Evidence map›Paper›PMID 28259923›Full record

ArticleOncology reports2017

Pleomorphic adenoma gene like-2 induces epithelial-mesenchymal transition via Wnt/β-catenin signaling pathway in human colorectal adenocarcinoma.

Yong-Peng Wang, Peng-Tao Guo, Zhi Zhu, Hao Zhang, Yan Xu, Yu-Ze Chen, Fang Liu, Si-Ping Ma

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  8. METTL14 Regulates PLAGL2/Journal of oncology · 2023
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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 1 institution in 1 country.

Yong-Peng WangDepartment of Colorectal Surgery, Cancer Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Peng-Tao GuoDepartment of Surgical Oncology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Zhi ZhuDepartment of Surgical Oncology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Hao ZhangDepartment of Colorectal Surgery, Cancer Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Yan XuDepartment of Surgical Oncology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Yu-Ze ChenDepartment of Colorectal Surgery, Cancer Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Fang LiuDepartment of Colorectal Surgery, Cancer Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
Si-Ping MaDepartment of Colorectal Surgery, Cancer Hospital of China Medical University, Shenyang, Liaoning, P.R. China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a critical step in the acquisition of metastatic and invasive power for tumor cells. Colorectal adenocarcinoma (CRC) is a common cancer where metastasis is directly linked to patient survival. Recent studies show that pleomorphic adenoma gene like-2 (PLAGL2) could induce tumor EMT and is an independent predictive factor associated with poor prognosis in cancer. In the present study, we confirmed the role of PLAGL2 in the prognosis of CRC patients and provide molecular evidence of PLAGL2 promoted EMT in CRC cell line SW480. We found that PLAGL2 expression was upregulated in the paraffin-embedded CRC tissues compared to borderline or benign tissues. Experimental EMT induced by PLAGL2 plasmid transfection proved PLAGL2 protein overexpression could enhance the cell scratch wound-healing and transwell ability and significantly upregulated mesenchymal marker proteins, N-cadherin and vimentin and concurrently downregulated epithelial marker of E-cadherin. Subsequently, through western blot assay, we found that PLAGL2 could activate the wnt-signaling component β-catenin in the nuclei. More CRC cell metastasis to the lungs was observed when the PLAGL2 overexpressing SW480 cells were injected into the tail vein of rats, compared with the cell control and PLAGL2 silence group. Our findings indicated that PLAGL2 might be a very upstream key molecule regulating EMT involved in Wnt/β‑catenin signaling pathway.

Indexed as

AdenocarcinomaAgedAged, 80 and overAnimalsbeta CateninCell Line, TumorCell MovementColorectal NeoplasmsDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm Metastasisbeta CateninDNA-Binding ProteinsPLAGL2 protein, humanRNA-Binding ProteinsTranscription FactorsVimentin

Identifiers

PMID28259923
PMCPMC5367359
OpenAlexW2591653114

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.