PMID- 31173286
OWN - NLM
STAT- MEDLINE
DCOM- 20200914
LR  - 20230907
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 10
DP  - 2019 May
TI  - MicroRNA-32 inhibits the proliferation, migration and invasion of human colon 
      cancer cell lines by targeting E2F transcription factor 5.
PG  - 4156-4163
LID - 17918 [pii]
LID - 10.26355/eurrev_201905_17918 [doi]
AB  - OBJECTIVE: MicroRNAs to be essential therapeutic targets for the treatment of 
      diseases such as cancer. Colon cancer is one of the prevalent cancers and causes 
      tremendous human mortality. The treatment of colon cancer is limited by late 
      diagnosis and lack of efficient therapeutic targets. Herein, the therapeutic 
      potential of the miR-32 was explored in colon cancer. PATIENTS AND METHODS: 
      Expression analysis was carried out by quantitative Real-time polymerase chain 
      reaction (qRT-PCR). Transfections were performed by Lipofectamine(R) 2000 reagent. 
      The cell counting kit 8 (CCK-8) assay was used to determine cell viability. The 
      4', 6-diamidino-2-phenylindole (DAPI) and annexin V/Propidium Iodide (PI) assays 
      were used for the detection of apoptosis. Transwell assays were used to determine 
      cell migration and invasion. The expression of the proteins was estimated by 
      Western blotting. RESULTS: The results showed that the expression of miR-32 was 
      aberrantly downregulated in all colon cancer cells. Overexpression of miR-32 
      caused significant (p<0.01) decline in the viability in SW-948 cells via 
      induction of apoptosis. The induction of apoptosis was also accompanied by the 
      upregulation of Bax and downregulation of Bcl-2 expression. Overexpression of 
      miR-32 also caused the arrest of the SW-498 cells in the G2/M phase of cell cycle 
      and inhibited their migration and invasion. TargetScan analysis showed E2F 
      transcription factor 5 (E2F5) to be the potential target of miR-32, which was 
      also confirmed by dual luciferase reporter assay. The expression of E2F5 was 
      significantly (p<0.01) upregulated in the colon cancer cells and overexpression 
      of miR-32 caused a considerable decline in the expression of E2F5 in the SW-948 
      cells. E2F5 silencing also inhibited the growth of the SW-948 cells via induction 
      of apoptosis and G2/M cell cycle arrest. MiR-32 overexpression also inhibited the 
      migration and invasion of the SW-948 cells. However, rescue assay revealed E2F5 
      to be essential for the tumor suppressive effects of miR-32. CONCLUSIONS: The 
      findings of the present study reveal that miR-32 acts as a tumor suppressor in 
      colon cancer cells and may have therapeutic implications in colon cancer 
      treatment.
FAU - Yang, F
AU  - Yang F
AD  - Department of Pediatric Surgery, The No. 1 Hospital of Jilin University, 
      Changchun, Jilin, China. zhwang53@yahoo.com.
FAU - Chen, L
AU  - Chen L
FAU - Wang, Z-J
AU  - Wang ZJ
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (BCL2 protein, human)
RN  - 0 (E2F Transcription Factors)
RN  - 0 (MIRN32 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
SB  - IM
RIN - Eur Rev Med Pharmacol Sci. 2021 Jan;25(2):568. PMID: 33577001
MH  - Apoptosis
MH  - Cell Division
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cell Survival
MH  - Colonic Neoplasms/epidemiology/*genetics
MH  - Down-Regulation
MH  - E2F Transcription Factors/*metabolism
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - MicroRNAs/*genetics/pharmacology
MH  - Neoplasm Invasiveness/*genetics
MH  - Prevalence
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Up-Regulation
EDAT- 2019/06/08 06:00
MHDA- 2020/09/15 06:00
CRDT- 2019/06/08 06:00
PHST- 2019/06/08 06:00 [entrez]
PHST- 2019/06/08 06:00 [pubmed]
PHST- 2020/09/15 06:00 [medline]
AID - 17918 [pii]
AID - 10.26355/eurrev_201905_17918 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 May;23(10):4156-4163. doi: 
      10.26355/eurrev_201905_17918.