Evidence map›Paper›PMID 23624915›Full record

ArticleOncogene2014

LRIG1 modulates aggressiveness of head and neck cancers by regulating EGFR-MAPK-SPHK1 signaling and extracellular matrix remodeling.

J J-C Sheu, C-C Lee, C-H Hua, C-I Li, M-T Lai, S-C Lee, J Cheng, C-M Chen, C Chan, S C-C Chao and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-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

40 citing papers in PubMed, 116 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

13 authors at 5 institutions in 1 country.

J J-C Sheu1] Human Genetic Center, China Medical University Hospital, Taichung, Taiwan [2] School of Chinese Medicine, China Medical University, Taichung, Taiwan [3] Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
C-C LeeNational Institute of Cancer Research, National Health Research Institutes, Zhunan Town, Taiwan.
C-H HuaDepartment of Otolaryngology, China Medical University Hospital, Taichung, Taiwan.
C-I LiNational Institute of Cancer Research, National Health Research Institutes, Zhunan Town, Taiwan.
M-T Lai1] Department of Pathology, Chung Shan Medical University Hospital, Taichung, Taiwan [2] School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
S-C LeeCollege of Medical Science and Technology, Chung Shan Medical University, Taichung, Taiwan.
J ChengHuman Genetic Center, China Medical University Hospital, Taichung, Taiwan.
C-M ChenHuman Genetic Center, China Medical University Hospital, Taichung, Taiwan.
C ChanHuman Genetic Center, China Medical University Hospital, Taichung, Taiwan.
S C-C ChaoHuman Genetic Center, China Medical University Hospital, Taichung, Taiwan.
J-Y ChenNational Institute of Cancer Research, National Health Research Institutes, Zhunan Town, Taiwan.
J-Y ChangNational Institute of Cancer Research, National Health Research Institutes, Zhunan Town, Taiwan.
C-H LeeNational Institute of Cancer Research, National Health Research Institutes, Zhunan Town, Taiwan.
National Health Research Institutes · TWChina Medical University · TWChina Medical University Hospital · TWChung Shan Medical University · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EGFR overexpression and chromosome 3p deletion are two frequent events in head and neck cancers. We previously mapped the smallest region of recurrent copy-number loss at 3p12.2-p14.1. LRIG1, a negative regulator of EGFR, was found at 3p14, and its copy-number loss correlated with poor clinical outcome. Inducible expression of LRIG1 in head and neck cancer TW01 cells, a line with low LRIG1 levels, suppressed cell proliferation in vitro and tumor growth in vivo. Gene expression profiling, quantitative RT-PCR, chromatin immunoprecipitation, and western blot analysis demonstrated that LRIG1 modulated extracellular matrix (ECM) remodeling and EGFR-MAPK-SPHK1 transduction pathway by suppressing expression of EGFR ligands/activators, MMPs and SPHK1. In addition, LRIG1 induction triggered cell morphology changes and integrin inactivation, which coupled with reduced SNAI2 expression. By contrast, knockdown of endogenous LRIG1 in TW06 cells, a line with normal LRIG1 levels, significantly enhanced cell proliferation, migration and invasiveness. Such tumor-promoting effects could be abolished by specific MAPK or SPHK1 inhibitors. Our data suggest LRIG1 as a tumor suppressor for head and neck cancers; LRIG1 downregulation in cancer cells enhances EGFR-MAPK-SPHK1 signaling and ECM remodeling activity, leading to malignant phenotypes of head and neck cancers.

Indexed as

Adaptor Proteins, Signal TransducingDown-RegulationErbB ReceptorsExtracellular MatrixGene Knockdown TechniquesHead and Neck NeoplasmsHumansMembrane GlycoproteinsMitogen-Activated Protein KinasesAdaptor Proteins, Signal TransducingErbB ReceptorsLRIG1 protein, humanMembrane GlycoproteinsMitogen-Activated Protein KinasesSPHKAP protein, human

Identifiers

PMID23624915
OpenAlexW2046659393

What OpenQuestion holds

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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.