PMID- 33660806
OWN - NLM
STAT- MEDLINE
DCOM- 20220105
LR  - 20220105
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 25
IP  - 4
DP  - 2021 Feb
TI  - SP1-induced lncRNA TUG1 regulates proliferation and apoptosis in islet cells of 
      type 2 diabetes mellitus via the miR-188-3p/FGF5 axis.
PG  - 1959-1966
LID - 25096 [pii]
LID - 10.26355/eurrev_202102_25096 [doi]
AB  - OBJECTIVE: To elucidate the role of TUG1 in the onset of type 2 diabetes mellitus 
      (T2DM) and the potential mechanism. MATERIALS AND METHODS: Relative levels of 
      TUG1 and SP1 in high-fat diet animal model and high-glucose cell model were 
      detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and their 
      correlation was analyzed. Potential binding sites in the promoter sequences of 
      TUG1 and SP1 were predicted using the JASPAR. Their interaction was further 
      confirmed by chromatin immunoprecipitation (ChIP) and Dual-Luciferase reporter 
      assay. The influences of TUG1 on proliferative and apoptotic potentials in Min6 
      cells were examined by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine 
      (EdU) assay and flow cytometry, respectively. Subsequently, the interaction in 
      the TUG1/miR-188-3p /FGF5 axis was similarly explored by Dual-Luciferase reporter 
      assay. RESULTS: SP1 and TUG1 were downregulated in high-fat and high-glucose 
      models, and they displayed a positive correlation. TUG1 bound E2 region in SP1 
      promoters. Knockdown of TUG1 inhibited proliferative rate and induced apoptosis 
      in high-glucose-treated Min6 cells. Furthermore, the TUG1 / miR-188-3p /FGF5 axis 
      was identified to be responsible for regulating Min6 cell functions. CONCLUSIONS: 
      SP1 induces TUG1 downregulation in T2DM cell models, which further regulates 
      proliferative and apoptotic potentials in islet cells by activating the 
      miR-188-3p/FGF5 axis.
FAU - Zhang, P
AU  - Zhang P
AD  - Department of Endocrinology, the First Affiliated Hospital of Soochow University, 
      Suzhou, China. 20174132030@stu.suda.edu.cn.
FAU - Li, Y-N
AU  - Li YN
FAU - Tu, S
AU  - Tu S
FAU - Cheng, X-B
AU  - Cheng XB
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Fgf5 protein, mouse)
RN  - 0 (MIRN188 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (TUG1 noncoding RNA, mouse)
RN  - 129653-64-1 (Fibroblast Growth Factor 5)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Diabetes Mellitus, Experimental/*metabolism/pathology
MH  - Diabetes Mellitus, Type 2/*metabolism/pathology
MH  - Fibroblast Growth Factor 5/genetics/*metabolism
MH  - Islets of Langerhans/*metabolism/pathology
MH  - Mice
MH  - MicroRNAs/genetics/*metabolism
MH  - RNA, Long Noncoding/genetics/*metabolism
MH  - Sp1 Transcription Factor/genetics/*metabolism
EDAT- 2021/03/05 06:00
MHDA- 2022/01/06 06:00
CRDT- 2021/03/04 08:40
PHST- 2021/03/04 08:40 [entrez]
PHST- 2021/03/05 06:00 [pubmed]
PHST- 2022/01/06 06:00 [medline]
AID - 25096 [pii]
AID - 10.26355/eurrev_202102_25096 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2021 Feb;25(4):1959-1966. doi: 
      10.26355/eurrev_202102_25096.