Evidence map›Paper›PMID 30444038›Full record

ArticleMolecular oncology2019

Pirin: a potential novel therapeutic target for castration-resistant prostate cancer regulated by miR-455-5p.

Takayuki Arai, Satoko Kojima, Yasutaka Yamada, Sho Sugawara, Mayuko Kato, Kazuto Yamazaki, Yukio Naya, Tomohiko Ichikawa, Naohiko Seki

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

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  11. Role of motor proteins in human cancers.Saudi journal of biological sciences · 2022
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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 2 institutions in 1 country.

Takayuki AraiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Japan.
Satoko KojimaDepartment of Urology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Yasutaka YamadaDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Japan.
Sho SugawaraDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Japan.
Mayuko KatoDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Japan.
Kazuto YamazakiDepartment of Pathology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Yukio NayaDepartment of Urology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Tomohiko IchikawaDepartment of Urology, Chiba University Graduate School of Medicine, Japan.
Naohiko SekiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Japan.
Chiba University · JPTeikyo University Chiba Medical Center · JP

Funding

KAKENHI 16H05462(B)KAKENHI 17K11160(C)KAKENHI 18K09160(C)KAKENHI 18K09338(C)KAKENHI 18K16685KAKENHI 18K16723KAKENHI 18K16724
6 · The paper itself

Abstract

Androgen deprivation therapy is frequently used to treat prostate cancer (PCa), but resistance can occur, a condition known as castration-resistant prostate cancer (CRPC). Thus, novel approaches for identification of CRPC are important for designing effective PCa treatments. Analysis of microRNA (miRNA) expression signatures by RNA sequencing showed that both passenger and guide strands of the miR-455-duplex (miR-455-5p and miR-455-3p, respectively) acted as antitumor miRNAs in PCa cells. The involvement of miRNA passenger strands in cancer pathogenesis is a novel concept for miRNA functionality. Based on a large patient cohort in The Cancer Genome Atlas, expression of eight miR-455-5p/-3p target genes (PIR: P = 0.0137, LRP8: P = 0.0495, IGFBP3: P = 0.0172, DMBX1: P = 0.0175, CCDC64: P = 0.0446, TUBB1: P = 0.0149, KIF21B: P = 0.0336, and NFAM1: P = 0.0013) was significantly associated with poor prognosis of PCa patients. Here, we focused on PIR (pirin), a highly conserved member of the cupin superfamily. PIR expression was directly regulated by miR-455-5p, and PIR overexpression was detected in hormone-sensitive prostate cancer (HSPC) surgical specimens and CRPC autopsy specimens. Loss-of-function assays using siRNA or an inhibitor (bisamide) showed that downregulation of PIR expression blocked cancer cell migration and invasion. Moreover, the miR-455-5p/PIR axis contributed to cancer cell aggressiveness. These results suggest that PIR might be a promising diagnostic marker for HSPC and CRPC. Furthermore, CRPC treatment strategies targeting PIR may be possible in the future. Identification of antitumor miRNAs, including miRNA passenger strands, may contribute to the development of new diagnostic markers and therapeutic strategies for CRPC.

Indexed as

Molecular Targeted TherapyAntineoplastic AgentsArgonaute ProteinsCarrier ProteinsCell Line, TumorDioxygenasesDisease-Free SurvivalGene Expression Regulation, NeoplasticHumansMaleMicroRNAsNuclear ProteinsOncogenesPrognosisProstatic Neoplasms, Castration-ResistantAGO2 protein, humanAntineoplastic AgentsArgonaute ProteinsCarrier ProteinsDioxygenasesMicroRNAsMIRN455 microRNA, humanNuclear ProteinsPIR protein, humanbisamidecastration-resistant prostate cancermiR-455-5ppirin

Identifiers

PMID30444038
PMCPMC6360383
OpenAlexW2900521889

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.