Evidence map›Paper›PMID 27012847›Full record

ArticleBMC cancer2016

The milk-derived fusion peptide, ACFP, suppresses the growth of primary human ovarian cancer cells by regulating apoptotic gene expression and signaling pathways.

Juan Zhou, Mengjing Zhao, Yigui Tang, Jing Wang, Cai Wei, Fang Gu, Ting Lei, Zhiwu Chen, Yide Qin

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-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

9 citing papers in PubMed, 15 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 3 institutions in 1 country.

Juan ZhouDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, Anhui, 230032, China.
Mengjing ZhaoDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, Anhui, 230032, China.
Yigui TangDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, Anhui, 230032, China.
Jing WangDepartment of Obstetrics and Gynecology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Cai WeiDepartment of Pharmacy, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230601, China.
Fang GuDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, Anhui, 230032, China.
Ting LeiDepartment of Pharmacy, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230601, China.
Zhiwu ChenDepartment of Pharmacology, Anhui Medical University, Hefei, Anhui, 230032, China.
Yide QinDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, Anhui, 230032, China. yideqin@ahmu.edu.cn.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CNSecond Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundACFP is an anti-cancer fusion peptide derived from bovine milk protein. This study was to investigate the anti-cancer function and underlying mechanisms of ACFP in ovarian cancer.

methodsFresh ovarian tumor tissues were collected from 53 patients who underwent initial debulking surgery, and primary cancer cells were cultured. Normal ovarian surface epithelium cells (NOSECs), isolated from 7 patients who underwent surgery for uterine fibromas, were used as normal control tissue. Anti-viabilities of ACFP were assessed by WST-1 (water-soluble tetrazolium 1), and apoptosis was measured using a flow cytometry-based assay. Gene expression profiles of ovarian cancer cells treated with ACFP were generated by cDNA microarray, and the expression of apoptotic-specific genes, such as bcl-xl, bax, akt, caspase-3, CDC25C and cyclinB1, was assessed by real time PCR and western blot analysis.

resultsTreatment with ACFP inhibited the viability and promoted apoptosis of primary ovarian cancer cells but exhibited little or no cytotoxicity toward normal primary ovarian cells. Mechanistically, the anti-cancer effects of ACFP in ovarian cells were shown to occur partially via changes in gene expression and related signal pathways. Gene expression profiling highlighted that ACFP treatment in ovarian cancer cells repressed the expression of bcl-xl, akt, CDC25C and cyclinB1 and promoted the expression of bax and caspase-3 in a time- and dose-dependent manner.

conclusionsOur results suggest that ACFP may represent a potential therapeutic agent for ovarian cancer that functions by altering the expression and signaling of cancer-related pathways in ovarian cancer cells.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCaspase 3Cattlecdc25 PhosphatasesCell ProliferationCell SurvivalCyclin B1FemaleGene Expression Regulation, NeoplasticHumansMilk ProteinsOligonucleotide Array Sequence AnalysisOvarian NeoplasmsPeptidesbcl-2-Associated X ProteinCaspase 3CDC25C protein, humancdc25 PhosphatasesCyclin B1Milk ProteinsPeptidesAnti-ovarian cancerApoptosiscDNA microarrayCell viabilityFusion peptide

Identifiers

PMID27012847
PMCPMC4806491
OpenAlexW2306873046

What OpenQuestion holds

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LicenceCC BY
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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.