Evidence map›Paper›PMID 32361789›Full record

ArticleInvestigational new drugs2020

Tivantinib inhibits the VEGF signaling pathway and induces apoptosis in gastric cancer cells with c-MET or VEGFA amplification.

Bum Jun Kim, Yoo Jin Kim, Sung-Hwa Sohn, Bohyun Kim, Hee Jung Sul, Hyeong Su Kim, Dae Young Zang

Abstract read
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In one paragraph

Article in Investigational new drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 17 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

7 authors at 2 institutions in 1 country.

Bum Jun Kim *Division of Internal Medicine, National Army Capital Hospital, The Armed Forces Medical Command, Sungnam, 13574, Republic of Korea.
Yoo Jin Kim *Hallym Translational Research Institute, Hallym University College of Medicine, Anyang-si, Gyeonggi-do, 14068, Republic of Korea.
Sung-Hwa Sohn *Hallym Translational Research Institute, Hallym University College of Medicine, Anyang-si, Gyeonggi-do, 14068, Republic of Korea.
Bohyun KimHallym Translational Research Institute, Hallym University College of Medicine, Anyang-si, Gyeonggi-do, 14068, Republic of Korea.
Hee Jung SulHallym Translational Research Institute, Hallym University College of Medicine, Anyang-si, Gyeonggi-do, 14068, Republic of Korea.
Hyeong Su KimDivision of Hematology-Oncology, Department of Internal Medicine, Hallym University Medical Center, Hallym University College of Medicine, Anyang-si, Gyeonggi-do, 14068, Republic of Korea.
Dae Young ZangHallym Translational Research Institute, Hallym University College of Medicine, Anyang-si, Gyeonggi-do, 14068, Republic of Korea. fhdzang@hallym.or.kr.ORCID http://orcid.org/0000-0002-2602-7848
Hallym University · KRHallym University Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tivantinib has been described as a selective inhibitor of c-Met and is being studied in various types of cancer. In this study, we evaluated the effects of tivantinib on the suppression of gastric cancer (GC) cell migration and apoptosis. We also examined the mechanism of action of tivantinib by oncogenic pathway analysis. We applied an RNA-sequencing approach in 34 GC patients to identify oncogenes that are differentially expressed in GC tissues. To examine the inhibitory effect of tivantinib on GC cells, we conducted apoptosis analysis using an annexin V-APC/PI apoptosis detection kit and trans-well migration assay with human GC cell lines. For oncogenic pathway analysis, Western blot and quantitative real-time PCR analysis were used to detect the expression of proteins and genes before and after tivantinib exposure. In the RNA-sequencing analysis of 34 GC patients, c-Met and VEGFA genes were expressed and positively correlated with each other. Cell migration and apoptosis analysis demonstrated that tivantinib induced the best inhibition effect in SNU620, MKN45 (carries VEGFB mutation), AGS, and MKN28 cells, but not in KATO III (carries VEGFB and VEGFC mutations) cells. Oncogenic pathway analysis showed that tivantinib, in addition to c-Met signaling pathway inhibition, also inhibits VEGF signaling and MYC expression in VEGFA-expressing GC cells. We found that tivantinib has anti-cancer activity not only in GC cells overexpressing c-Met but also in non-c-Met GC cells by inhibition of the VEGF signaling pathway.

Indexed as

Antineoplastic AgentsApoptosisCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansOncogenesProtein Kinase InhibitorsProto-Oncogene Proteins c-metPyrrolidinonesQuinolinesSequence Analysis, RNAStomach NeoplasmsVascular Endothelial Growth Factor AAntineoplastic AgentsARQ 197MET protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-metPyrrolidinonesQuinolinesVascular Endothelial Growth Factor AVEGFA protein, humanC-metGastric cancerTivantinibVEGF

Identifiers

PMID32361789
OpenAlexW3023733300

What OpenQuestion holds

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Registered trials

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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.