Evidence map›Paper›PMID 32606981›Full record

ArticleCancer management and research2020

Anlotinib Suppresses Colorectal Cancer Proliferation and Angiogenesis via Inhibition of AKT/ERK Signaling Cascade.

Qian Yang, Laichao Ni, Saber Imani, Zhangqiang Xiang, Rui Hai, Ruilin Ding, Shaozhi Fu, Jing Bo Wu, Qinglian Wen

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 48 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

9 authors at 1 institution in 1 country.

Qian Yang *Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Laichao Ni *Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.ORCID 0000-0002-5260-8291
Saber Imani *Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Zhangqiang XiangDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Rui HaiDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Ruilin DingDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Shaozhi FuDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.ORCID 0000-0002-8666-4304
Jing Bo WuDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Qinglian WenDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Affiliated Hospital of Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnlotinib is a highly potent multi-target tyrosine kinase inhibitor, with very good anti-tumor activity against a variety of solid tumors. However, its effect on colorectal cancer (CRC) is not yet clearly understood. The objective of this study was to investigate the anti-tumor effect and underlying mechanism of anlotinib in the pathogenesis of CRC. MATERIALS AND

methodsEffects of anlotinib on CT26 cells proliferation and microvessel formation in endothelial cells were determined by MTT assay and tube formation assay. Cell migration and invasion were analyzed by using the wound healing assay and transwell assay. Cell cycle and apoptosis were detected by flow cytometry. A CRC xenograft mouse model was used for conducting in-vivo studies to verify the effect of anlotinib. The expression of Ki-67 and CD31 in the tumor tissue was detected by immunohistochemistry and protein expression was measured by Western blot.

resultsIn-vitro studies revealed that anlotinib inhibited the proliferation, migration, and invasion of CT26 cells and the tube formation of HUVECs in a dose-dependent manner. Anlotinib also significantly induced cell apoptosis and G2/M arrest. It effectively inhibited tumor growth and prolonged survival time in the CRC xenograft mouse model. Immunohistochemical analysis of the tumor tissue revealed that anlotinib downregulated CD31 and Ki-67 which are the biomarkers of microvessel density and proliferation. Furthermore, anlotinib was able to inhibit the activation of VEGFR-2/AKT and FGFR, PDGFRβ and their downstream signaling ERK.

conclusionThe findings of the present study suggested that anlotinib suppressed cell proliferation and angiogenesis via inhibition of AKT/ERK signaling pathway in colorectal cancer and could be a novel therapeutic strategy for treatment of CRC.

Indexed as

angiogenesisanlotinibcolorectal cancerproliferationtyrosine kinase inhibitor

Identifiers

PMID32606981
PMCPMC7321688
OpenAlexW3035871032

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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.