Evidence map›Paper›PMID 30565428›Full record

ArticleCancer medicine2019

CCNG1 (Cyclin G1) regulation by mutant-P53 via induction of Notch3 expression promotes high-grade serous ovarian cancer (HGSOC) tumorigenesis and progression.

Ying Xu, Qing Zhang, Chunying Miao, Samina Dongol, Yinuo Li, Chenjuan Jin, Ruifeng Dong, Yingwei Li, Xingsheng Yang, Beihua Kong

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 37 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 1 institution in 1 country.

Ying XuDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Qing ZhangDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Chunying MiaoDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Samina DongolDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Yinuo LiDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Chenjuan JinDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Ruifeng DongDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Yingwei LiDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Xingsheng YangDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.
Beihua KongDepartment of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, China.ORCID 0000-0002-1627-1150
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TP53 mutation is considerably common in advanced high-grade serous ovarian cancer (HGSOC) and significantly associated with a poor prognosis. In this study, we investigated the role of Cyclin G1 (CCNG1), a target gene of wild-type TP53 (P53wt), in HGSOC and the possible regulatory mechanism between TP53 mutant (P53mt) and CCNG1 in the progression of HGSOC. High expression level of CCNG1 was found in 61.3% of HGSOC tissues and only 18.2% in fimbriae of fallopian tubes. Additionally, overexpression of CCNG1 was significantly associated with a shorter overall survival (P < 0.0001) and progression-free survival (P < 0.0004) in HGSOC patients. In vitro, CCNG1 promoted both tumor cell motility by inducing epithelial-mesenchymal transition (EMT) and resistance to cisplatin (CDDP). In vivo, knockdown expression of CCNG1 inhibited cancer metastasis. Furthermore, P53mt increased the expression of CCNG1 by regulating Notch3 expression, and a positive correlation between CCNG1 and Notch3 protein expression was observed by Immunohistochemistry (IHC) (r = 0.39, P: 0.01528). In conclusion, the activation of P53mt-Notch3-CCNG1 pathway was responsible for tumor progression to advanced disease with correlation with worse prognosis in patients with HGSOC. These data suggest a possible molecular mechanism of disease and highlights CCNG1's potential role as a therapeutic target in HGSOC.

Indexed as

Antineoplastic AgentsCarcinogenesisCell Line, TumorCell MovementCell SurvivalCisplatinCyclin G1Disease ProgressionDrug Resistance, NeoplasmFemaleHumansMiddle AgedMutationOvarian NeoplasmsPrognosisReceptor, Notch3Antineoplastic AgentsCCNG1 protein, humanCisplatinCyclin G1NOTCH3 protein, humanReceptor, Notch3Tumor Suppressor Protein p53Cyclin G1high-grade serous ovarian cancermetastasisNotch3P53mtprognosis

Identifiers

PMID30565428
PMCPMC6346265
OpenAlexW2904939440

What OpenQuestion holds

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LicenceCC BY
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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.