Evidence map›Paper›PMID 39237880›Full record

ArticleCellular & molecular biology letters2024

Hsa_circ_0000520 suppresses vasculogenic mimicry formation and metastasis in bladder cancer through Lin28a/PTEN/PI3K signaling.

Chunyu Zhang, Jiao Hu, Zhi Liu, Hao Deng, Jiatong Xiao, Zhenglin Yi, Yunbo He, Zicheng Xiao, Jinliang Huang, Haisu Liang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

The trial behind it

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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

10 citing papers in PubMed.

  1. Article
  2. Acta pharmaceutica Sinica. B · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
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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

14 authors.

Chunyu ZhangDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Jiao HuDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Zhi LiuDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Hao DengDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Jiatong XiaoDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Zhenglin YiDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Yunbo HeDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Zicheng XiaoDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Jinliang HuangDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Haisu LiangDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Benyi FanDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China.
Zhihua WangDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. zhwang_hust@hotmail.com.
Jinbo ChenDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China. chenjinbo@csu.edu.cn.
Xiongbing ZuDepartment of Urology, Xiangya Hospital, Central South University, Changsha, China. zuxbxy@csu.edu.cn.

Funding

Central South University Innovation-Driven Research Program 2023CXQD071Hunan Province key research and development plan 2023SK2016Hunan Province Young talents Program 2021RC3027Natural Science Foundation of Hunan Province 2023JJ30870
6 · The paper itself

Abstract

backgroundVasculogenic mimicry (VM) is a potential cause of resistance to antiangiogenic therapy and is closely related to the malignant progression of tumors. It has been shown that noncoding RNAs play an important role in the formation of VM in malignant tumors. However, the role of circRNAs in VM of bladder cancer and the regulatory mechanisms are unclear.

methodsFirstly, hsa_circ_0000520 was identified to have circular character by Sanger sequencing and Rnase R assays. Secondly, the potential clinical value of hsa_circ_0000520 was explored by quantitative real-time polymerase chain reaction (qRT-PCR) and fluorescence in situ hybridization (FISH) of clinical specimens. Thirdly, the role of hsa_circ_0000520 in bladder cancer invasion, migration, and VM formation was examined by in vivo and in vitro experiments. Finally, the regulatory mechanisms of hsa_circ_0000520 in the malignant progression of bladder cancer were elucidated by RNA binding protein immunoprecipitation (RIP), RNA pulldown, co-immunoprecipitation (co-IP), qRT-PCR, Western blot (WB), and fluorescence co-localization.

resultsHsa_circ_0000520 was characterized as a circular RNA and was lowly expressed in bladder cancer compared with the paracancer. Bladder cancer patients with high expression of hsa_circ_0000520 had better survival prognosis. Functionally, hsa_circ_0000520 inhibited bladder cancer invasion, migration, and VM formation. Mechanistically, hsa_circ_0000520 acted as a scaffold to promote binding of UBE2V1/UBC13 to Lin28a, further promoting the ubiquitous degradation of Lin28a, improving PTEN mRNA stability, and inhibiting the phosphorylation of the PI3K/AKT pathway. The formation of hsa_circ_0000520 in bladder cancer was regulated by RNA binding protein QKI.

conclusionsHsa_circ_0000520 inhibits metastasis and VM formation in bladder cancer and is a potential target for bladder cancer diagnosis and treatment.

Indexed as

Cell MovementPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseRNA-Binding ProteinsRNA, CircularSignal TransductionUrinary Bladder NeoplasmsAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMice, NudeLin28A protein, humanPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePTEN protein, humanRNA-Binding ProteinsRNA, CircularBladder cancerHsa_circ_0000520MetastasisPI3K/AKT pathwayVasculogenic mimicry

Identifiers

PMID39237880
PMCPMC11378395

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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.