PMID- 29750311
OWN - NLM
STAT- MEDLINE
DCOM- 20180927
LR  - 20181114
IS  - 1791-2431 (Electronic)
IS  - 1021-335X (Linking)
VI  - 40
IP  - 1
DP  - 2018 Jul
TI  - MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal
      cancer cells by targeting iASPP.
PG  - 252-260
LID - 10.3892/or.2018.6406 [doi]
AB  - In the present study, the function of miR-150 and its downstream target iASPP in 
      the growth and metastasis of colorectal cancer (CRC) cells was investigated. The 
      expression of miR-150 and iASPP was first investigated in clinical CRC samples.
      Subsequently, the effects of miR-150 overexpression and iASPP inhibition on cell 
      viability, cell cycle distribution, apoptosis, migration and invasion were
      detected with CCK-8, flow cytometry, scratch and Transwell assays. The
      interaction between miR-150 and iASPP was confirmed using a dual-luciferase
      assay. Subsequently, the key role of iASPP in the anti-CRC function of miR-150
      was assessed by inducing the expression of the gene in miR-150 overexpressed
      SW480 cells. In clinical samples, the level of miR-150 was downregulated, while
      iASPP was induced. Enforced expression of miR-150 decreased the viability,
      induced G1 cell cycle arrest and apoptosis, and inhibited the migration and
      invasion of SW480 cells. Knockdown of iASPP exerted a similar effect on SW480
      cells to that of the overexpression of miR-150. Dual-luciferase assay
      demonstrated that miR-150 directly bound to iASPP and inhibited its
      transcription. The function of miR-150 depended on the inhibition of iASPP;
      induced expression of iASPP in miR-150-knockdown SW480 and HCT116 cells restored 
      cell viability, migration and invasion while inhibiting G1 cell cycle arrest and 
      apoptosis. Increased expression of miR-150 suppressed viability, proliferation,
      migration and invasion of SW480 cells. Furthermore, iASPP was a direct target of 
      miR-150 and played a key role in its anti-CRC function. miR-150 may be a
      promising predictor of prognosis in CRC patients.
FAU - Li, Chen
AU  - Li C
AD  - Department of Surgery, Clinical Division, The Chinese People's Liberation Army
      General Hospital, Beijing 100853, P.R. China.
FAU - Du, Xiaohui
AU  - Du X
AD  - Department of Surgery, Clinical Division, The Chinese People's Liberation Army
      General Hospital, Beijing 100853, P.R. China.
FAU - Xia, Shaoyou
AU  - Xia S
AD  - Department of Surgery, Clinical Division, The Chinese People's Liberation Army
      General Hospital, Beijing 100853, P.R. China.
FAU - Chen, Lin
AU  - Chen L
AD  - Department of Surgery, Clinical Division, The Chinese People's Liberation Army
      General Hospital, Beijing 100853, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180430
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (MIRN150 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (PPP1R13L protein, human)
RN  - 0 (Repressor Proteins)
SB  - IM
MH  - Apoptosis
MH  - Biomarkers, Tumor/*genetics
MH  - Cell Cycle Checkpoints/genetics
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Cell Survival/genetics
MH  - Colorectal Neoplasms/*genetics/pathology
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockdown Techniques
MH  - HCT116 Cells
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/antagonists & inhibitors/*genetics
MH  - MicroRNAs/*genetics
MH  - Neoplasm Invasiveness/genetics/pathology
MH  - Neoplasm Metastasis
MH  - Prognosis
MH  - Protein Binding/genetics
MH  - Repressor Proteins/antagonists & inhibitors/*genetics
PMC - PMC6059748
EDAT- 2018/05/12 06:00
MHDA- 2018/09/28 06:00
CRDT- 2018/05/12 06:00
PHST- 2017/08/14 00:00 [received]
PHST- 2018/04/19 00:00 [accepted]
PHST- 2018/05/12 06:00 [pubmed]
PHST- 2018/09/28 06:00 [medline]
PHST- 2018/05/12 06:00 [entrez]
AID - 10.3892/or.2018.6406 [doi]
PST - ppublish
SO  - Oncol Rep. 2018 Jul;40(1):252-260. doi: 10.3892/or.2018.6406. Epub 2018 Apr 30.