Evidence map›Paper›PMID 29872080›Full record

ArticleScientific reports2018

Alcohol consumption promotes colorectal carcinoma metastasis via a CCL5-induced and AMPK-pathway-mediated activation of autophagy.

Haodong Zhao, Danlei Chen, Rui Cao, Shiqing Wang, Dandan Yu, Yakun Liu, Yu Jiang, Mei Xu, Jia Luo, Siying Wang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Haodong ZhaoDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Danlei ChenDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Rui CaoDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Shiqing WangDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Dandan YuDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Yakun LiuDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Yu JiangDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China.
Mei XuDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, Kentucky, 40536, USA.
Jia LuoDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, Kentucky, 40536, USA. jialuo888@uky.edu.ORCID 0000-0002-6968-3618
Siying WangDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China. sywang@ahmu.edu.cn.
Anhui Medical University · CNUniversity of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a definite relationship between alcohol consumption and colorectal cancer (CRC) development. We investigated effect of alcohol consumption on CRC patients' progression and prognosis by utilizing epidemiological data and found patients with alcohol consumption increased risks of tumor-node-metastasis (TNM), organ metastasis and poorer prognosis. Because their tumor tissues displayed increased expression of C-C chemokine ligand 5 (CCL5), we hypothesized CCL5 might participate in cancer progression in such patients. Ethanol increased the secretion of CCL5 in two CRC cell lines, HT29 and DLD-1. Treatment with CCL5 directly increased migratory ability of these cells, whereas neutralization or knockdown of CCL5 can partially block alcohol-stimulated migration. We further investigated underlying mechanism of CCL5-induced migration. Our results indicated that effects of CCL5 on migration are mediated by the ability of CCL5 to induce autophagy, a cellular process known to be critical for migration. Using high-throughput sequencing and western blotting, we found induction of autophagy by CCL5 takes place via AMPK pathway. Aforementioned ethanol increases CCL5 secretion, CCL5 activates autophagy through AMPK pathway, and autophagy increases migration was confirmed by experiments with autophagy or AMPK inhibitors. To sum up, our study demonstrates that chronic alcohol consumption may promote metastasis of CRC through CCL5-induced autophagy.

Indexed as

AutophagyAlcohol DrinkingAMP-Activated Protein KinasesBlotting, WesternCell Line, TumorCell MovementChemokine CCL5Colorectal NeoplasmsEthanolGene Expression ProfilingHigh-Throughput Nucleotide SequencingHumansNeoplasm MetastasisAMP-Activated Protein KinasesCCL5 protein, humanChemokine CCL5Ethanol

Identifiers

PMID29872080
PMCPMC5988731
OpenAlexW2806172426

What OpenQuestion holds

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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.