Evidence map›Paper›PMID 30034549›Full record

ArticleTherapeutic advances in medical oncology2018

HDAC3-mediated silencing of miR-451 decreases chemosensitivity of patients with metastatic castration-resistant prostate cancer by targeting NEDD9.

Dong-Qin Chen, Chen Yu, Xue-Feng Zhang, Zhong-Fang Liu, Rui Wang, Min Jiang, Hao Chen, Feng Yan, Min Tao, Long-Bang Chen and 2 more

Abstract read
In one paragraph

Article in Therapeutic advances in medical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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  11. Regulation ofCancers · 2019
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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

12 authors.

Dong-Qin ChenDepartment of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.
Chen YuDepartment of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.
Xue-Feng ZhangWake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, USA.
Zhong-Fang LiuDepartment of Medical Oncology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Rui WangDepartment of Medical Oncology, Nanjing University, Nanjing, China.
Min JiangDepartment of Medical Oncology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Hao ChenDepartment of Urology, the First Hospital of Jiaxing, Jiaxing, China.
Feng YanDepartment of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.
Min TaoDepartment of Medical Oncology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Long-Bang ChenDepartment of Medical Oncology, Nanjing University, Nanjing, China.
Hong ZhuThe First Affiliated Hospital of Soochow University, 899 Pinghai Road, Suzhou 215006, China.
Ji-Feng FengJiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, 42 Baiziting Road, Nanjing 210009, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTreatment of metastatic castration-resistant prostate cancer (mCRPC) with docetaxel often fails due to the emergence of chemoresistance. Thus, restoring chemosensitivity to docetaxel-based therapies remains a challenge in mCRPC treatment.

methodsmicroRNA (miR)-451 expression was measured in docetaxel-treated prostate cancer cells and tumor tissues by quantitative reverse-transcription polymerase chain reaction . Cell-counting kit 8 assay was performed to determine docetaxel chemoresistance. Neural-precursor-cell-expressed developmentally downregulated protein 9 (NEDD9) was identified as a novel target of miR-451 by dual-luciferase reporter system. Chromatin immunoprecipitation and co-immunoprecipitation assay were performed to confirm that histone deacetylase 3 (HDAC3)/Sp1 (a highly evolutionarily conserved transcription factor) interacted with the Sp1 binding sites in miR-451 promoter.

resultsmiR-451 was found to be silenced in docetaxel-treated prostate cancer cells and mCRPC tissues. Low miR-451 expression was closely associated with a high Gleason score, high Eastern Cooperative Oncology Group performance status score, visceral metastasis and poor prognosis. Low expression of miR-451 was significantly correlated with short progression-free survival (PFS) and overall survival (OS) according to Kaplan-Meier analysis, and miR-451 was determined to be an independent poor prognostic factor for PFS and OS in mCRPC patients by univariate and multivariate Cox regression analyses. NEDD9 was identified as a new and functional target of miR-451. Restoration of NEDD9 partially reversed the effects of miR-451 on enhancing chemosensitivity of prostate cancer cells. HDAC3 was confirmed to be involved in silencing of miR-451 expression in prostate cancer cells.

conclusionsThe current data revealed a new HDAC3/Sp1/miR-451/NEDD9 signaling axis that regulates the chemosensitivity of prostate cancer cells and represents a novel therapeutic target for chemosensitizing mCRPC.

Indexed as

chemosensitivityHDAC3miR-451NEDD9prostate cancer

Identifiers

PMID30034549
PMCPMC6048672

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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.