Evidence map›Paper›PMID 32038836›Full record

ArticleToxicological research2009

Cytotoxic Effects on HL-60 Cells of Myosin Light Chain Kinase Inhibitor ML-7 Alone and in Combination with Flavonoids.

Joong Won Lee, Yang Jee Kim, Young Joo Choi, Hae Dong Woo, Gye Eun Kim, Tae Kyung Ha, Young Hyun Lee, Hai Won Chung

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 85% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
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 1 institution in 1 country.

Joong Won LeeSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Yang Jee KimSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Young Joo ChoiSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Hae Dong WooSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Gye Eun KimSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Tae Kyung HaSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Young Hyun LeeSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Hai Won ChungSchool of Public Health and Institute of Health and Environment, Seoul National University, 28 Yongon-dong, Jongno-gu, Seoul, 110-460 Korea.
Korea National Institute of Health · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncontrolled cell growth and increased cell proliferation are major features of cancer that are dependent on the stable structure and dynamics of the cytoskeleton. Since stable cytoskeleton structure and dynamics are partly regulated by myosin light chain kinase (MLCK), many current studies focused on MLCK inhibition as a chemotherapeutic target. As a potent and selective MLCK inhibitor, ML-7 [1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazapine hydrochloride] is a promising candidate for an anticancer agent, which would induce apoptosis as well as prevents invasion and metastasis in certain types of cancer cells. This study assessed cytotoxic effects of ML-7 against HL-60 cells and therapeutic efficacy of ML-7 as a potential antileukemia agent. Trypan-blue exclusion assays showed dose- and time- dependent decreases in ML-7 treated HL-60 cells (p < 0.05). Comet assays revealed a significant increase in DNA damage in HL-60 cells after treatment with 40 µM ML-7 for 2 h. Sub-G1 fractions, analyzed by flow cytometry increased in a dose-dependent manner, suggesting that ML-7 can induce apoptotic cell death in HL-60 cells. ML-7 was selectively cytotoxic towards HL-60 cells; not affecting normal human lymphocytes. That selective effect makes it a promising potential anti-leukemia agent. In addition, anticancer efficacy of ML-7 in combination with flavonoids (genistein or quercetin) or anticancer drugs (cisplatin or AraC) against HL-60 cells was assessed. Combination of ML-7 with flavonoids increased the anticancer effect of ML-7 to a greater extent than combination with the anticancer drugs. This implies that ML-7 in combination with flavonoids could increase the efficacy of anticancer treatment, while avoiding side effects cansed by conventional anticancer drug-containing combination chemotherapy.

Indexed as

1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazapine hydrochloride (ML-7)ApoptosisDNA damageFlavonoidsHL-60 cellsMyosin light chain kinase inhibitor

Identifiers

PMID32038836
PMCPMC7006274
OpenAlexW2103646381

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.