Evidence map›Paper›PMID 31952105›Full record

ArticleMolecules (Basel, Switzerland)2020

Casticin Induces DNA Damage and Affects DNA Repair Associated Protein Expression in Human Lung Cancer A549 Cells (Running Title: Casticin Induces DNA Damage in Lung Cancer Cells).

Zheng-Yu Cheng, Yung-Ting Hsiao, Yi-Ping Huang, Shu-Fen Peng, Wen-Wen Huang, Kuo-Ching Liu, Te-Chun Hsia, Tzong-Der Way, Jing-Gung Chung

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-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

12 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Zheng-Yu ChengDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.
Yung-Ting HsiaoDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.
Yi-Ping HuangDepartment of Physiology, College of Medicine, China Medical University, Taichung 404, Taiwan.
Shu-Fen PengDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.
Wen-Wen HuangDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.
Kuo-Ching LiuDepartment of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 404, Taiwan.
Te-Chun HsiaDepartment of Respiratory Therapy, China Medical University, Taichung 404, Taiwan.
Tzong-Der WayDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.
Jing-Gung ChungDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.ORCID 0000-0002-7303-2287
China Medical University · TW

Funding

China Medical University, Taiwan CMU107-ASIA-17 and CMU107-BC-3Experiments and data analysis were performed in part through the use of the Medical Research Core Facilities Center, Office of Research & Development at China Medical University, Taichung, Taiwan N/A
6 · The paper itself

Abstract

Casticin was obtained from natural plants, and it has been shown to exert biological functions; however, no report concerns the induction of DNA damage and repair in human lung cancer cells. The objective of this study was to investigate the effects and molecular mechanism of casticin on DNA damage and repair in human lung cancer A549 cells. Cell viability was determined by flow cytometric assay. The DNA damage was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and electrophoresis which included comet assay and DNA gel electrophoresis. The protein levels associated with DNA damage and repair were analyzed by western blotting. The expression and translocation of p-H2A.X were observed by confocal laser microscopy. Casticin reduced total viable cell number and induced DNA condensation, fragmentation, and damage in A549 cells. Furthermore, casticin increased p-ATM at 6 h and increased p-ATR and BRCA1 at 6-24 h treatment but decreased p-ATM at 24-48 h, as well as decreased p-ATR and BRCA1 at 48 h. Furthermore, casticin decreased p-p53 at 6-24 h but increased at 48 h. Casticin increased p-H2A.X and MDC1 at 6-48 h treatment. In addition, casticin increased PARP (cleavage) at 6, 24, and 48 h treatment, DNA-PKcs and MGMT at 48 h in A549 cells. Casticin induced the expressions and nuclear translocation of p-H2AX in A549 cells by confocal laser microscopy. Casticin reduced cell number through DNA damage and condensation in human lung cancer A549 cells.

Indexed as

ApoptosisDNA DamageDNA RepairA549 CellsCell SurvivalFlavonoidsGene Expression Regulation, NeoplasticHistonesHumansLung NeoplasmsNeoplasm ProteinscasticinFlavonoidsH2AX protein, humanHistonesNeoplasm ProteinscasticinDNA condensation and repairDNA damagehuman lung cancer A549 cells

Identifiers

PMID31952105
PMCPMC7024307
OpenAlexW3000558035

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.