Evidence map›Paper›PMID 37000262›Full record

ArticleJournal of cancer research and clinical oncology2023

YAP inhibitor verteporfin suppresses tumor angiogenesis and overcomes chemoresistance in esophageal squamous cell carcinoma.

Xue-Wei Wang, Rong Zhao, Zi-Yi Yang, Ting Li, Jia-Cheng Yang, Xiu-Li Wang, Xin-Ting Li, Xin-Ran Zhao, Xiao-Zhong Li, Xiao-Xia Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Targeting the YAP/TAZ mechanotransducers in solid tumour therapeutics.Journal of cellular and molecular medicine · 2023
    Article
  8. Review
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

10 authors at 1 institution in 1 country.

Xue-Wei WangDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Rong ZhaoDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Zi-Yi YangDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Ting LiDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Jia-Cheng YangDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Xiu-Li WangDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Xin-Ting LiDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Xin-Ran ZhaoDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China.
Xiao-Zhong LiDepartment of Infectious Diseases, Shanxi Provincial People's Hospital, Taiyuan, China.
Xiao-Xia WangDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China. wxiaoxia99007@126.com.
Shanxi Medical University · CN

Funding

National Natural Science Foundation of China 82272911Natural Science Foundation of Shanxi Province 202103021224385
6 · The paper itself

Abstract

purposeTargeting angiogenesis is an attractive strategy for the effective treatment of cancer. This study aimed to investigate the anti-cancer activities of YAP inhibitor verteporfin (VP) in esophageal squamous cell carcinoma (ESCC) cells through its inhibitory effect on tumor angiogenesis.

methodsCell proliferation, apoptosis, migration and invasion abilities were estimated by MTT, colony formation, DAPI staining, wound healing and transwell assays, respectively. Human umbilical vein endothelial cell (HUVEC) tube formation assay and chick embryo chorioallantoic membrane (CAM) model were used to observe angiogenesis in vitro and in vivo. The interactions between ESCC cells and HUVECs were assessed by cell chemotactic migration and adhesion assays. The expression levels of angiogenesis-related molecules were detected by Western blot.

resultsWe found that VP was potential to inhibit ESCC cell proliferation, migration, invasion and induce apoptosis in the dose-dependent fashion. VP also significantly suppressed proliferation, migration, and tube formation of HUVECs and promoted apoptosis of HUVECs, and reduced angiogenesis in CAM. Moreover, VP inhibited ESCC cell-induced angiogenesis in vitro by decreasing HUVEC chemotactic migration, adhesion and tube formation, and also reduced ESCC cell-induced neovascularization of the CAM in vivo. In addition, VP suppressed the expression of pro-angiogenic molecules such as VEGFA, MMP-2 and β-catenin in ESCC cells. Furtherly, VP increased the chemosensitivity of ESCC-resistant cells to paclitaxel (PTX). The combination of VP and PTX attenuated the resistant cell-mediated angiogenesis in vitro and in vivo.

conclusionThese results reveal for the first time that VP potently inhibits malignant progression and overcomes chemoresistance of ESCC cells via inhibition of tumor angiogenesis. It provides insight into a new strategy for the treatment of ESCC that VP could be a potential drug candidate for targeting tumor angiogenesis.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsCell Line, TumorCell MovementCell ProliferationChick EmbryoDrug Resistance, NeoplasmHumansNeovascularization, PathologicPaclitaxelVerteporfinPaclitaxelVerteporfinChemoresistanceEsophageal squamous cell carcinomaTumor angiogenesisVerteporfin

Identifiers

PMID37000262
PMCPMC11796746
OpenAlexW4362459119

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.