PMID- 30675291
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 17
IP  - 2
DP  - 2019 Feb
TI  - Oncogenic miR-744 promotes prostate cancer growth through direct targeting of 
      LKB1.
PG  - 2257-2265
LID - 10.3892/ol.2018.9822 [doi]
AB  - Prostate cancer (PCa) is one of the most common malignancies worldwide, and with 
      a limited number of treatments for this type of cancer, its incidence is rapidly 
      increasing. Patients presenting with PCa are likely to experience disease 
      recurrence, which represents a considerable clinical challenge. MicroRNAs 
      (miRNAs) have been widely characterized as a critical regulator in a number of 
      types of cancer, including PCa. miRNA-744 (miR-744) has been reported to be 
      involved in cancer regulation; however, its role in PCa remained poorly 
      understood. In a recent study, it was demonstrated that miR-744 was overexpressed 
      in prostate tissue from PCa patients when compared with the surrounding tissues, 
      and knockdown of miR-744 resulted in reduced cell growth. In addition, an 
      increased population of apoptotic cells was detected upon miR-744 knockdown, 
      together with a decrease in cell proliferation. Cell cycle analysis demonstrated 
      a higher number of cells in the G1 phase and lower numbers in the S phase 
      following miR-744 silencing. The levels of key proteins involved in cell cycle 
      progression (cyclin D1, cyclin-dependent kinase 4, and proliferating cell nuclear 
      antigen) were increased, whereas those proteins responsible for cell cycle 
      inhibition (cyclin-dependent kinase inhibitor p21) were decreased. The tumor 
      suppressor liver kinase B1 (LKB1) was revealed to be a potential target of 
      miR-744, suggesting its potential mechanism of action. LKB1 levels were 
      negatively correlated with miR-744, and LKB1 was indicated to be a direct target 
      of miR-744. Furthermore, it was revealed that by targeting LKB1, miR-744 may 
      regulate adenosine monophosphate-activated protein kinase (AMPK); the AMPK 
      signaling pathway was activated by miR-744 knockdown, with subsequent inhibition 
      of the mammalian target of rapamycin (mTOR) signaling pathway. Taken together, 
      these results demonstrated that miR-744 promoted cell growth through the AMPK 
      signaling pathway, by targeting LKB1. The present study revealed a novel insight 
      into the biological function of miR-744 in PCa, and that miR-744 may be a 
      potential therapeutic target.
FAU - Zhang, Minglei
AU  - Zhang M
AD  - Department of Orthopedics, China and Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130000, P.R. China.
FAU - Li, Hai
AU  - Li H
AD  - Department of Urology, China and Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130000, P.R. China.
FAU - Zhang, Yun
AU  - Zhang Y
AD  - Department of Urology, China and Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130000, P.R. China.
FAU - Li, Hongyan
AU  - Li H
AD  - Department of Urology, China and Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130000, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20181211
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC6341651
OTO - NOTNLM
OT  - adenosine monophosphate-activated protein kinase signaling pathway
OT  - cell growth
OT  - liver kinase B1
OT  - microRNA-744
OT  - prostate cancer
EDAT- 2019/01/25 06:00
MHDA- 2019/01/25 06:01
PMCR- 2018/12/11
CRDT- 2019/01/25 06:00
PHST- 2017/12/26 00:00 [received]
PHST- 2018/10/25 00:00 [accepted]
PHST- 2019/01/25 06:00 [entrez]
PHST- 2019/01/25 06:00 [pubmed]
PHST- 2019/01/25 06:01 [medline]
PHST- 2018/12/11 00:00 [pmc-release]
AID - OL-0-0-9822 [pii]
AID - 10.3892/ol.2018.9822 [doi]
PST - ppublish
SO  - Oncol Lett. 2019 Feb;17(2):2257-2265. doi: 10.3892/ol.2018.9822. Epub 2018 Dec 
      11.