Evidence map›Paper›PMID 27186290›Full record

ArticleAmerican journal of translational research2016

Galectin-1 mediates TGF-β-induced transformation from normal fibroblasts into carcinoma-associated fibroblasts and promotes tumor progression in gastric cancer.

Lingyan Zheng, Cong Xu, Zhonghai Guan, Xingyun Su, Zhenzhen Xu, Jiang Cao, Lisong Teng

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  17. Galectins as Molecular Targets for Therapeutic Intervention.International journal of molecular sciences · 2018
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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

7 authors at 1 institution in 1 country.

Lingyan ZhengDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
Cong XuDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
Zhonghai GuanDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
Xingyun SuDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
Zhenzhen XuDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
Jiang CaoClinical Research Center, The Second Affiliated Hospital of Zhejiang University School of Medicine Hangzhou, Zhejiang, China.
Lisong TengDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rcinoma-associated fibroblasts (CAFs) are a major constituent of the tumor microenvironment. Cancer cells can induce the transformation from normal fibroblasts (NFs) into CAFs, reciprocally, CAFs promote tumor invasion and proliferation. TGF-β has been the mostly accepted factor to fuel NFs transformation into CAFs. Galectin-1 (Gal1) is highly upregulated in CAFs of multiple human cancers, and overexpression of Gal1 in CAFs promotes tumor progression. The effect of Gal1 on TGF-β-induced CAFs activation has not yet been established in gastric cancer (GC). In this study, we show that Gal1 expression in stroma is positively related to TGF-β in epithelial cells by retrospective analysis of GC patient samples. Meanwhile, conditioned media (CMs) from gastric cancer cells induce expression of both Gal1 and the CAFs marker alpha smooth muscle actin (α-SMA) in NFs via TGF-β secretion. Knockdown of Gal1 prevents TGF-β-induced the conversion of NFs to CAFs. CMs from fibroblasts overexpressing Gal1 inhibits cancer cells apoptosis, promotes migration and invasion in vitro. Thus, Gal1 is significantly involved in the development of tumor-promoting microenvironment by enhancing TGF-β signaling in a positive feedback loop. Targeting Gal1 in tumor stroma should be considered as a potential therapeutic target for GC.

Indexed as

carcinoma-associated fibroblastgalectin-1normal fibroblastStric cancerTGF-βtransformation

Identifiers

PMID27186290
PMCPMC4859895
OpenAlexW2398317880

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.