PMID- 28000876
OWN - NLM
STAT- MEDLINE
DCOM- 20170323
LR  - 20181202
IS  - 1791-2431 (Electronic)
IS  - 1021-335X (Linking)
VI  - 37
IP  - 2
DP  - 2017 Feb
TI  - miR-196b/miR-1290 participate in the antitumor effect of resveratrol via 
      regulation of IGFBP3 expression in acute lymphoblastic leukemia.
PG  - 1075-1083
LID - 10.3892/or.2016.5321 [doi]
AB  - MicroRNAs play critical roles in the progression of acute lymphoblastic leukemia 
      (ALL). Previous studies have indicated that miR-196b and miR-1290 play critical 
      roles in T-cell ALL (T-ALL) and B-cell ALL (B-ALL), respectively. Resveratrol, a 
      natural edible polyphenolic phytoalexin, possesses certain anticancer activities. 
      Nevertheless, the mechanism involved in the regulation of ALL by resveratrol is 
      still poorly understood. The present study aimed to reveal the potential 
      mechanism underlying the antitumor effect of resveratrol in ALL focusing on 
      miRNAs. Research indicates that insulin-like growth factor binding protein 3 
      (IGFBP3) plays a critical role in the aetiology of ALL. In the present study, we 
      first demonstrated that the expression of IGFBP3 was decreased in ALL patients. 
      We further identified that miR-196b and miR-1290 were overexpressed in T-ALL 
      TALL-104 and B-ALL SUP-B15 cell lines, respectively. Moreover, resveratrol 
      markedly decreased the overexpression of miR-196b/miR-1290 and elevated IGFBP3 
      expression in the ALL cell lines. As an miR-196b/miR-1290 inhibitor, resveratrol 
      was further demonstrated to exert antitumor effects on ALL cells including 
      antiproliferation, cell cycle arrest, apoptosis and inhibition of migration. 
      Dual-luciferase reporter assay revealed that miR-196b/miR-1290 directly bound to 
      the 3'-untranslated (3'-UTR) region of IGFBP3 mRNA. Moreover, we observed that 
      IGFBP3 short interfering RNA reversed the antitumor activity of resveratrol 
      against ALL cells. Taken together, the present study provides evidence that 
      resveratrol targets miR-196b and miR-1290 for its antitumor activity in T-ALL and 
      B-ALL, respectively. The present study also confirms that both miR‑196b and 
      miR-1290 target the IGFBP3 3'-UTR and are potential therapeutic targets for ALL.
FAU - Zhou, Wei
AU  - Zhou W
AD  - Department of Hematology, Guangzhou First People's Hospital, Guangzhou Medical 
      University, Guangzhou, Guangdong 510180, P.R. China.
FAU - Wang, Shunqing
AU  - Wang S
AD  - Department of Hematology, Guangzhou First People's Hospital, Guangzhou Medical 
      University, Guangzhou, Guangdong 510180, P.R. China.
FAU - Ying, Yi
AU  - Ying Y
AD  - Department of Hematology, Guangzhou First People's Hospital, Guangzhou Medical 
      University, Guangzhou, Guangdong 510180, P.R. China.
FAU - Zhou, Ruiqing
AU  - Zhou R
AD  - Department of Hematology, Guangzhou First People's Hospital, Guangzhou Medical 
      University, Guangzhou, Guangdong 510180, P.R. China.
FAU - Mao, Ping
AU  - Mao P
AD  - Department of Hematology, Guangzhou First People's Hospital, Guangzhou Medical 
      University, Guangzhou, Guangdong 510180, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20161215
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Antineoplastic Agents, Phytogenic)
RN  - 0 (IGFBP3 protein, human)
RN  - 0 (Insulin-Like Growth Factor Binding Protein 3)
RN  - 0 (MIRN1290 microRNA, human)
RN  - 0 (MIRN196 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Stilbenes)
RN  - Q369O8926L (Resveratrol)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Antineoplastic Agents, Phytogenic/pharmacology
MH  - Case-Control Studies
MH  - Cell Line, Tumor
MH  - Gene Expression Regulation, Leukemic/drug effects
MH  - Humans
MH  - Insulin-Like Growth Factor Binding Protein 3/genetics/*metabolism
MH  - MicroRNAs/*genetics
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/*drug therapy/genetics
MH  - RNA, Small Interfering
MH  - Resveratrol
MH  - Stilbenes/*pharmacology
EDAT- 2016/12/22 06:00
MHDA- 2017/03/24 06:00
CRDT- 2016/12/22 06:00
PHST- 2016/06/29 00:00 [received]
PHST- 2016/08/13 00:00 [accepted]
PHST- 2016/12/22 06:00 [pubmed]
PHST- 2017/03/24 06:00 [medline]
PHST- 2016/12/22 06:00 [entrez]
AID - 10.3892/or.2016.5321 [doi]
PST - ppublish
SO  - Oncol Rep. 2017 Feb;37(2):1075-1083. doi: 10.3892/or.2016.5321. Epub 2016 Dec 15.