Evidence map›Paper›PMID 26379394›Full record

ArticleWorld journal of gastroenterology2015

Dexamethasone inhibits hypoxia-induced epithelial-mesenchymal transition in colon cancer.

Jung Ho Kim, You-Jin Hwang, Sang Hoon Han, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Se-Hee Kim

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 14% 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, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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  19. Effects of initiating time and dosage ofWorld journal of gastroenterology · 2017
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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

10 authors at 1 institution in 1 country.

Jung Ho KimJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
You-Jin HwangJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Sang Hoon HanJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Young Eun LeeJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Saerom KimJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Yoon Jae KimJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Jae Hee ChoJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Kwang An KwonJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Ju Hyun KimJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Se-Hee KimJung Ho Kim, Young Eun Lee, Saerom Kim, Yoon Jae Kim, Jae Hee Cho, Kwang An Kwon, Ju Hyun Kim, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 405-760, South Korea.
Jeju National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo elucidate the effects of dexamethasone on hypoxia-induced epithelial-to-mesenchymal transition (EMT) in colon cancer.

methodsHuman colon cancer HCT116 and HT29 cells were exposed to normoxic (21%) and hypoxic (1%) conditions. First, the effect of dexamethasone on cell viability was examined by MTT cell proliferation assay. In order to measure the expression levels of EMT markers (Snail, Slug, Twist, E-cadherin, and integrin αVβ6) and hypoxia-related genes [Hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF)] by dexamethasone, quantitative real-time polymerase chain reaction and western blot analysis were performed. Furthermore, the morphological changes of colon cancer cells and the expression pattern of E-cadherin by dexamethasone were detected through immunocytochemistry. Finally, the effects of dexamethasone on the invasiveness and migration of colon cancer cells were elucidated using matrigel invasion, migration, and wound healing migration assays.

resultsUnder hypoxia, dexamethasone treatment inhibited HIF-1α protein level and its downstream gene, VEGF mRNA level in the colon cancer cell lines, HCT116 and HT29. In addition, the presence of dexamethasone down-regulated the mRNA levels of hypoxia-induced Snail, Slug, and Twist, all transcriptional factors of EMT, as well as hypoxia-induced integrin αVβ6 protein level, a well-known EMT marker for colon cancer cells. Furthermore, reduced E-cadherin in hypoxic condition was found to be recoverable by treating with dexamethasone in both colon cancer cell lines. Similarly, under hypoxic conditions, dexamethasone restored the growth pattern and morphological phenotype reminiscent of colon cancer cells grown under normoxic conditions; dexamethasone blocked the migration and invasion of both colorectal cancer cell lines in hypoxia.

conclusionOur study suggested that dexamethasone has inhibitory effects on cell migration and invasion by suppressing EMT of colon cancer cell lines in hypoxic condition.

Indexed as

Tumor MicroenvironmentAntigens, CDAntineoplastic AgentsCadherinsCell HypoxiaCell MovementCell ProliferationCell ShapeCell SurvivalColonic NeoplasmsDexamethasoneDose-Response Relationship, DrugEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsAntigens, CDAntineoplastic AgentsCadherinsCDH1 protein, humanDexamethasoneHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor AVEGFA protein, humanColon cancerDexamethasoneEpithelial-mesenchymal transitionHypoxiaHypoxia-inducible factor-1α

Identifiers

PMID26379394
PMCPMC4566382
OpenAlexW2395337368

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.