Evidence map›Paper›PMID 25344917›Full record

ArticleOncotarget2014

TM4SF4 overexpression in radiation-resistant lung carcinoma cells activates IGF1R via elevation of IGF1.

Soo-Im Choi, Seo-Yeon Kim, Jaeha Lee, Eun-Wie Cho, In-Gyu Kim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  20. Implications of Insulin-like Growth Factor 1 Receptor Activation in Lung Cancer.The Malaysian journal of medical sciences : MJMS · 2016
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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

5 authors at 3 institutions in 1 country.

Soo-Im ChoiDepartment of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute (KAERI), Daedeok-daero, Yuseong-gu, Daejeon, South Korea. Department of Radiation Biotechnology and Applied Radioisotope, Korea University of Science and Technology, Daedeok-daero, Yuseong-gu, Daejeon, South Korea.
Seo-Yeon KimDepartment of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute (KAERI), Daedeok-daero, Yuseong-gu, Daejeon, South Korea.
Jaeha LeeDepartment of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute (KAERI), Daedeok-daero, Yuseong-gu, Daejeon, South Korea. Department of Radiation Biotechnology and Applied Radioisotope, Korea University of Science and Technology, Daedeok-daero, Yuseong-gu, Daejeon, South Korea.
Eun-Wie ChoEpigenomics Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Gwahak-ro, Yuseong-gu, Daejeon, South Korea.
In-Gyu KimDepartment of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute (KAERI), Daedeok-daero, Yuseong-gu, Daejeon, South Korea. Department of Radiation Biotechnology and Applied Radioisotope, Korea University of Science and Technology, Daedeok-daero, Yuseong-gu, Daejeon, South Korea.
Korea Atomic Energy Research Institute · KRKorea Research Institute of Bioscience and Biotechnology · KRKorea University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transmembrane 4 L six family member 4 (TM4SF4) is a member of the tetraspanin L6 domain family. Other members of this family, TM4SF1 (also known as L6-Ag) and TM4SF5, have been shown to be upregulated in multiple tumors and involved in epithelial-to-mesenchymal transition and cell migration. However, unlike its homologs, little is known about TM4SF4. Here, we show that TM4SF4 was highly expressed in radiation-resistant lung adenocarcinoma cells, such as A549 and Calu-3 cells, and its expression activated cell growth, migration, and invasion. Overexpression of TM4SF4 in A549 cells increased the activation of PI3K, AKT, and NF-kappaB and the expression of PTEN. IGF1R was clearly activated by overexpression of TM4SF4, although EGFR was also slightly activated. TM4SF4 expression was correlated with the increased expression of IGF1, consequently resulting in IGF1R activation. Tumorigenic activity of TM4SF4 in lung adenocarcinoma cells was also demonstrated by xenograft assay; however, this activity was almost completely suppressed by treatment with anti-TM4SF4 antibody. Our results suggest that TM4SF4 overexpression in lung carcinoma cells results in resistance to radiotherapy via IGF1-induced IGF1R activation and blocking the activity of TM4SF4 using specific antibody can be a promising therapeutics against TM4SF4-overexpressing lung adenocarcinoma.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsAntibodiesCell Line, TumorCell MovementCell ProliferationDNA MethylationFemaleHumansInsulin-Like Growth Factor ILung NeoplasmsMembrane GlycoproteinsMiceMice, Inbred BALB CMice, NudeAntibodiesIGF1 protein, humanIGF1R protein, humanInsulin-Like Growth Factor IMembrane GlycoproteinsReceptor, IGF Type 1Receptors, SomatomedinTM4SF4 protein, human

Identifiers

PMID25344917
PMCPMC4259440
OpenAlexW1829044527

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.