Evidence map›Paper›PMID 29383839›Full record

ArticleJournal of cellular and molecular medicine2018

Interplay between Trx-1 and S100P promotes colorectal cancer cell epithelial-mesenchymal transition by up-regulating S100A4 through AKT activation.

Zhigui Zuo, Peili Zhang, Feiyan Lin, Wenjing Shang, Ruichun Bi, Fengying Lu, Jianbo Wu, Lei Jiang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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 1 institution in 1 country.

Zhigui ZuoDepartment of Colorectal Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Peili ZhangCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Feiyan LinCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenjing ShangCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Ruichun BiCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Fengying LuCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Jianbo WuCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Lei JiangCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0001-9588-2015
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported a novel positive feedback loop between thioredoxin-1 (Trx-1) and S100P, which promotes the invasion and metastasis of colorectal cancer (CRC). However, the underlying molecular mechanisms remain poorly understood. In this study, we examined the roles of Trx-1 and S100P in CRC epithelial-to-mesenchymal transition (EMT) and their underlying mechanisms. We observed that knockdown of Trx-1 or S100P in SW620 cells inhibited EMT, whereas overexpression of Trx-1 or S100P in SW480 cells promoted EMT. Importantly, S100A4 and the phosphorylation of AKT were identified as potential downstream targets of Trx-1 and S100P in CRC cells. Silencing S100A4 or inhibition of AKT phosphorylation eliminated S100P- or Trx-1-mediated CRC cell EMT, migration and invasion. Moreover, inhibition of AKT activity reversed S100P- or Trx-1-induced S100A4 expression. The expression of S100A4 was higher in human CRC tissues compared with their normal counterpart tissues and was significantly correlated with lymph node metastasis and poor survival. The overexpression of S100A4 protein was also positively correlated with S100P or Trx-1 protein overexpression in our cohort of CRC tissues. In addition, overexpression of S100P reversed the Trx-1 knockdown-induced inhibition of S100A4 expression, EMT and migration and invasion in SW620 cells. The data suggest that interplay between Trx-1 and S100P promoted CRC EMT as well as migration and invasion by up-regulating S100A4 through AKT activation, thus providing further potential therapeutic targets for suppressing the EMT in metastatic CRC.

Indexed as

Calcium-Binding ProteinsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionHumansNeoplasm InvasivenessNeoplasm ProteinsOncogene Protein v-aktPhosphorylationProto-Oncogene Proteins c-aktS100 Calcium-Binding Protein A4ThioredoxinsCalcium-Binding ProteinsNeoplasm ProteinsOncogene Protein v-aktProto-Oncogene Proteins c-aktS100A4 protein, humanS100 Calcium-Binding Protein A4S100P protein, humanThioredoxinsTXN protein, humancolorectal cancerepithelial-mesenchymal transitionS100A4S100Pthioredoxin-1

Identifiers

PMID29383839
PMCPMC5867135
OpenAlexW2794035430

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.