Evidence map›Paper›PMID 33154652›Full record

ArticleOncoTargets and therapy2020

Therapeutic Potential of Apatinib Against Colorectal Cancer by Inhibiting VEGFR2-Mediated Angiogenesis and β-Catenin Signaling.

Xiaomin Cai, Bin Wei, Lele Li, Xiaofeng Chen, Jing Yang, Xiaofei Li, Xiaozheng Jiang, Mu Lv, Mingyang Li, Yumeng Lin and 3 more

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 13 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

13 authors at 3 institutions in 1 country.

Xiaomin Cai *Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Bin Wei *Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Lele Li *Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Xiaofeng ChenDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.ORCID 0000-0001-6137-5234
Jing YangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Xiaofei LiDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Xiaozheng JiangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Mu LvDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Mingyang LiDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Yumeng LinState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, People's Republic of China.
Qiang XuState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, People's Republic of China.
Wenjie GuoState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, People's Republic of China.ORCID 0000-0001-8506-3905
Yanhong GuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Jiangsu Province Hospital · CNNanjing University · CNHuaian First People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeApatinib is an inhibitor of VEGFR2 (vascular endothelial growth factor receptor 2) that has attracted a great deal of attention due to its promotion of anticancer activity. In the present study, we investigated the therapeutic effects of apatinib against colorectal cancer (CRC) and examined the underlying mechanism. MATERIALS AND

methodsBoth in vivo and in vitro assays were conducted to study the effect of apatinib on CRC. To elucidate the associated mechanism, RNA-seq (transcriptome) analysis was conducted on apatinib-treated HCT116 cells.

resultsApatinib showed antiproliferative and proapoptotic effects, induced G0/G1 arrest and blocked cell migration and invasion in CRC. An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3β levels, which further increased β-catenin ubiquitination and reduced the nuclear translocation of β-catenin. Furthermore, apatinib strongly suppressed CT26 cell growth in mouse xenograft models by inhibiting β-catenin signaling and angiogenesis.

conclusionOverall, the results of the present study here indicated that by inhibiting the VEGFR2-β-catenin-mediated malignant phenotype, apatinib significantly suppresses the growth of CRC, suggesting that the use of apatinib is a promising therapeutic strategy for CRC.

Indexed as

angiogenesisapatinibcolorectal cancerVEGFR2β-catenin

Identifiers

PMID33154652
PMCPMC7606303
OpenAlexW3095316681

What OpenQuestion holds

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LicenceCC BY-NC
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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.