Evidence map›Paper›PMID 34318593›Full record

ArticleJournal of cellular and molecular medicine2021

Anti-growth and pro-apoptotic effects of dasatinib on human oral cancer cells through multi-targeted mechanisms.

Nam-Sook Park, Yu-Kyung Park, Anil Kumar Yadav, Young-Min Shin, David Bishop-Bailey, Jong-Soon Choi, Jong Wook Park, Byeong-Churl Jang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. 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
1.3field-weighted citation impact, top 22% 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, 16 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Advances in Small Molecular Agents against Oral Cancer.Molecules (Basel, Switzerland) · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
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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

8 authors at 4 institutions in 2 countries.

Nam-Sook ParkDepartment of Molecular Medicine, College of Medicine, Keimyung University, Daegu, Korea.
Yu-Kyung ParkDepartment of Molecular Medicine, College of Medicine, Keimyung University, Daegu, Korea.
Anil Kumar YadavDepartment of Molecular Medicine, College of Medicine, Keimyung University, Daegu, Korea.
Young-Min ShinDepartment of Dentistry, College of Medicine, Keimyung University, Daegu, Korea.
David Bishop-BaileyNorth Cornwall Research Institute, Cornwall, UK.
Jong-Soon ChoiBiological Disaster Analysis Group, Division of Convergence Biotechnology, Korea Basic Science Institute, Daejeon, Korea.
Jong Wook ParkDepartment of Immunology, College of Medicine, Keimyung University, Daegu, Korea.
Byeong-Churl JangDepartment of Molecular Medicine, College of Medicine, Keimyung University, Daegu, Korea.ORCID 0000-0002-2691-5503
Keimyung University · KRChungnam National University · KRCornwall Council · GBKeimyung College University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dasatinib is an inhibitor of Src that has anti-tumour effects on many haematological and solid cancers. However, the anti-tumour effects of dasatinib on human oral cancers remain unclear. In this study, we investigated the effects of dasatinib on different types of human oral cancer cells: the non-tumorigenic YD-8 and YD-38 and the tumorigenic YD-10B and HSC-3 cells. Strikingly, dasatinib at 10 µM strongly suppressed the growth and induced apoptosis of YD-38 cells and inhibited the phosphorylation of Src, EGFR, STAT-3, STAT-5, PKB and ERK-1/2. In contrast, knockdown of Src blocked the phosphorylation of EGFR, STAT-5, PKB and ERK-1/2, but not STAT-3, in YD-38 cells. Dasatinib induced activation of the intrinsic caspase pathway, which was inhibited by z-VAD-fmk, a pan-caspase inhibitor. Dasatinib also decreased Mcl-1 expression and S6 phosphorylation while increased GRP78 expression and eIF-2α phosphorylation in YD-38 cells. In addition, to its direct effects on YD-38 cells, dasatinib also exhibited anti-angiogenic properties. Dasatinib-treated YD-38 or HUVEC showed reduced HIF-1α expression and stability. Dasatinib alone or conditioned media from dasatinib-treated YD-38 cells inhibited HUVEC tube formation on Matrigel without affecting HUVEC viability. Importantly, dasatinib's anti-growth, anti-angiogenic and pro-apoptotic effects were additionally seen in tumorigenic HSC-3 cells. Together, these results demonstrate that dasatinib has strong anti-growth, anti-angiogenic and pro-apoptotic effects on human oral cancer cells, which are mediated through the regulation of multiple targets, including Src, EGFR, STAT-3, STAT-5, PKB, ERK-1/2, S6, eIF-2α, GRP78, caspase-9/3, Mcl-1 and HIF-1α.

Indexed as

Antineoplastic AgentsBiomarkers, TumorCarcinoma, Squamous CellCell Line, TumorDasatinibHumansMouth NeoplasmsProtein Kinase InhibitorsAntineoplastic AgentsBiomarkers, TumorDasatinibProtein Kinase InhibitorsapoptosisdasatinibHIF-1αHSC-3SrcYD-38

Identifiers

PMID34318593
PMCPMC8419177
OpenAlexW3185462939

What OpenQuestion holds

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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.