Evidence map›Paper›PMID 34782718›Full record

ArticleOncogene2022

Tight junction protein 1 promotes vasculature remodeling via regulating USP2/TWIST1 in bladder cancer.

Xue-Qi Liu, Xin-Rong Shao, Ye Liu, Zhao-Xia Dong, Sze-Hoi Chan, Yuan-Yuan Shi, Shu-Na Chen, Lin Qi, Li Zhong, Yue Yu and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-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

14 citing papers in PubMed, 18 citations in OpenAlex.

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    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 2 countries.

Xue-Qi Liu *Molecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0002-8295-032X
Xin-Rong Shao *Molecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0003-0334-8339
Ye Liu *Department of Pathology, Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Zhao-Xia DongMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Sze-Hoi ChanMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Yuan-Yuan ShiMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Shu-Na ChenMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0002-0051-0153
Lin QiMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Li ZhongState Key Laboratory of Oncology in South China, Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.ORCID http://orcid.org/0000-0002-1646-2862
Yue YuMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Ting LvDepartment of Pathology, Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Peng-Fei YangDepartment of Pathology, Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Li-Yan LiMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Xiao-Bin WangAndrology section, Center of Reproductive Medicine, Shengjing Hospital of China Medical University, Shenyang, China.
Xu-Dong ZhangMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.
Xin LiMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0001-8328-4894
Wenxue ZhaoMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0001-5380-1176
Lalit SehgalDivision of Hematology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH, USA.ORCID http://orcid.org/0000-0002-1151-5427
Miao LiThe First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, China. limiao27@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-7227-3460
Xing-Ding ZhangMolecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China. zhangxd39@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-2759-5185
Sun Yat-sen University · CNChina Medical University · CNShenzhen University Health Science Center · CNThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder cancer (BLCA) is the most common malignant tumor of the urinary system and is characterized by high metastatic rates and poor prognosis. The expression of tight junction protein 1 (TJP1) is associated with bladder cancer invasion; however, the mechanism by which TJP1 affects vasculature remodeling remains unknown. In this study, we found that TJP1 expression correlated with tumor angiogenesis and poor overall survival in clinical samples. Furthermore, TJP1 overexpression promoted tumor angiogenesis in BLCA cells and stimulated recruitment of macrophages to tumors by upregulating CCL2 expression. Mechanistically, TJP1 interacted with TWIST1 and enhanced the transcriptional activity of CCL2. The impairment of tumor angiogenesis caused by knockdown of TJP1 was dramatically rescued by overexpression of TWIST1. Furthermore, TJP1 recruited USP2, which deubiquitinated TWIST1, thereby protecting TWIST1 from proteasome-mediated protein degradation. In conclusion, our results suggest that TJP1 controls angiogenesis in BLCA via TWIST1-dependent regulation of CCL2. We demonstrate that TJP1 functions as a scaffold for the interaction between USP2 and TWIST1 and this may provide potential therapeutic targets in bladder cancer.

Indexed as

AnimalsCell Line, TumorDisease Models, AnimalHumansMiceMice, NudeTransfectionUbiquitin ThiolesteraseUrinary Bladder NeoplasmsZonula Occludens-1 ProteinTjp1 protein, mouseUbiquitin ThiolesteraseUsp2 protein, mouseZonula Occludens-1 Protein

Identifiers

PMID34782718
OpenAlexW3213878098

What OpenQuestion holds

Textmetadata
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.