Evidence map›Paper›PMID 32491253›Full record

ArticleMolecular oncology2020

The STAT3-miR-223-TGFBR3/HMGCS1 axis modulates the progression of cervical carcinoma.

Ju Zhang, Ming Jiang, Lili Qian, Xiao Lin, Weiguo Song, Yunfeng Gao, Ying Zhou

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
  5. The emerging role of cholesterol metabolism in gynecologic cancer development and therapy.Apoptosis : an international journal on programmed cell death · 2026
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  16. Role of exosomal non-coding RNAs from tumor cells and tumor-associated macrophages in the tumor microenvironment.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    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

7 authors at 3 institutions in 1 country.

Ju ZhangDepartment of Laboratory Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Ming JiangSchool of Life Science, University of Science and Technology of China, Hefei, China.ORCID 0000-0001-6794-3116
Lili QianDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Anhui Provincial Hospital, Hefei, China.
Xiao LinDepartment of Laboratory Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Weiguo SongDepartment of Gynaecology and Obstetrics, The Second Hospital of Anhui Medical University, Hefei, China.
Yunfeng GaoChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Ying ZhouDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Anhui Provincial Hospital, Hefei, China.
University of Science and Technology of China · CNAnhui Medical University · CNChina-US (Henan) Hormel Cancer Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is induced by persistent infections with high-risk human papillomaviruses (HPVs), which produce the early protein 6 of HPVs (E6)/E7 protein that is involved in cell transformation by interacting with several oncoproteins or tumor suppressors. However, the role of noncoding RNA in mediating the pathogenesis of cervical cancer remains unclear. Here, we report that the novel signal transducer and activator of transcription 3 (STAT3)-microRNA-223-3p (miR-223)-TGFBR3/HMGCS1 axis regulated by the E6 protein controls cervical carcinogenesis. miR-223 was highly expressed in cervical tumor tissues, whereas TGFBR3 or HMGCS1 was significantly downregulated. miR-223 targeted the 3'-UTRs of TGFBR3 and HMGCS1 and suppressed their expression, leading to increased anchorage-independent growth and cervical squamous cell carcinoma (CSCC) tumor growth in vitro and in vivo. The increased expression of miR-223 was mediated by the transcription factor STAT3, whose activity was enhanced by E6 in the context of interleukin (IL)-6 stimulation. In addition, exosomal miR-223 derived from CSCC cells induced IL-6 secretion by monocyte/macrophage in a coculture system in vitro, and IL-6 secretion, in turn, led to enhanced STAT3 activity in CSSC cells, forming a positive feedback loop. Furthermore, modified miR-223 inhibitor effectively suppressed tumor growth in cell line-derived xenograft model, suggesting that miR-223 is a potential promising therapeutic target in CSCC. In conclusion, our results demonstrate that the STAT3-miR-223-HMGCS1/TGFBR3 axis functions as a key signaling pathway in cervical cancer progression and provides a new therapeutic target.

Indexed as

Disease ProgressionAnimalsBase SequenceCarcinoma, Squamous CellCell Line, TumorExosomesFemaleGene Expression Regulation, NeoplasticHumansHydroxymethylglutaryl-CoA SynthaseInterleukin-6MacrophagesMice, NudeMicroRNAsModels, BiologicalMonocytesbetaglycanHMGCS1 protein, humanHydroxymethylglutaryl-CoA SynthaseInterleukin-6MicroRNAsMIR223, humanProteoglycansReceptors, Transforming Growth Factor betaSTAT3 protein, humanSTAT3 Transcription Factorcervical cancerHMGCS1miR-223TGFBR3

Identifiers

PMID32491253
PMCPMC7463355
OpenAlexW3030613244

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.