Evidence map›Paper›PMID 36434686›Full record

ArticleBiology direct2022

CXCL1 promotes colon cancer progression through activation of NF-κB/P300 signaling pathway.

Changhua Zhuo, Qiang Ruan, Xiangqian Zhao, Yangkun Shen, Ruirong Lin

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 67 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

5 authors at 3 institutions in 1 country.

Changhua ZhuoDepartment of Gastrointestinal Surgical Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, Fujian, 350014, People's Republic of China. czhuo12@outlook.com.
Qiang RuanFuzhou University, College of Chemistry, Fuzhou, 350108, People's Republic of China.
Xiangqian ZhaoFujian Normal University Qishan Campus, College of Life Science, Biomedical Research Center of South China, Fuzhou, 350117, People's Republic of China.
Yangkun ShenFujian Normal University Qishan Campus, College of Life Science, Biomedical Research Center of South China, Fuzhou, 350117, People's Republic of China. 1205370146@qq.com.
Ruirong LinDepartment of Gastrointestinal Surgical Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, Fujian, 350014, People's Republic of China.
Fujian Normal University · CNFuzhou University · CNFujian Medical University · CN

Funding

Medical Innovation Project of Fujian Province 2022CXA060the Joint for the innovation of Science and Technology of Fujian Province 2018Y9106the Natural Science Funds of Fujian Province 2019J01198
6 · The paper itself

Abstract

backgroundThe upregulated expression of CXCL1 has been validated in colorectal cancer patients. As a potential biotherapeutic target for colorectal cancer, the mechanism by which CXCL1 affects the development of colorectal cancer is not clear.

methodsExpression data of CXCL1 in colorectal cancer were obtained from the GEO database and verified using the GEPIA database and the TIMER 2.0 database. Knockout and overexpression of CXCL1 in colorectal cancer cells by CRISPR/Cas and "Sleeping Beauty" transposon-mediated gene editing techniques. Cell biological function was demonstrated by CCK-8, transwell chamber and Colony formation assay. RT-qPCR and Western Blot assays measured RNA and protein expression. Protein localization and expression were measured by immunohistochemistry and immunofluorescence.

resultsBioinformatics analysis showed significant overexpression of CXCL1 in the colorectal cancer tissues compared to normal human tissues, and identified CXCL1 as a potential therapeutic target for colorectal cancer. We demonstrate that CXCL1 promotes the proliferation and migration of colon cancer cells and has a facilitative effect on tumor angiogenesis. Furthermore, CXCL1 elevation promoted the migration of M2-tumor associated macrophages (TAMs) while disrupting the aggregation of CD4+ and CD8+ T cells at tumor sites. Mechanistic studies suggested that CXCL1 activates the NF-κB pathway. In the in vivo colon cancer transplantation tumor model, treatment with the P300 inhibitor C646 significantly inhibited the growth of CXCL1-overexpressing colon cancer.

conclusionCXCL1 promotes colon cancer development through activation of NF-κB/P300, and that CXCL1-based therapy is a potential novel strategy to prevent colon cancer development.

Indexed as

Colonic NeoplasmsColorectal NeoplasmsChemokine CXCL1HumansNF-kappa BSignal TransductionChemokine CXCL1CXCL1 protein, humanNF-kappa BC646Colon cancerCXCL1NF-κBP300

Identifiers

PMID36434686
PMCPMC9701058
OpenAlexW4310046092

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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.