Evidence map›Paper›PMID 28332364›Full record

ArticleYonsei medical journal2017

Potential Antitumor Activity of SIM-89 in Non-Small Cell Lung Cancer Cells.

Jun Pei, Tianqing Chu, Minhua Shao, Jiajun Teng, Huifang Sha, Aiqing Gu, Rong Li, Jialin Qian, Weifeng Mao, Ying Li and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Yonsei medical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 96% 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

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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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

11 authors at 3 institutions in 1 country.

Jun PeiDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Tianqing ChuDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Minhua ShaoDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Jiajun TengDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Huifang ShaDepartment of Basic Research, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Aiqing GuDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Rong LiDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Jialin QianDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Weifeng MaoDepartment of Biology, East China Normal University, Shanghai, China.
Ying LiDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Baohui HanDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China. hanbh520@163.com.
Shanghai Chest Hospital · CNShanghai Jiao Tong University · CNEast China Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposec-Met and its ligand, hepatocyte growth factor (HGF), play a critical role in oncogenesis and metastatic progression. The aim of this study was to identify inhibited enzymogram and to test the antitumor activity of SIM-89 (a c-Met receptor tyrosine kinase inhibitor) in non-small cell lung cancer. MATERIALS AND

methodsZ'-LYTE kinase assay was employed to screen the kinase enzymogram, and mechanism of action (MOA) analysis was used to identify the inhibited kinases. Cell proliferation was then analyzed by CCK8 assay, and cell migration was determined by transwell assay. The gene expression and the phosphorylation of c-Met were examined by realtime-PCR and western blotting, respectively. Finally, the secretion of HGF was detected by ELISA assay.

resultsc-Met, activated protein kinase (AMPK), and tyrosine kinase A (TRKA) were inhibited by SIM-89 with the IC₅₀ values of 297 nmol/L, 1.31 μmol/L, and 150.2 nmol/L, respectively. SIM-89 exerted adenosine triphosphate (ATP) competitive inhibition on c-Met. Moreover, the expressions of STAT1, JAK1, and c-Met in H460 cells were decreased by SIM-89 treatment, and c-Met phosphorylation was suppressed in A549, H441, H1299, and B16F10 cells by the treatment. In addition, SIM-89 treatment significantly decreased the level of HGF, which accounted for the activation of c-Met receptor tyrosine kinase. Finally, we showed cell proliferation inhibition and cell migration suppression in H460 and H1299 cells after SIM-89 treatment.

conclusionIn conclusion, SIM-89 inhibits tumor cell proliferation, migration and HGF autocrine, suggesting it's potential antitumor activity.

Indexed as

Cell Line, TumorAntineoplastic AgentsBlotting, WesternCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationEnzyme-Linked Immunosorbent AssayHepatocyte Growth FactorHumansLung NeoplasmsPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-metSignal TransductionXenograft Model Antitumor AssaysAntineoplastic AgentsHepatocyte Growth FactorHGF protein, humanMET protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-metantitumorcell migrationcell proliferationc-Metlung cancer

Identifiers

PMID28332364
PMCPMC5368144
OpenAlexW2603770170

What OpenQuestion holds

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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.