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The role of miR-24 as a race related genetic factor in prostate cancer

  • Yutaka Hashimoto
    ,
  • Marisa Shiina
    ,
  • Taku Kato
    ,
  • Soichiro Yamamura
    ,
  • Yuichiro Tanaka
    ,
  • Shahana Majid
*Corresponding author for this work
  • VA Medical Center
    ,
  • University of California at San Francisco
    ,
  • North Carolina Central University
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

The incidence of prostate cancer (PCa) among African-Americans (AfA) is significantly higher than Caucasian-Americans (CaA) but the genetic basis for this disparity is not known. To address this problem, we analyzed miRNA expression in AfA (n = 81) and CaA (n = 51) PCa patients. Here, we found that miR-24 is differentially expressed in AfA and CaA PCa patients and attempt to clarify its role in AfA patients. Also, the public sequencing data of the miR-24 promoter confirmed that it was highly methylated and down-regulated in PCa patients. Utilizing a VAMCSF and NDRI patient cohorts, we discovered that miR-24 expression was linked to a racial difference between AfA/CaA PCa patients. Interestingly, miR-24 was restored after treatment of PCa cells with 5Aza-CdR in an AfA cell line (MDA-PCa-2b), while restoration of miR-24 was not observed in CaA cells, DU-145. Ectopic expression of miR-24 showed decreased growth and induced apoptosis, though the effect was less in the CaA cell line compared to the AfA cell line. Finally, we found unique changes in biological pathways and processes associated with miR-24 transfected AfA cells by quantitative PCR-based gene expression array. Evaluation of the altered pathways showed that AR, IGF1, IGFBP5 and ETV1 were markedly decreased in the AfA derived cell line compared with CaA cells, and there was a reciprocal regulatory relationship of miR-24/target expression in prostate cancer patients. These results demonstrate that miR-24 may be a central regulator of key events that contribute to race-related tumorigenesis and has potential to be a therapeutic agent for PCa treatment.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 16581-16593 (13 pages)

Journal (Volume, Issue Number)

Oncotarget (Volume 8, Issue 10)

Publication milestones

  • Published - 2017

Publication status

Published - 2017

ISSN

1949-2553

Publication IDs

  • Scopus: 85014698940
  • PubMed: 28157714

Publication metrics

Metrics

Scopus
citations
SciVal
FWCI
0.71
SciVal
Author count
16
SciVal
citations
10
SciVal
Paper percentile
75
Fractional count
1
Fractional count
0.06
Fractional count
15
Fractional count
0.94
Fractional count
1
Fractional count
1

PlumX, opens in new tab

Captures
24
Citation count
21

Funding Details

We appreciate Dr. Roger Erickson for his support and assistance with the preparation of the manuscript. This work was supported by the National Cancer Institute at the National Institutes of Health through grant numbers UO1CA184966, RO1CA138642, RO1CA194730 and VA funded program project number (BX001604).
FundersFunding numbers
NIH
UO1CA184966, BX001604, RO1CA138642
NCI
U01CA194730