Evidence map›Paper›PMID 40542346›Full record

ArticleJournal of translational medicine2025

Overexpression of oncogenic polo-like kinase 1 disrupts the invasiveness, cell cycle, and apoptosis in synovial sarcoma.

Jun Zhang, Zhong Li, Ming-Yu Xie, Ning Wang, Hao Liu, Feng Li, Li-Juan Pang, Yan Qi

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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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

8 authors.

Jun Zhang *Department of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524000, Guangdong, China.
Zhong Li *Department of Pathology, Xiongan Xuanwu Hospital, Baoding, Hebei Province, China.
Ming-Yu XieDepartment of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524000, Guangdong, China.
Ning WangDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, Shihezi, 832002, Xinjiang, China.
Hao LiuDepartment of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524000, Guangdong, China.
Feng LiDepartment of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524000, Guangdong, China.
Li-Juan PangDepartment of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524000, Guangdong, China.
Yan QiDepartment of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524000, Guangdong, China. qiyanyan-1998@163.com.

Funding

Natural Science Foundation of Guangdong Province 2025A1515012466the National Natural Science Foundation of China 82472793Zhanjiang Central People's Hospital High-level Personnel Research start-up funding project 2022A24
6 · The paper itself

Abstract

backgroundSynovial sarcoma (SS) is an aggressive malignant soft tissue sarcoma of undetermined tissue origin that harbors potential metastases and recurrences, leading to a poor prognosis. Polo-like kinase 1 (PLK1) is an essential member of the serine/threonine kinase family, which plays a key role in cell cycle progression and other cellular processes. Therefore, PLK1 could act as a promising target for treating various cancers, including a low incidence of sarcoma.

methodsSS paraffin-embedded tissue samples were selected to detect the expression of PLK1 and apoptosis- and autophagy-related proteins using immunohistochemistry. We analyzed the effects of low PLK1 expression on the SS cell cycle and function using the PLK1 inhibitor BI2536 in SW982 and SSX1 cells (cells with high expression of the SYT-SSX1 fusion gene). Western blotting was used to detect the expression of PLK1 and apoptotic proteins in different groups. Finally, the antitumor effects and safety of BI2536 were evaluated using xenograft tumor experiments in nude mice.

resultsIn SS tissues, PLK1 was overexpressed and autophagy-related proteins were expressed at low levels, leading to poor prognosis. Suppressing PLK1 expression using the PLK1 inhibitor BI2536 decreased the proliferation, migration, and invasion abilities of SW982 and SYT-SSX1 cells and promoted the expression of the apoptotic protein Bax. Meanwhile, we confirmed that SS cell apoptosis increased and G2/M cycle arrest occurred after PLK1 expression was inhibited. We found that BI2536 significantly inhibited the growth of SS-xenografted tumors in nude mice, and the expression of stem cell-related factors significantly decreased.

conclusionPLK1 overexpression was closely associated with poor prognosis. Suppressing PLK1 expression significantly inhibited the growth, invasion, and migration of SS cells, promoted apoptosis, and blocked the G2/M phase of the cell cycle.

Indexed as

ApoptosisCell CycleCell Cycle ProteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsSarcoma, SynovialAdultAnimalsAutophagyCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleBI 2536Cell Cycle ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsPteridinesApoptosisBI2536Cell cycleInvasivenessPLK1Synovial sarcoma

Identifiers

PMID40542346
PMCPMC12181926

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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.