Evidence map›Paper›PMID 26378810›Full record

ArticleOncotarget2015

sMEK1 inhibits endothelial cell proliferation by attenuating VEGFR-2-dependent-Akt/eNOS/HIF-1α signaling pathways.

Boh-Ram Kim, Seung Hee Seo, Mi Sun Park, Seung-Hoon Lee, Youngjoo Kwon, Seung Bae Rho

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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, 31 citations in OpenAlex.

  1. Review
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  3. Arteriosclerosis, thrombosis, and vascular biology · 2024
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  6. SMEK1 promotes lung adenocarcinoma proliferation and invasion by activating Wnt/β-catenin signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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 1 country.

Boh-Ram KimResearch Institute, National Cancer Center, Ilsan-ro, Ilsandong-gu, Goyang-si Gyeonggi-do, Republic of Korea.
Seung Hee SeoResearch Institute, National Cancer Center, Ilsan-ro, Ilsandong-gu, Goyang-si Gyeonggi-do, Republic of Korea.
Mi Sun ParkResearch Institute, National Cancer Center, Ilsan-ro, Ilsandong-gu, Goyang-si Gyeonggi-do, Republic of Korea.
Seung-Hoon LeeDepartment of Life Science, Yong In University, Samga-dong, Cheoin-gu, Yongin-si Gyeonggi-do, Republic of Korea.
Youngjoo KwonCollege of Pharmacy, Graduate School of Pharmaceutical Sciences, Ewha Global Top 5 Program, Ewha Womans University, Seoul, Republic of Korea.
Seung Bae RhoResearch Institute, National Cancer Center, Ilsan-ro, Ilsandong-gu, Goyang-si Gyeonggi-do, Republic of Korea.
National Cancer Center · KREwha Womans University · KRYong In University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The suppressor of MEK null (sMEK1) protein possesses pro-apoptotic activities. In the current study, we reveal that sMEK1 functions as a novel anti-angiogenic factor by suppressing vascular endothelial growth factor (VEGF)-induced cell proliferation, migration, and capillary-like tubular structure in vitro. In addition, sMEK1 inhibited the phosphorylation of the signaling components up- and downstream of Akt, including phospholipase Cγ1 (PLC-γ1), 3-phosphoinositide-dependent protein kinase 1 (PDK1), endothelial nitric oxide synthetase (eNOS), and hypoxia-inducible factor 1 (HIF-1α) during ovarian tumor progression via binding with vascular endothelial growth factor receptor 2 (VEGFR-2). Furthermore, sMEK1 decreased tumor vascularity and inhibited tumor growth in a xenograft human ovarian tumor model. These results supply convincing evidence that sMEK1 controls endothelial cell function and subsequent angiogenesis by suppressing VEGFR-2-mediated PI3K/Akt/eNOS signaling pathway. Taken together, our results clearly suggest that sMEK1 might be a novel anti-angiogenic and anti-tumor agent for use in ovarian tumor.

Indexed as

Cell ProliferationAnimalsApoptosisBlotting, WesternCell MovementCells, CulturedFemaleHumansHuman Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1, alpha SubunitImmunoenzyme TechniquesImmunoprecipitationMiceMice, Inbred BALB CMice, NudeNeovascularization, PathologicHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNitric Oxide Synthase Type IIINOS3 protein, humanPhosphoprotein PhosphatasesPPP4R3A protein, humanProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2VEGFA protein, humananti-angiogenic activityhypoxic conditionovarian tumorsMEK1 tumor suppressorxenograft model

Identifiers

PMID26378810
PMCPMC4741643
OpenAlexW2287741923

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.