843 860
expression can occur without the need for additional factors
in cellular splicing machinery like
Malat1
, due to genomic
duplication in the
AR
locus
[28].
5.
Conclusions
In summary, these results suggest that targeting the
Malat1
/AR-v7 axis
via Malat1
-siRNA or ASC-J9 can be
developed as a new therapy to better suppress the EnzR-
PCa progression.
Author contributions:
Chawnshang Chang had full access to all the data
in the study and takes responsibility for the integrity of the data and the
accuracy of the data analysis.
Study concept and design:
Chang, Sun.
Acquisition of data:
Wang, Lin, Lin, Antonarakis, Luo.
Analysis and interpretation of data:
Sun, Li, Antonarakis, Luo.
Drafting of the manuscript:
Wang, Sun, Chang.
Critical revision of the manuscript for important intellectual content:
Chang.
Statistical analysis:
Luo, Antonarakis.
Obtaining funding:
Chang.
Administrative, technical, or material support:
Niu, Yeh.
Supervision:
None.
Other:
None.
Financial disclosures:
Chawnshang Chang certifies that all conflicts of
interest, including specific financial interests and relationships and
affiliations relevant to the subject matter or materials discussed in the
manuscript (eg, employment/affiliation, grants or funding, consultan-
cies, honoraria, stock ownership or options, expert testimony, royalties,
or patents filed, received, or pending), are the following: ASC-J9 was
patented by the University of Rochester, University of North Carolina,
and AndroScience, and then licensed to AndroScience. All authors
declare there are no potential conflicts of interest related to this
manuscript.
Funding/Support and role of the sponsor:
This work was supported by
NIH Grants (CA127300 and CA156700), Taiwan Department of Health
Clinical Trial and Research Center of Excellence Grant DOH99-TD-B-111-
004 (China Medical University, Taichung, Taiwan).
Appendix A. Supplementary data
Supplementary data associated with this article can be
found, in the online version, at
http://dx.doi.org/10.1016/j. eururo.2016.04.035.
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