Evidence map›Paper›PMID 29216925›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

Silencing of miR-193a-5p increases the chemosensitivity of prostate cancer cells to docetaxel.

Zhan Yang, Jin-Suo Chen, Jin-Kun Wen, Hai-Tao Gao, Bin Zheng, Chang-Bao Qu, Kai-Long Liu, Man-Li Zhang, Jun-Fei Gu, Jing-Dong Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 10% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
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  6. Exploring the miRNAs Profile in Dark-Cutting Beef.Foods (Basel, Switzerland) · 2024
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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

14 authors at 2 institutions in 1 country.

Zhan YangDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Jin-Suo ChenDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Jin-Kun WenDepartment of Biochemistry and Molecular Biology, Ministry of Education of China, Hebei Medical University, No. 361 Zhongshan E Rd, Shijiazhuang, 050017, China.
Hai-Tao GaoDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Bin ZhengDepartment of Biochemistry and Molecular Biology, Ministry of Education of China, Hebei Medical University, No. 361 Zhongshan E Rd, Shijiazhuang, 050017, China.
Chang-Bao QuDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Kai-Long LiuDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Man-Li ZhangDepartment of Biochemistry and Molecular Biology, Ministry of Education of China, Hebei Medical University, No. 361 Zhongshan E Rd, Shijiazhuang, 050017, China.
Jun-Fei GuDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Jing-Dong LiDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Yan-Ping ZhangDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Wei LiDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Xiao-Lu WangDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China.
Yong ZhangDepartment of Urology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, China. zhangyong89@sina.com.
Second Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

The National Natural Science Foundation of China 81600237The National Natural Science Foundation of China 81672555
6 · The paper itself

Abstract

backgroundDocetaxel-based chemotherapy failure in advanced prostate carcinoma has partly been attributed to the resistance of prostate cancer (PC) cells to docetaxel-induced apoptosis. Hence, there is an urgent need to identify mechanisms of docetaxel chemoresistance and to develop new combination therapies.

methodsmiR-193a-5p level was evaluated by qPCR in prostate tissues and cell lines, and its expression in the tissues was also examined by in situ hybridization. PC cell line (PC3 cell) was transfected with miR-193a-5p mimic or its inhibitor, and then cell apoptosis and the expression of its downstream genes Bach2 and HO-1 were detected by TUNEL staining and Western blotting. Luciferase reporter assay was used to detect the effect of miR-193a-5p and Bach2 on HO-1 expression. Xenograft animal model was used to test the effect of miR-193a-5p and docetaxel on PC3 xenograft growth.

resultsmiR-193a-5p was upregulated in PC tissues and PC cell lines, with significant suppression of PC3 cell apoptosis induced by oxidative stress. Mechanistically, miR-193a-5p suppressed the expression of Bach2, a repressor of the HO-1 gene, by directly targeting the Bach2 mRNA 3'-UTR. Docetaxel treatment modestly decreased Bach2 expression and increased HO-1 level in PC3 cells, whereas a modest increase of HO-1 facilitated docetaxel-induced apoptosis. Notably, docetaxel-induced miR-193a-5p upregulation, which in turn inhibits Bach2 expression and thus relieves Bach2 repression of HO-1 expression, partly counteracted docetaxel-induced apoptosis, as evidenced by the increased Bcl-2 and decreased Bax expression. Accordingly, silencing of miR-193a-5p enhanced sensitization of PC3 cells to docetaxel-induced apoptosis. Finally, depletion of miR-193a-5p significantly reduced PC xenograft growth in vivo.

conclusionsSilencing of miR-193a-5p or blockade of the miR-193a-5p-Bach2-HO-1 pathway may be a novel therapeutic approach for castration-resistant PC.

Indexed as

AgedAnimalsAntineoplastic AgentsDisease Models, AnimalDocetaxelGene SilencingHumansMaleMiceMicroRNAsMiddle AgedProstatic Neoplasms, Castration-ResistantTaxoidsTransfectionUp-RegulationXenograft Model Antitumor AssaysAntineoplastic AgentsDocetaxelMicroRNAsMIRN1934 microRNA, humanTaxoidsBach2ChemoresistanceDocetaxelHO-1miR-193a-5pProstate cancer

Identifiers

PMID29216925
PMCPMC5721613
OpenAlexW2774140051

What OpenQuestion holds

Textmetadata
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.