Evidence map›Paper›PMID 30541589›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Isoalantolactone induces apoptosis through ROS-mediated ER stress and inhibition of STAT3 in prostate cancer cells.

Wei Chen, Ping Li, Yi Liu, Yu Yang, Xueting Ye, Fangyi Zhang, Hang Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 73 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

7 authors at 2 institutions in 1 country.

Wei ChenDepartment of Urology, |The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Ping LiDepartment of Urology, |The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Yi LiuDepartment of Gynaecology and Obstetrics, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yu YangDepartment of Urology, |The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Xueting YeDepartment of Urology, |The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Fangyi ZhangDepartment of Urology, |The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Hang HuangDepartment of Urology, |The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China. wzhuanghang@163.com.
First Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CN

Funding

Natural Science Foundation of Zhejiang Province LY16H050008
6 · The paper itself

Abstract

backgroundProstate cancer is one of the most commonly diagnosed cancers in men worldwide. Currently available therapies for metastatic prostate cancer are only marginally effective. Therefore, new therapeutic agents are urgently needed to improve patient outcome. Isoalantolactone (IATL), an active sesquiterpene naturally present in many vegetables and medicinal plants, is known to induce cell death and apoptosis in various cancer cell lines. Nevertheless, antitumor mechanisms initiated by IATL in cancer cells have not been fully defined.

methodsCell apoptosis and cellular ROS levels were analyzed by flow cytometry. Western blot and qRT-PCR were used to analyze the protein and mRNA levels of indicated molecules, respectively. Nude mice xenograft model was used to test the effects of IATL on prostate cancer cell growth in vivo.

resultsIn this study, we found that IATL dose-dependently inhibited cancer cell growth and induced apoptosis in PC-3 and DU145 cells. Mechanistically, our data found that IATL induced reactive oxygen species (ROS) production, resulting in the activation of endoplasmic reticulum stress pathway and eventually cell apoptosis in prostate cancer cells. IATL also decreased the protein expression levels of p-STAT3 and STAT3, and the effects of IATL were reversed by pretreatment with N-acetyl-L-cysteine (NAC). In vivo, we found that IATL inhibited the growth of prostate cancer xenografts without exhibiting toxicity. Treatment of mice bearing human prostate cancer xenografts with IATL was also associated with induction of ER stress and inhibtion of STAT3.

conclusionIn summary, our results unveil a previously unrecognized mechanism underlying the biological activity of IATL, and provide a novel anti-cancer candidate for the treatment of prostate cancer.

Indexed as

AnimalsCell Line, TumorEndoplasmic Reticulum StressHumansMaleMiceMice, NudeProstatic NeoplasmsRandom AllocationReactive Oxygen SpeciesSesquiterpenesSTAT3 Transcription FactorisoalantolactoneReactive Oxygen SpeciesSesquiterpenesSTAT3 protein, humanSTAT3 Transcription FactorER stressIsoalantolactoneProstate cancerReactive oxygen speciesSTAT3

Identifiers

PMID30541589
PMCPMC6292114
OpenAlexW2903662205

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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.