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UCA1 involved in the metformin-regulated bladder cancer cell proliferation and glycolysis.

Abstract Despite great scientific advances have been achieved in cancer treatment in recent years, the death rate of bladder cancer has been staying at a high level. Metformin, a widely-used and low-cost diabetes medicine, might have the potential of anticancer. The aim of this study was to evaluate the effects of metformin on bladder cancer cells and to identify potential molecular targets and signaling pathways. Bladder cancer 5637 cells transfected with either pcDNA/UCA1 vector or pcDNA3.1 empty vector were treated with various doses of metformin for different periods of time, and then cell proliferation and glycolysis were assessed. Reverse transcription polymerase chain reaction and Western blotting were applied to examine the expression of long non-coding RNA UCA1 and mammalian target of rapamycin-signal transducer and activator of transcription pathway molecules. We found metformin inhibited bladder cancer cell proliferation in a dose- and time-dependent manner. UCA1-overexpressed 5637 cells showed increased proliferation and glycolysis compared with control cells. Metformin downregulated both endogenous and exogenous UCA1 expression, leading to the inhibition of mammalian target of rapamycin-signal transducer and activator of transcription 3-hexokinase 2 signaling pathway. Our study provided the first evidence that metformin inhibited proliferation and glycolysis in cancer cells through regulation of long non-coding RNA UCA1. The discovery also suggested the important roles of long non-coding RNA in chemoprevention, which is a property of metformin.
PMID
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Authors

Mayor MeshTerms
Keywords

Metformin

UCA1

bladder cancer

hexokinase 2

mammalian target of rapamycin

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28641488
OWN - NLM
STAT- MEDLINE
DA  - 20170623
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - UCA1 involved in the metformin-regulated bladder cancer cell proliferation and
      glycolysis.
PG  - 1010428317710823
LID - 10.1177/1010428317710823 [doi]
AB  - Despite great scientific advances have been achieved in cancer treatment in
      recent years, the death rate of bladder cancer has been staying at a high level. 
      Metformin, a widely-used and low-cost diabetes medicine, might have the potential
      of anticancer. The aim of this study was to evaluate the effects of metformin on 
      bladder cancer cells and to identify potential molecular targets and signaling
      pathways. Bladder cancer 5637 cells transfected with either pcDNA/UCA1 vector or 
      pcDNA3.1 empty vector were treated with various doses of metformin for different 
      periods of time, and then cell proliferation and glycolysis were assessed.
      Reverse transcription polymerase chain reaction and Western blotting were applied
      to examine the expression of long non-coding RNA UCA1 and mammalian target of
      rapamycin-signal transducer and activator of transcription pathway molecules. We 
      found metformin inhibited bladder cancer cell proliferation in a dose- and
      time-dependent manner. UCA1-overexpressed 5637 cells showed increased
      proliferation and glycolysis compared with control cells. Metformin downregulated
      both endogenous and exogenous UCA1 expression, leading to the inhibition of
      mammalian target of rapamycin-signal transducer and activator of transcription
      3-hexokinase 2 signaling pathway. Our study provided the first evidence that
      metformin inhibited proliferation and glycolysis in cancer cells through
      regulation of long non-coding RNA UCA1. The discovery also suggested the
      important roles of long non-coding RNA in chemoprevention, which is a property of
      metformin.
FAU - Li, Tian
AU  - Li T
AD  - 1 Department of Urology, The Fifth Affiliated Hospital of Guangzhou Medical
      University, Guangzhou, China.
AD  - 2 Minimally Invasive Technique and Product Translational Center, Guangzhou
      Medical University, Guangzhou, China.
FAU - Sun, Xiangzhou
AU  - Sun X
AD  - 3 Department of Urology, The First Affiliated Hospital of Sun Yat-sen University,
      Guangzhou, China.
FAU - Jiang, Xianhan
AU  - Jiang X
AD  - 1 Department of Urology, The Fifth Affiliated Hospital of Guangzhou Medical
      University, Guangzhou, China.
AD  - 2 Minimally Invasive Technique and Product Translational Center, Guangzhou
      Medical University, Guangzhou, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (UCA1 RNA, human)
RN  - 9100L32L2N (Metformin)
RN  - EC 2.7.1.1 (Hexokinase)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Cell Line, Tumor
MH  - Cell Proliferation/*drug effects/genetics
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Glycolysis/drug effects
MH  - Hexokinase/*genetics
MH  - Humans
MH  - Metformin/*administration & dosage
MH  - RNA, Long Noncoding/*biosynthesis/genetics
MH  - Signal Transduction/drug effects
MH  - Urinary Bladder Neoplasms/drug therapy/*genetics/pathology
OTO - NOTNLM
OT  - Metformin
OT  - UCA1
OT  - bladder cancer
OT  - hexokinase 2
OT  - mammalian target of rapamycin
EDAT- 2017/06/24 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/24 06:00
AID - 10.1177/1010428317710823 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317710823. doi: 10.1177/1010428317710823.