Carcinogenesis Research Group, Khon Kaen University, Khon Kaen, Thailand.
Natcha PatarapadungkitHPV & EBV and Carcinogenesis Research Group, Khon Kaen University, Khon Kaen, Thailand.
Chamsai PientongDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.ORCID 0000-0003-2797-043X
Khon Kaen University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small non-coding RNAs that function to down-regulate gene expression involving in various cellular processes related to carcinogenesis. Recently, miR-22 was identified as a tumor-suppressing miRNA in many human cancers. However, the regulatory mechanism and the specific function of this miRNA in cervical cancer remain unclear. In the present study, we carried out gene transfection, western blot and quantitative RT-PCR to explore the regulatory mechanism and the functional role of miR-22 in cervical cancer. We verified that miR-22 was down-regulated in cervical cancer tissues and cervical cancer cell lines relative to matched non-tumor tissues and normal human cervical keratinocyte line (HCK1T). By contrast, histone deacetylase 6 (HDAC6) was inversely correlated with miR-22 in both cervical tissues and cancer cell lines. Mechanically, HDAC6 was down-regulated by miR-22 at the post-transcriptional level, via a specific target site within the 3'UTR, identified by a luciferase reporter assay. Moreover, we also showed that the correlation between miR-22 and HDAC6 expression was regulated by an E6/p53 pathway in HCK1Ts expressing HPV16 E6. For functional study, an ectopic expression of miR-22 could inhibit cell proliferation and migration, and could induce apoptosis of cervical cancer cell lines. These findings demonstrated that miR-22 was down-regulated in cervical cancer and inversely collated with its downstream target HDAC6. MiR-22 acts as tumor suppressor by inhibiting proliferation and migration, and by inducing apoptosis of cervical cancer cell lines by targeting the 3'UTR of HDAC6. This newly identified E6/p53/miR-22/HDAC6 regulatory network might be a candidate therapeutic target for cervical cancer.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorCell MovementCell ProliferationFemaleHistone Deacetylase 6HumansKeratinocytesMicroRNAsOncogene Proteins, ViralRepressor ProteinsSignal TransductionTumor Suppressor Protein p53Uterine Cervical NeoplasmsE6 protein, Human papillomavirus type 16HDAC6 protein, humanHistone Deacetylase 6MicroRNAsMIRN22 microRNA, humanOncogene Proteins, ViralRepressor ProteinsTumor Suppressor Protein p53

Identifiers

PMID30379969
PMCPMC6209303
OpenAlexW2899354526

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.