Evidence map›Paper›PMID 26632346›Full record

ArticleCell adhesion & migration2015

Histone deacetylase inhibitor valproic acid (VPA) promotes the epithelial mesenchymal transition of colorectal cancer cells via up regulation of Snail.

Jutao Feng, Junhua Cen, Jun Li, Rujin Zhao, Canhua Zhu, Zongxin Wang, Jiafen Xie, Wei Tang

Open access · goldAbstract read
In one paragraph

Article in Cell adhesion & migration, 2015. 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
3.2field-weighted citation impact, top 8% 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, 47 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

8 authors at 3 institutions in 1 country.

Jutao Fenga Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Junhua Cena Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Jun Lia Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Rujin Zhaoa Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Canhua Zhua Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Zongxin Wanga Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Jiafen Xiea Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Wei Tanga Hepatobiliary Surgery Department ; The First Affiliated Hospital of Guangzhou Medical University ; Guangzhou , China.
Guangzhou Medical University · CNSecond Military Medical University · CNEastern Hepatobiliary Surgery Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACIs) have been shown to have antiproliferative activity through cell-cycle arrest, differentiation, and apoptosis in colorectal cancer (CRC) cells. Our present study revealed that one HDAC inhibitor, valproic acid (VPA), can obviously promote in vitro motility of HCT-116 and SW480 cells. VPA treatment significantly down regulates the expression of epithelial markers E-Cadherin (E-Cad) and Zona occludin-1(ZO-1) while up regulates the mesenchymal markers Vimentin (Vim) and N-cadherin (N-Cad), suggesting that VPA can trigger the epithelial-mesenchymal transition (EMT) of CRC cells. VPA treatment significantly increases the expression and nuclear localization of Snail, the key transcription factors of EMT. Snail knockdown by siRNAs obviously reverses VPA induced EMT of HCT-116 and SW480 cells. Further, VPA can decrease the ubiquitination, increase the acetylation, and then elevate the stabilization of Snail. VPA also increases the phosphorylation of Akt/GSK-3β. The inhibitor of PI3K/Akt, LY2994002, significantly attenuates VPA induced phosphorylation of Akt and GSK-3β and up regulation of Snail and Vim. Collectively, our data reveal that VPA can trigger the EMT of CRC cells via up regulation of Snail through AKT/GSK-3β signals and post-transcriptional modification. It suggests that more attention should be paid when VPA used as a new anticancer drug for CRC patients.

Indexed as

Cell MovementColorectal NeoplasmsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHCT116 CellsHistone Deacetylase InhibitorsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSnail Family Transcription FactorsTranscription FactorsValproic AcidGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanHistone Deacetylase InhibitorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSnail Family Transcription FactorsTranscription FactorsValproic AcidAkt/GSK-3βcolorectal cancerEMTSnailVPA

Identifiers

PMID26632346
PMCPMC4955961
OpenAlexW2181788738

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.