Evidence map›Paper›PMID 27013588›Full record

ArticleOncotarget2016

Sciellin mediates mesenchymal-to-epithelial transition in colorectal cancer hepatic metastasis.

Chuan-Kai Chou, Chi-Chen Fan, Pei-Shan Lin, Pei-Yu Liao, Jia-Chen Tung, Chang-Hsun Hsieh, Mien-Chie Hung, Chung-Hsuan Chen, Wei-Chao Chang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 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

9 authors at 6 institutions in 2 countries.

Chuan-Kai ChouNational Applied Research Laboratories, National Laboratory Animal Center, Taipei, Taiwan.
Chi-Chen FanSuperintendent Office, Mackay Memorial Hospital, Taipei, Taiwan.
Pei-Shan LinCenter for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan.
Pei-Yu LiaoNational Applied Research Laboratories, National Laboratory Animal Center, Taipei, Taiwan.
Jia-Chen TungGraduate Institute of Cancer Biology, China Medical University, Taichung, Taiwan.
Chang-Hsun HsiehDepartment of Orthopaedic Surgery, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan.
Mien-Chie HungCenter for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan.
Chung-Hsuan ChenGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Wei-Chao ChangCenter for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan.
China Medical University Hospital · TWNational Applied Research Laboratories · TWChina Medical University · TWGenomics Research Center, Academia Sinica · TWMackay Memorial Hospital · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic metastasis is the major cause of mortality in colorectal cancer (CRC) patients. Using proteomic analysis, we found sciellin (SCEL) to be specifically expressed in hepatic metastatic CRC cell lines. SCEL knockdown increased CRC cell migration and invasion, while overexpression had the opposite effect. SCEL knockdown also caused cancer cells to form more invasive structures within 3D cultures, increased the mesenchymal marker vimentin, and attenuated the epithelial marker E-cadherin. SCEL increased WNT signaling by activating β-catenin and its downstream target c-myc, and activated mesenchymal-to-epithelial transition (MET) through a SCEL-β-catenin-E-cadherin axis. SCEL showed higher expression in late stage primary CRC than in its hepatic metastatic counterpart. SCEL expression is dynamically modulated by TGF-β1 and hypoxia, revealing a plastic MET mechanism for tumor colonization. Intrahepatic injection in immunodeficient mice revealed that SCEL is necessary for metastatic CRC tumor growth in the liver. These results demonstrate that SCEL is a MET inducer dynamically regulated through the metastasis process. They suggest SCEL may be a useful therapeutic target for preventing or eliminating CRC hepatic metastasis.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCarrier ProteinsCell Line, TumorCell MovementCell TransdifferentiationColorectal NeoplasmsHeterograftsHumansLiver NeoplasmsMiceMice, Inbred BALB CMice, NudeNeoplasm MetastasisCarrier ProteinsSCEL protein, humancolorectal cancerhepatic metastasismesenchymal-to-epithelial transitionSCEL

Identifiers

PMID27013588
PMCPMC5041940
OpenAlexW2303355011

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.