Evidence map›Paper›PMID 25940797›Full record

ArticleOncotarget2015

Thyroid hormone-mediated regulation of lipocalin 2 through the Met/FAK pathway in liver cancer.

I-Hsiao Chung, Cheng-Yi Chen, Yang-Hsiang Lin, Hsiang-Cheng Chi, Ya-Hui Huang, Pei-Ju Tai, Chia-Jung Liao, Chung-Ying Tsai, Syuan-Ling Lin, Meng-Han Wu and 2 more

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 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 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

12 authors at 2 institutions in 1 country.

I-Hsiao ChungDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Cheng-Yi ChenDepartment of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan.
Yang-Hsiang LinDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Hsiang-Cheng ChiDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Ya-Hui HuangLiver Research Center, Department of Hepato-Gastroenterology, Chang-Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
Pei-Ju TaiDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Chia-Jung LiaoDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Chung-Ying TsaiDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Syuan-Ling LinDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Meng-Han WuDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Ching-Ying ChenDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Kwang-Huei LinDepartment of Biochemistry, School of Medicine, Chang-Gung University, Taoyuan, Taiwan.
Chang Gung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The thyroid hormone, 3,3',5-triiodo-L-thyronine (T3), regulates cell growth, development and differentiation via interactions with thyroid hormone receptors (TR), but the mechanisms underlying T3-mediated modulation of cancer progression are currently unclear. Lipocalin 2 (LCN2), a tumor-associated protein, is overexpressed in a variety of cancer types. Oligonucleotide microarray, coupled with proteomic analysis, has revealed that LCN2 is positively regulated by T3/TR. However, the physiological role and pathway of T3-mediated regulation of LCN2 in hepatocellular carcinogenesis remain to be characterized. Upregulation of LCN2 after T3 stimulation was observed in a time- and dose-dependent manner. Additionally, TRE on the LCN2 promoter was identified at positions -1444/-1427. Overexpression of LCN2 enhanced tumor cell migration and invasion, and conversely, its knockdown suppressed migration and invasion, both in vitro and in vivo. LCN2-induced migration occurred through activation of the Met/FAK cascade. LCN2 was overexpressed in clinical hepatocellular carcinoma (HCC) patients, compared with normal subjects, and positively correlated with TRα levels. Both TRα and LCN2 showed similar expression patterns in relation to survival rate, tumor grade, tumor stage and vascular invasion. Our findings collectively support a potential role of T3/TR in cancer progression through regulation of LCN2 via the Met/FAK cascade. LCN2 may thus be effectively utilized as a novel marker and therapeutic target in HCC.

Indexed as

Acute-Phase ProteinsAnimalsBlotting, WesternCell Line, TumorCell MovementFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticHep G2 CellsHumansLipocalin-2LipocalinsLiver NeoplasmsMice, SCIDNeoplasm InvasivenessProto-Oncogene ProteinsProto-Oncogene Proteins c-metAcute-Phase ProteinsFocal Adhesion Kinase 1LCN2 protein, humanLipocalin-2LipocalinsMET protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-metPTK2 protein, humanReceptors, Thyroid HormoneThyroid HormonesTriiodothyronineLCN2Met/FAK cascadethyroid hormone receptor

Identifiers

PMID25940797
PMCPMC4558135
OpenAlexW2108316991

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.