Evidence map›Paper›PMID 34162426›Full record

ArticleJournal of ovarian research2021

TCP1 regulates PI3K/AKT/mTOR signaling pathway to promote proliferation of ovarian cancer cells.

Huixi Weng, Xiushan Feng, Yu Lan, Zhiqun Zheng

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
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

15 citing papers in PubMed, 21 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

4 authors at 1 institution in 1 country.

Huixi Weng *Department of Ob & Gyn, Fujian Medical University Union Hospital, 29#, Xinquan Road, Gulou District, Fuzhou, 350001, Fujian, China.
Xiushan Feng *Department of Ob & Gyn, Fujian Medical University Union Hospital, 29#, Xinquan Road, Gulou District, Fuzhou, 350001, Fujian, China.
Yu LanDepartment of Ob & Gyn, Fujian Medical University Union Hospital, 29#, Xinquan Road, Gulou District, Fuzhou, 350001, Fujian, China.
Zhiqun ZhengDepartment of Ob & Gyn, Fujian Medical University Union Hospital, 29#, Xinquan Road, Gulou District, Fuzhou, 350001, Fujian, China. z-zhiqun@163.com.ORCID http://orcid.org/0000-0002-2309-7162
Fujian Medical University · CN

Funding

Fujian Provincial Department of Science and Technology (CN) 2100201
6 · The paper itself

Abstract

objectiveTCP1 is one of the eight subunits of the TCP1 ring complex (TRiC) or the multi-protein mammalian cytosolic chaperone complex. TRiC participates in protein folding and regulates the expression of multiple signaling proteins and cytoskeletal components in cells. Although the clinical importance of its subunits has been clarified in various carcinomas, the function of TCP1 in ovarian cancer (OC) remains unclear. We aimed to identify the association between the expression of TCP1 and the development of epithelial OC (EOC) and patient prognosis, and explore the underlying mechanisms of TCP1 on the tumor progression of OC cells.

methodsTCP1 protein expression was tested in various ovarian tissues by immunohistochemistry, and the correlation between TCP1 expression and clinical physiologic or pathologic parameters of patients with EOC was analyzed. The relationship between TCP1 expression and the prognosis of patients with OC was investigated and analyzed using the Kaplan-Meier (KM) plotter online database. The expression level of TCP1 was then tested in different OC cell lines by Western blotting. Further, a model using OC cell line A2780 was constructed to study the functions of TCP1 in growth, migration, and invasion of human EOC cells. Finally, the possible regulating signaling pathways were discussed.

resultsTCP1 protein expression in OC or borderline tissues was significantly higher than that in benign ovarian tumors and normal ovarian tissue. The upregulated expression of TCP1 in OC was positively associated with the differentiation grade and FIGO stage of tumors and predicted poor clinical outcomes. Compared with IOSE-80 cells, TCP1 protein was overexpressed in A2780 cells. TCP1 knockdown using shRNA lentivirus inhibited the viability of A2780 cells. Western blotting showed that the phosphatidylinositol-3 kinase (PI3K) signaling pathway was activated in the tumor invasion in EOC driven by TCP1.

conclusionUpregulated TCP1 is correlated with the poor prognosis of patients with OC. The mechanism of cancer progression promoted by TCP1 upregulation may be linked to the activation of the PI3K signaling pathway, and TCP1 may serve as a novel target for the treatment of OC.

Indexed as

Cell Line, TumorCell ProliferationChaperonin Containing TCP-1FemaleHumansMiddle AgedOvarian NeoplasmsPhosphatidylinositol 3-KinasePrognosisProto-Oncogene Proteins c-aktSignal TransductionSurvival AnalysisTOR Serine-Threonine KinasesChaperonin Containing TCP-1MTOR protein, humanPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktTCP1 protein, humanTOR Serine-Threonine KinasesOvarian cancerPI3K/AKT/mTOR signaling pathwayPrognostic biomarkerTCP1

Identifiers

PMID34162426
PMCPMC8223286
OpenAlexW3176207014

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.