Evidence map›Paper›PMID 30176898›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3.

Bo Ma, Hang Zhang, Yu Wang, Ang Zhao, Zhiming Zhu, Xiaowen Bao, Yang Sun, Lin Li, Qi Zhang

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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 94 citations in OpenAlex.

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  15. Apoptosis mechanisms induced by 15d-PMJFrontiers in pharmacology · 2023
    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

9 authors at 1 institution in 1 country.

Bo MaSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Hang ZhangSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Yu WangSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Ang ZhaoSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Zhiming ZhuSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Xiaowen BaoSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Yang SunSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China.
Lin LiInstitute of Advanced Materials (IAM), Nanjing Tech University, Nanjing, 210009, People's Republic of China. iamlli@njtech.edu.cn.
Qi ZhangSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 210009, People's Republic of China. nancyzhang03@hotmail.com.
Nanjing Tech University · CN

Funding

Jiangsu Synergetic Innovation Center for Advanced Bio-Manufacture XTD1819National Natural Science Foundation of China 81672508National Natural Science Foundation of China 81773802
6 · The paper itself

Abstract

backgroundThe development of potent non-toxic chemotherapeutic drugs against castration resistant prostate cancer (CRPC) remains a major challenge. Corosolic acid (CA), a natural triterpenoid, has anti-cancer activity with limited side effects. However, CA anti-prostate cancer activities and mechanisms, particularly in CRPC, are not clearly understood. In this study, we investigated CA anti-tumor ability against human CRPC and its mechanism of action.

methodsThe cell apoptosis and proliferation effects were evaluated via MTT detection, colony formation assay and flow cytometry. Western blot, gene transfection and immunofluorescence assay were applied to investigate related protein expression of Endoplasmic reticulum stress. A xenograft tumor model was established to investigate the inhibitory effect of CA on castration resistant prostate cancer in vivo.

resultsThe results showed that CA inhibited cell growth and induced apoptosis in human prostate cancer cell (PCa) line PC-3 and DU145, as well as retarded tumor growth in a xenograft model, exerting a limited toxicity to normal cells and tissues. Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. IRE-1, PERK or CHOP knockdown partially attenuated CA cytotoxicity against PCa cells. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death. CHOP silencing resulted in PCa cells sensitive to CA-induced apoptosis.

conclusionOur data demonstrated, for the first time, that CA might represent a novel drug candidate for the development of an anti-CRPC therapy.

Indexed as

AnimalsApoptosisCell Cycle ProteinsCell Line, TumorCell ProliferationeIF-2 KinaseEndoplasmic Reticulum StressEndoribonucleasesGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Kinase 4MiceProstatic Neoplasms, Castration-ResistantProtein Serine-Threonine KinasesRepressor ProteinsCell Cycle Proteinscorosolic acidDDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseEndoribonucleasesERN1 protein, humanMAP Kinase Kinase 4Protein Serine-Threonine KinasesRepressor ProteinsTranscription Factor CHOPTRIB3 protein, humanTriterpenesCastration resistant PCa (CRPC)CCAAT-enhancer-binding protein homologous protein (CHOP)Corosolic acid (CA)Endoplasmic reticulum stress (ER stress)Protein kinase RNA-like endoplasmic reticulum kinase (PERK)Tribbles homolog 3 (TRIB3)

Identifiers

PMID30176898
PMCPMC6122202
OpenAlexW2888856643

What OpenQuestion holds

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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.