PMID- 36162632
OWN - NLM
STAT- MEDLINE
DCOM- 20221118
LR  - 20230131
IS  - 1879-1220 (Electronic)
IS  - 0960-0760 (Linking)
VI  - 225
DP  - 2023 Jan
TI  - LINC01146/F11R facilitates growth and metastasis of prostate cancer under the 
      regulation of TGF-beta.
PG  - 106193
LID - S0960-0760(22)00144-3 [pii]
LID - 10.1016/j.jsbmb.2022.106193 [doi]
AB  - The effect of long intergenic non-protein coding RNAs (lncRNAs) was verified in 
      prostate cancer (PCa), but the mechanism of LINC01146 in PCa is unclear. 
      Bioinformatics was applied to analyze LINC01146 expression in PCa and predict 
      target genes of LINC01146, followed by the verification of qRT-PCR, RNA pull-down 
      and co-immunoprecipitation (Co-IP). The correlation between LINC01146 expression 
      and clinicopathological characteristics was investigated. The location of 
      LINC01146 in PCa cells was detected by fluorescence in situ hybridization (FISH). 
      After interference with LINC01146 or/and F11 receptor (F11R) or treated with 
      transforming growth factor beta 1 (TGF-beta1), the function of LINC01146 in PCa in 
      vitro or in vivo was determined by CCK-8, colony formation, flow cytometry, 
      scratch test, transwell assay, xenograft experiment and western blot. LINC01146 
      and F11R were over-expressed in PCa and positively correlated with poor 
      prognosis. LINC01146 located in the cytoplasm and combined with F11R. LINC01146 
      overexpression impeded apoptosis, facilitated viability, proliferation, migration 
      and invasion in PCa cells in vitro, promoted tumor growth in vivo, downregulated 
      E-cadherin, Bax and Cleaved caspase-3, and upregulated N-cadherin, Vimentin and 
      PCNA, but LINC01146 silencing did the opposite. F11R was positively regulated by 
      LINC01146 and F11R depletion negated the effect of LINC01146 overexpression on 
      malignant phenotypes of PCa cells. The expression of LINC01146 and F11R was 
      regulated by TGF-beta1. The promoting role of TGF-beta1 in migration, invasion and F11R 
      in PCa cells was reversed by LINC01146 silencing. LINC01146 upregulated F11R to 
      facilitate malignant phenotypes of PCa cells, which was regulated by TGF-beta.
CI  - Copyright (c) 2022. Published by Elsevier Ltd.
FAU - Guo, Xiaohua
AU  - Guo X
AD  - Department of Urology, Second Hospital of Shanxi Medical University, China. 
      Electronic address: guoxiaoh_huaxg@163.com.
FAU - Gu, Yong
AU  - Gu Y
AD  - Department of Urology, Second Hospital of Shanxi Medical University, China.
FAU - Guo, Chao
AU  - Guo C
AD  - Department of Urology, Second Hospital of Shanxi Medical University, China.
FAU - Pei, Liang
AU  - Pei L
AD  - Department of Urology, Second Hospital of Shanxi Medical University, China.
FAU - Hao, Chuan
AU  - Hao C
AD  - Department of Urology, Second Hospital of Shanxi Medical University, China.
LA  - eng
PT  - Journal Article
DEP - 20220923
PL  - England
TA  - J Steroid Biochem Mol Biol
JT  - The Journal of steroid biochemistry and molecular biology
JID - 9015483
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Junctional Adhesion Molecule A)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (MicroRNAs)
RN  - 0 (F11R protein, human)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Cell Adhesion Molecules)
SB  - IM
MH  - Male
MH  - Humans
MH  - Transforming Growth Factor beta/metabolism
MH  - Transforming Growth Factor beta1/genetics
MH  - *Junctional Adhesion Molecule A/genetics/metabolism
MH  - Gene Expression Regulation, Neoplastic
MH  - Cell Movement/genetics
MH  - In Situ Hybridization, Fluorescence
MH  - Cell Line, Tumor
MH  - *Prostatic Neoplasms/metabolism
MH  - *RNA, Long Noncoding/genetics
MH  - Cell Proliferation/genetics
MH  - *MicroRNAs/genetics
MH  - Receptors, Cell Surface/genetics
MH  - Cell Adhesion Molecules/genetics/metabolism
OTO - NOTNLM
OT  - F11 receptor
OT  - Long intergenic non-protein coding RNA 1146
OT  - Malignant phenotypes
OT  - Prostate cancer
OT  - Transforming growth factor beta
COIS- Conflict of Interest Statement The authors declare no conflicts of interest.
EDAT- 2022/09/27 06:00
MHDA- 2022/11/19 06:00
CRDT- 2022/09/26 19:35
PHST- 2022/04/14 00:00 [received]
PHST- 2022/09/20 00:00 [revised]
PHST- 2022/09/21 00:00 [accepted]
PHST- 2022/09/27 06:00 [pubmed]
PHST- 2022/11/19 06:00 [medline]
PHST- 2022/09/26 19:35 [entrez]
AID - S0960-0760(22)00144-3 [pii]
AID - 10.1016/j.jsbmb.2022.106193 [doi]
PST - ppublish
SO  - J Steroid Biochem Mol Biol. 2023 Jan;225:106193. doi: 
      10.1016/j.jsbmb.2022.106193. Epub 2022 Sep 23.