Evidence map›Paper›PMID 27041866›Full record

ArticlePharmacognosy magazine2016

Endoplasmic reticulum stress-induced apoptotic pathway and mitochondrial dysregulation in HeLa cells treated with dichloromethane extract of Dillenia suffruticosa.

Wan Abd Ghani Wan Nor Hafiza, Latifah Saiful Yazan, Yin Sim Tor, Jhi Biau Foo, Nurdin Armania, Heshu Sulaiman Rahman

Abstract read
In one paragraph

Article in Pharmacognosy magazine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
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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

6 authors.

Wan Abd Ghani Wan Nor HafizaDepartment of Biomedical Sciences, Faculty of Medicine and Health Science, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; College of Medical Laboratory Technology, Institute for Medical Research, Jin Pahang, 50588 Kuala Lumpur, Malaysia.
Latifah Saiful YazanDepartment of Biomedical Sciences, Faculty of Medicine and Health Science, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Laboratory of Molecular Biomedicine, Institute of Bioscience, 43400 UPM Serdang, Selangor, Malaysia.
Yin Sim TorLaboratory of Molecular Biomedicine, Institute of Bioscience, 43400 UPM Serdang, Selangor, Malaysia.
Jhi Biau FooLaboratory of Molecular Biomedicine, Institute of Bioscience, 43400 UPM Serdang, Selangor, Malaysia.
Nurdin ArmaniaDepartment of Biomedical Sciences, Faculty of Medicine and Health Science, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Laboratory of Molecular Biomedicine, Institute of Bioscience, 43400 UPM Serdang, Selangor, Malaysia.
Heshu Sulaiman RahmanDepartment of Microbiology and Pathology, Faculty of Veterinary Medicine, 43400 UPM Serdang, Selangor, Malaysia; UPM-MAKNA Cancer Research Laboratory, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ethyl acetate and dichloromethane extract of Dillenia suffruticosa (EADS and DCMDS, respectively) can be a potential anticancer agent. The effects of EADS and DCMDS on the growth of HeLa cervical cancer cells and the expression of apoptotic-related proteins had been investigated in vitro. Cytotoxicity of the extracts toward the cells was determined by 5-diphenyltetrazolium bromide assay, the effects on cell cycle progression and the mode of cell death were analyzed by flow cytometry technique, while the effects on apoptotic-related genes and proteins were evaluated by quantitative real-time polymerase chain reaction, and Western blot and enzyme-linked immunosorbent assay, respectively. Treatment with DCMDS inhibited (P < 0.05) proliferation and induced apoptosis in HeLa cells. The expression of cyclin B1 was downregulated that led to G2/M arrest in the cells after treatment with DCMDA. In summary, DCMDS induced apoptosis in HeLa cells via endoplasmic reticulum stress-induced apoptotic pathway and dysregulation of mitochondria. The data suggest the potential application of DCMDS in the treatment of cervical cancer.

Indexed as

Apoptosiscell cycle arrestcervical cancerDillenia suffruticosaendoplasmic reticulum stress

Identifiers

PMID27041866
PMCPMC4792007

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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.