Evidence map›Paper›PMID 34923985›Full record

ArticleCancer cell international2021

Cervical cancer-derived exosomal miR-663b promotes angiogenesis by inhibiting vinculin expression in vascular endothelial cells.

Xuewu You, Wenxiong Sun, Ying Wang, Xiaoli Liu, Aihong Wang, Lu Liu, Sai Han, Yu Sun, Junhua Zhang, Lingyu Guo and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 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

11 authors at 3 institutions in 1 country.

Xuewu YouDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Wenxiong SunDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Ying WangDepartment of Obstetrics and Gynecology, Yidu Central Hospital of Weifang, Weifang, 262500, Shandong, People's Republic of China.
Xiaoli LiuDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Aihong WangDepartment of Obstetrics and Gynecology, Feicheng Hospital Affiliated to Shandong First Medical University, Taian, 271600, Shandong, People's Republic of China.
Lu LiuDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Sai HanDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Yu SunDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Junhua ZhangDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Lingyu GuoDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.
Youzhong ZhangDepartment of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China. zhangyouzhong@sdu.edu.cn.ORCID http://orcid.org/0000-0002-6132-141X
Shandong University · CNShandong First Medical University · CNYidu Central Hospital of Weifang · CN

Funding

the Health Commission of Weifang wfwsjs-2018053the Key research project of shandong provence 2017CXGC1210
6 · The paper itself

Abstract

backgroundAngiogenesis provides essential nutrients and oxygen for tumor growth and has become the main mechanism of tumor invasion and metastasis. Exosomes are nanoscale membrane vesicles containing proteins, lipids, mRNA and microRNA (miRNA), which mediate intercellular communication and play an important role in tumor progression. Accumulated evidence indicates that tumor-derived exosomal miRNAs participate in the tumor microenvironment and promote angiogenesis.

methodsBioinformatic target prediction and dual luciferase reporter assays were performed to identify the binding site between miR-663b and the 3'-UTR of vinculin (VCL). VCL overexpression lentivirus and miR-663b overexpression/inhibition lentivirus were used to create a VCL overexpression model and miR-663b overexpression/inhibition model in-vitro. Immunohistochemistry (IHC) assays and western blot assays were used to detect protein expression. Exosome-cell cocultures, wound healing assays, tube formation assays and transwell assays were used to measure the migration and tube formation ability of vascular endothelial cells [human umbilical vein endothelial cells (HUVECs)]. siRNA targeted VCL was used to knockdown VCL.

resultsIn the present study, we found that miR-663b was elevated in cervical cancer tissue and exosomes. miR-663b could bind the 3'-UTR of VCL and inhibit its expression. VCL is downregulated in cervical cancer, and decreased VCL has a negative correlation with a high level of miR-663b. Further studies demonstrated that exosomes secreted by cervical cancer cells can deliver miR-663b to HUVECs and inhibit the expression of VCL, thereby promoting angiogenesis and tumor growth.

conclusionsmiR-663b derived from cancer cell exosomes acts as a driving factor for angiogenesis and a potential target of antiangiogenic therapy in cervical cancer. Our findings illustrated a new signaling pathway, including exosomes, miRNAs and target genes, which provides potential targets for antiangiogenic therapy.

Identifiers

PMID34923985
PMCPMC8684657
OpenAlexW4200223105

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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.