Evidence map›Paper›PMID 28899430›Full record

ArticleJournal of ovarian research2017

The aberrant upstream pathway regulations of CDK1 protein were implicated in the proliferation and apoptosis of ovarian cancer cells.

Ruitao Zhang, Huirong Shi, Fang Ren, Minghui Zhang, Pengcheng Ji, Wenwen Wang, Chuanna Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-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

25 citing papers in PubMed, 46 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

7 authors at 1 institution in 1 country.

Ruitao ZhangDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China. z211019zhangruitao1@126.com.ORCID http://orcid.org/0000-0001-5610-9433
Huirong ShiDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China.
Fang RenDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China.
Minghui ZhangDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China.
Pengcheng JiDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China.
Wenwen WangDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China.
Chuanna LiuDepartment of Gynecology, First Affiliated Hospital, Zhengzhou University, NO.1 Jianshe Road, Zhengzhou, 450052, Henan, People's Republic of China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUpregulation of Cyclin dependent kinase 1 (CDK1) protein is closely related with the prognosis of several malignant tumors. Chk1-CDC25C-CDK1 signaling and P53-P21WAF1-CDK1 signaling pathways are closely related with the cell cycle G2/M phase regulation. The present study aimed to analyze the relationship between CDK1 and the proliferation and apoptosis of ovarian cancer cells, investigate its molecular mechanism preliminarily.

methodsThe specific short-hair RNA (shRNA) plasmids and negative control plasmid of CDK1, checkpoint kinase 1 (CHK1) and p53 genes were transfected into ovarian cancer SK-OV-3 and OVCAR-3 cells respectively. The expressions of CDK1, CHK1 and p53 mRNA and CDK1, Chk1 and P53 protein were detected by sqRT-PCR and Western blot, levels of phospho-CDK1(Thr14/Tyr15), CyclinB1, phospho-Chk1(ser345), cell division cycle 25C (CDC25C), phospho-CDC25C(ser216), P21WAF1, phospho-P53(ser15), proliferating cell nuclear antigen (PCNA), Ki-67, Bcl-2, Bax, Caspase8, Cleaved-caspase3 and Cytochrome C were examined by Western blot. The cell proliferation was measured by MTT and Trypan blue exclusion assay respectively, the cell cycle phase distribution and cell apoptosis rate were detected by flow cytometry (FCM) assay.

resultsAs results of CDK1 inhibition by shRNA, the cell proliferation was repressed, the cell numbers of G2/M phase and cell apoptosis rate were increased in both SK-OV-3 and OVCAR-3 cells. After knockdown of CDK1, expressions of PCNA, Ki-67 and Bcl-2 protein were downregulated, expressions of Bax, Caspase8, Cleaved-caspase3 and Cytochrome C were upregulated. While knockdown the CHK1 and p53 by shRNA respectively, the similar effects were observed on the cell proliferation, cell cycle phase distribution and apoptosis in both SK-OV-3 and OVCAR-3 cells, as well as the expressions of the proliferation and apoptosis related proteins mentioned above. Moreover, the levels of p-CDK1(Thr14/Tyr15) were increased after either CHK1 inhibition or p53 inhibition.

conclusionsAbnormal activation of CDK1 was implicated in the proliferation and apoptosis regulation of ovarian cancer cells, which might be due to the aberrant regulations of the upstream Chk1-CDC25C and P53-P21WAF1 signaling pathway.

Indexed as

ApoptosisCell ProliferationCDC2 Protein KinaseCell Line, TumorCheckpoint Kinase 1FemaleHumansOvarian NeoplasmsSignal TransductionTumor Suppressor Protein p53CDC2 Protein KinaseCDK1 protein, humanCheckpoint Kinase 1CHEK1 protein, humanTumor Suppressor Protein p53ApoptosisCyclin dependent kinases 1G2/M phase regulationOvarian epithelial cancerProliferation

Identifiers

PMID28899430
PMCPMC5596843
OpenAlexW2756036573

What OpenQuestion holds

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LicenceCC BY
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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.