Evidence map›Paper›PMID 30488243›Full record

ArticleInvestigational new drugs2019

A mediator of phosphorylated Smad2/3, evodiamine, in the reversion of TAF-induced EMT in normal colonic epithelial cells.

Wanbin Yang, Xiuli Gong, Xiulian Wang, Chao Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Investigational new drugs, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The Role of Zuo Jin Wan in Modulating the Tumor Microenvironment of Colorectal Cancer.Combinatorial chemistry & high throughput screening · 2025
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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

4 authors at 3 institutions in 1 country.

Wanbin YangInstitute of Tropical Diseases, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People's Republic of China.
Xiuli GongDepartment of Spleen and Stomach Diseases, Second Hospital of Traditional Chinese Medicine of Guangdong, Guangzhou, Guangdong, 510000, People's Republic of China.
Xiulian WangDepartment of Traditional Chinese Medicine, Affiliated Bao'an Hospital of Traditional Chinese Medicine of Shenzhen, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, 518000, People's Republic of China.
Chao HuangCentral Laboratory, Affiliated Bao'an Hospital of Shenzhen, Southern Medical University, Shenzhen, Guangdong, 518000, People's Republic of China. huangchao06@163.com.ORCID 0000-0003-3371-6462
Guangzhou University of Chinese Medicine · CNGuangdong Provincial Hospital of Traditional Chinese Medicine · CNSouthern Medical University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose Transdifferentiation exists within stromal cells in the tumour microenvironment. Transforming growth factor-β (TGF-β) secreted by tumour-associated fibroblasts (TAFs) affects the differentiation states of epithelial cells, including epithelial-mesenchymal transition (EMT). Evodiamine, a natural drug, can regulate differentiation. However, the specific effects and relative mechanisms of evodiamine remain unknown. Design We used four models to observe the influence of TAF-like CCD-18Co cells on the colon epithelial cell line HCoEpiC: the 3D- and 2D-mono-culture system, Transwell and direct co-culture model. Additionally, we established conditioned medium from CCD-18Co cells. The TGF-β pathway inhibitor LY364947 and evodiamine were added. Morphological changes and classical EMT markers were observed and detected using phase contrast microscopy and immunofluorescence. Cell migration was measured by the wound-healing assay. Western blotting was performed to detect the TGF-β/Smad signalling pathway. Results CCD-18Co cells induced EMT-like changes in the 2D- and 3D-cultured epithelial cell line HCoEpiC, accompanied by high expression of ZEB1 and Snail and the enhancement of migration. Moreover, CCD-18Co-derived conditioned medium caused dysfunction of TGF-β/Smad signalling in EMT. Evodiamine inhibited these EMT-like HCoEpiC and their migration. Additionally, evodiamine down-regulated the expression of ZEB1/Snail and up-regulated the expression of phosphorylated Smad2/3 (pSmad2/3). Evodiamine also increased the ratios of pSmad2/Smad2 and pSmad3/Smad3. Conclusion Based on our observations, evodiamine can reverse the TAF-induced EMT-like phenotype in colon epithelial cells, which may be associated with its mediation of phosphorylated Smad2 and Smad3 expression.

Indexed as

ApoptosisCancer-Associated FibroblastsCell MovementCell ProliferationColonEpithelial CellsEpithelial-Mesenchymal TransitionHumansPhosphorylationQuinazolinesSignal TransductionSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaTumor Cells, CulturedevodiamineQuinazolinesSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor betaEpithelial-mesenchymal transitionEvodiamineTransdifferentiationTransforming growth factor-βTumour-associated fibroblastsTumour microenvironment

Identifiers

PMID30488243
OpenAlexW2903496054

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.