Evidence map›Paper›PMID 31228347›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Anti-Proliferation and Pro-Apoptotic Effects of Diosmetin via Modulating Cell Cycle Arrest and Mitochondria-Mediated Intrinsic Apoptotic Pathway in MDA-MB-231 Cells.

Chunjing Wang, Shujing Li, Huanhuan Ren, Yue Sheng, Tiantian Wang, Min Li, Qiang Zhou, Hongxian He, Changqing Liu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 32 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

9 authors at 1 institution in 1 country.

Chunjing WangDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Shujing LiDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Huanhuan RenDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Yue ShengDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Tiantian WangDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Min LiDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Qiang ZhouDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Hongxian HeDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Changqing LiuDepartment of Life Sciences, Bengbu Medical College, Bengbu, Anhui, China (mainland).
Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Breast cancer is one of the most malignant tumors worldwide. The natural flavonoid diosmetin has been reported to exhibit various pharmacological activities, including anti-cancer effects. This study aimed to investigate the anti-breast cancer effects of diosmetin on MDA-MB-231 cells and to explore the underlying molecular mechanisms of cell apoptosis. MATERIAL AND METHODS The MDA-MB-231 cells were incubated with diosmetin for 24 h. Then, cell viability and lactate dehydrogenase (LDH) leakage were detected using CCK-8 and LDH assay kits, respectively. Inverted fluorescence microscopy and flow cytometry were used to measure the mitochondrial membrane potential (MMP) and intracellular reactive oxygen species (ROS). Cell apoptosis and cell cycle were determined by flow cytometry. The expressions of apoptosis and cell cycle-related genes were determined by Western blotting and qRT-PCR. RESULTS The results revealed that diosmetin exerts significant cytotoxic effects on MDA-MB-231 cells, as indicated by decreased cell viability, increased intracellular ROS accumulation and LDH release, as well as cell cycle arrest in G0/G1 phase, inducing mitochondrial dysfunction and apoptosis. Moreover, diosmetin treatment significantly downregulated the expression levels of Bcl-2 and Cyclin D1, and upregulated that of p53, Bax, caspase 3, cleaved caspase 9, and cleaved caspase 3. CONCLUSIONS These findings demonstrate that diosmetin has anti-proliferative and pro-apoptotic activities against MDA-MB-231 cells via cell cycle arrest and the mitochondria-mediated intrinsic apoptotic pathway. Our results extend the understanding of the anti-tumor mechanism of diosmetin and suggest that it may be of use as an active natural agent for the prevention or treatment of human breast cancer.

Indexed as

Apoptosisbcl-2-Associated X ProteinBreast NeoplasmsCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalCytochromes cFemaleFlavonoidsHumansMembrane Potential, MitochondrialMitochondriaProto-Oncogene Proteins c-bcl-2Reactive Oxygen Speciesbcl-2-Associated X ProteinBCL2 protein, humanCytochromes cdiosmetinFlavonoidsProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Identifiers

PMID31228347
PMCPMC6601365
OpenAlexW2952684089

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.