Evidence map›Paper›PMID 25605013›Full record

ArticleOncotarget2015

Galectin-1 is overexpressed in CD133+ human lung adenocarcinoma cells and promotes their growth and invasiveness.

Xuefeng Zhou, Dan Li, Xianguo Wang, Bo Zhang, Hua Zhu, Jinping Zhao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
2.5field-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, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Identification of novel therapeutic target genes in acquired lapatinib-resistant breast cancer by integrative meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Pooled it
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  14. The emerging role of galectins in high-fatality cancers.Cellular and molecular life sciences : CMLS · 2018
    Review
  15. Role of galectins in lung cancer.Oncology letters · 2017
    Article
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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

6 authors at 3 institutions in 2 countries.

Xuefeng ZhouDepartment of Thoracic and Cardiovascular Surgery, Zhongnan Hospital, Wuhan University, Wuhan, China.
Dan LiDepartment of Thoracic and Cardiovascular Surgery, Zhongnan Hospital, Wuhan University, Wuhan, China.
Xianguo WangDepartment of Thoracic and Cardiovascular Surgery, Zhongnan Hospital, Wuhan University, Wuhan, China.
Bo ZhangDepartment of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Hua ZhuDepartment of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Jinping ZhaoDepartment of Thoracic and Cardiovascular Surgery, Zhongnan Hospital, Wuhan University, Wuhan, China.
The Ohio State University Wexner Medical Center · USWuhan University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies demonstrated that a subpopulation of cancer cells, which are CD133 positive (CD133+) feature higher invasive and metastatic abilities, are called cancer stem cells (CSCs). By using tumor cells derived from patients with lung adenocarcinoma, we found that galectin-1 is highly overexpressed in the CD133+ cancer cells as compared to the normal cancer cells (CD133-) from the same patients. We overexpressed galectin-1 in CD133- cancer cells and downregulated it in CSCs. We found that overexpression of galectin-1 promoted invasiveness of CD133- cells, while knockdown of galectin-1 suppressed proliferation, colony formation and invasiveness of CSCs. Furthermore, tumor growth was significantly inhibited in CSCs xenografts with knockdown of galectin-1 as compared to CSCs treated with scramble siRNAs. Biochemical studies revealed that galectin-1 knockdown led to the suppression of COX-2/PGE2 and AKT/mTOR pathways, indicating galectin-1 might control the phenotypes of CSCs by regulating these signaling pathways. Finally, a retrospective study revealed that galectin-1 levels in blood circulation negatively correlates with overall survival and positively correlates with lymph node metastasis of the patients. Taken together, these findings suggested that galectin-1 plays a major role on the tumorigenesis and invasiveness of CD133+ cancer cells and might serve as a potential therapeutic target for treatment of human patients with lung adenocarcinoma.

Indexed as

Cell MovementCell ProliferationAC133 AntigenAdenocarcinomaAdenocarcinoma of LungAdultAgedAnimalsAntigens, CDBiomarkers, TumorFemaleGalectin 1Gene Knockdown TechniquesGlycoproteinsHumansLung NeoplasmsAC133 AntigenAntigens, CDBiomarkers, TumorGalectin 1GlycoproteinsPeptidesPROM1 protein, humanProm1 protein, mouse

Identifiers

PMID25605013
PMCPMC4413641
OpenAlexW1500351868

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.