Evidence map›Paper›PMID 33190089›Full record

ArticleNeoplasia (New York, N.Y.)2021

CBP-mediated Wnt3a/β-catenin signaling promotes cervical oncogenesis initiated by Piwil2.

Dingqing Feng, Keqin Yan, Haiyan Liang, Jing Liang, Wenhui Wang, Huan Yu, Ying Zhou, Weidong Zhao, Zhongjun Dong, Bin Ling

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

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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

10 authors at 5 institutions in 1 country.

Dingqing FengDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China.
Keqin YanDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China.
Haiyan LiangDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China.
Jing LiangDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China.
Wenhui WangDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Huan YuDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China.
Ying ZhouDepartment of Obstetrics and Gynecology, the First Affiliated Hospital of University of Science and Technology of China, Hefei, China.
Weidong ZhaoDepartment of Gynecology and Oncology, Anhui Provincial Cancer Hospital, Hefei, China.
Zhongjun DongSchool of Medicine, Tsinghua University, Beijing, China.
Bin LingDepartment of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, China; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. Electronic address: lingbin.ling@vip.sina.com.
China-Japan Friendship Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNAnhui Provincial Hospital · CNTsinghua University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous work demonstrated that Piwil2 reactivated by the human papillomavirus oncoproteins E6 and E7 may reprogram somatic cells into tumor-initiating cells (TICs), which contribute to cervical neoplasia lesions. Maintaining the stemness of TICs is critical for the progression of cervical lesions. Here, we determined that canonical Wnt signaling was aberrantly activated in HaCaT cells transfected with lentivirus expressing Piwil2 and in cervical lesion specimens of low-grade squamous intraepithelial lesion, high-grade squamous intraepithelial lesion, and invasive carcinoma. Blocking the β-catenin and CREB binding protein interaction with ICG-001 significantly downregulated the reprogramming factors c-Myc, Nanog, Oct4, Sox2, and Klf4, thus leading to cell differentiation and preventing tumorigenicity in Piwil2-overexpressing HaCaT cells. Similarly, Piwil2 also critically regulated the canonical Wnt signaling pathway in cervical cancer. We further demonstrated that ICG-001 increased cisplatin sensitivity and significantly suppressed tumor growth of cervical cancer alone or in combination with cisplatin both in vitro and in vivo. The β-catenin/ CREB binding protein-mediated transcription activated by Piwil2 is essential for the maintenance of TICs, therefore contributing to the progression of cervical oncogenesis.

Indexed as

Gene Expression Regulation, NeoplasticWnt Signaling PathwayAnimalsAntineoplastic AgentsArgonaute ProteinsBiomarkers, TumorCell Line, TumorCell SurvivalCell Transformation, NeoplasticCREB-Binding ProteinDisease Models, AnimalDisease SusceptibilityDrug Resistance, NeoplasmFemaleHumansImmunohistochemistryAntineoplastic AgentsArgonaute ProteinsBiomarkers, TumorCREB-Binding ProteinCREBBP protein, humanKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4PIWIL2 protein, humanCBPCervical cancerPiwil2Tumor initiating cellWnt signaling

Identifiers

PMID33190089
PMCPMC7674161
OpenAlexW3105846960

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.