Evidence map›Paper›PMID 34294689›Full record

ArticleCell death & disease2021

PSMC2/CCND1 axis promotes development of ovarian cancer through regulating cell growth, apoptosis and migration.

Dawei Zhu, Jie Huang, Ning Liu, Wei Li, Limei Yan

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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  10. [Overexpression of lncRNA FEZF1-AS1 promotes progression of non-small cell lung cancerNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

5 authors at 3 institutions in 1 country.

Dawei Zhu *Department of Gynaecology and Obstetrics, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Jie Huang *Department of Gynaecology and Obstetrics, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Ning Liu *Department of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Heping District, Shenyang, 110004, Liaoning, China.
Wei LiDepartment of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Heping District, Shenyang, 110004, Liaoning, China.
Limei YanDepartment of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Heping District, Shenyang, 110004, Liaoning, China. lmyan@cmu.edu.cn.
China Medical University · CNArmy Medical University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is known as one of the most common malignancies of the gynecological system, whose treatment is still not satisfactory because of the unclear understanding of molecular mechanism. PSMC2 is an essential component of 19 S regulatory granules in 26 S proteasome and its relationship with ovarian cancer is still not clear. In this study, we found that PSMC2 was upregulated in ovarian cancer tissues, associated with tumor grade and could probably predict poor prognosis. Knocking down the endogenous PSMC2 expression in ovarian cancer cells could decrease colony formation ability, cell motility and cell proliferation rate, along with increasing cell apoptosis rate. Cells models or xenografts formed by cells with relatively lower expression of PSMC2 exhibited weaker oncogenicity and slower growth rate in vivo. Moreover, gene microarray was used to analyze the alteration of gene expression profiling of ovarian cancer induced by PSMC2 knockdown and identify CCND1 as a potential downstream of PSMC2. Further study revealed the mutual regulation between PSMC2 and CCND1, and demonstrated that knockdown of CCND1 could enhance the regulatory effects induced by PSMC2 knockdown and overexpression of CCND1 reverses it. In summary, PSMC2 may promote the development of ovarian cancer through CCND1, which may predict poor prognosis of ovarian cancer patients.

Indexed as

ApoptosisCell MovementSignal TransductionAnimalsATPases Associated with Diverse Cellular ActivitiesCarcinogenesisCell Line, TumorCell ProliferationCyclin D1Down-RegulationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeATPases Associated with Diverse Cellular ActivitiesCCND1 protein, humanCyclin D1Proteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktPSMC2 protein, human

Identifiers

PMID34294689
PMCPMC8298468
OpenAlexW3183835718

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.