Evidence map›Paper›PMID 31736008›Full record

ArticleGenes & genomics2020

MUC16 facilitates cervical cancer progression via JAK2/STAT3 phosphorylation-mediated cyclooxygenase-2 expression.

Hui Shen, Meng Guo, Lu Wang, Xinyue Cui

Abstract read
PubMed Publisher
In one paragraph

Article in Genes & genomics, 2020. 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
2.1field-weighted citation impact, top 12% 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, 42 citations in OpenAlex.

  1. Article
  2. Chemoradiotherapy facilitates siglec-10Cancer immunology, immunotherapy : CII · 2026
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  15. [MUC16: The Novel Target for Tumor Therapy].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022
    Review
  16. Article
  17. Article
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  19. Review
  20. Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    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

4 authors at 1 institution in 1 country.

Hui ShenDepartment of Gynaecology and Obstetrics, The Affiliated Sir Run Run Hospital of Nanjing Medical University, No. 109 Longmian Avenue, Jiangning District, Nanjing, 211166, China. HuiShender@163.com.
Meng GuoDepartment of Gynaecology and Obstetrics, The Affiliated Sir Run Run Hospital of Nanjing Medical University, No. 109 Longmian Avenue, Jiangning District, Nanjing, 211166, China.
Lu WangDepartment of Gynaecology and Obstetrics, The Affiliated Sir Run Run Hospital of Nanjing Medical University, No. 109 Longmian Avenue, Jiangning District, Nanjing, 211166, China.
Xinyue CuiDepartment of Gynaecology and Obstetrics, The Affiliated Sir Run Run Hospital of Nanjing Medical University, No. 109 Longmian Avenue, Jiangning District, Nanjing, 211166, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMUC16 (mucin 16, also known as CA-125, cancer antigen 125, carcinoma antigen 125, or carbohydrate antigen 125) has been predicted as tumor biomarker for therapy. We determined to investigate effects and regulatory mechanism of MUC16 on cervical tumorigenesis.

methodsExpression levels of MUC16 in cervical cancer cell lines was analyzed via qRT-PCR (quantitative real-time polymerase chain reaction). Knockdown of MUC16 was conducted via shRNA (Short hairpin RNA) transfection. MTT and colony formation assays were used to investigate effect of MUC16 on cell proliferation. Wound healing assay was utilized to detect migration and transwell assay to detect invasion. The underlying mechanism was demonstrated via western blot analysis.

resultsMUC16 was elevated in cervical cancer cell lines. MUC16 knockdown inhibited cell proliferation, invasion and migration. Gain- and loss-of functional assays revealed that over-expression of MUC16 activated Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) via phosphorylation, thus facilitating cyclooxygenase-2 (COX-2) expression, while knockdown of MUC16 demonstrated the reverse effect on JAK2/STAT3 activation and COX-2 expression. Moreover, inhibition of JAK2/STAT3 attenuated the regulation of MUC16 on COX-2.

conclusionsMUC16 enhanced proliferation and invasion of cervical cancer cells via JAK2/STAT3 phosphorylation-mediated cyclooxygenase-2 expression, suggesting the potential therapeutic target ability of MUC16 to treat cervical cancer.

Indexed as

CA-125 AntigenCell Line, TumorCell MovementCell ProliferationCyclooxygenase 2Disease ProgressionFemaleHeLa CellsHumansJanus Kinase 2Membrane ProteinsNeoplasm InvasivenessPhosphorylationSTAT3 Transcription FactorUterine Cervical NeoplasmsCA-125 AntigenCyclooxygenase 2JAK2 protein, humanJanus Kinase 2Membrane ProteinsMUC16 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorCervical cancerCOX-2JAK2/STAT3MUC16Progression

Identifiers

PMID31736008
OpenAlexW2988726335

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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.