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MiR-613 suppresses retinoblastoma cell proliferation, invasion, and tumor formation by targeting E2F5.

Abstract Retinoblastoma is a common intraocular malignancy that occurs during childhood. MicroRNAs play critical roles in the regulation of retinoblastoma initiation and progression, and aberrant expression of miR-613 had been reported in various types of cancer. However, the role and mechanism of its function in retinoblastoma are still unclear. In this study, we found that miR-613 was downregulated in retinoblastoma tissues and cell lines. Overexpression of miR-613 suppressed retinoblastoma cell proliferation, migration, and invasion and induced cell cycle arrest in vitro. Additionally, overexpressed miR-613 also inhibited tumor formation of retinoblastoma cells in vivo. We further identified E2F5 as a direct target of miR-613. Reintroduction of E2F5 without 3'-untranslated region reversed the inhibitory effects of miR-613 on cell proliferation and invasion. Our data collectively indicate that miR-613 functions as a tumor suppressor in retinoblastoma through downregulating E2F5, supporting the targeting of the novel miR-613/E2F5 axis as a potentially effective therapeutic approach for retinoblastoma.
PMID
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Authors

Mayor MeshTerms
Keywords

E2F5

Retinoblastoma

miR-613

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




PMID- 28351331
OWN - NLM
STAT- MEDLINE
DA  - 20170329
DCOM- 20170407
LR  - 20170407
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 3
DP  - 2017 Mar
TI  - MiR-613 suppresses retinoblastoma cell proliferation, invasion, and tumor
      formation by targeting E2F5.
PG  - 1010428317691674
LID - 10.1177/1010428317691674 [doi]
AB  - Retinoblastoma is a common intraocular malignancy that occurs during childhood.
      MicroRNAs play critical roles in the regulation of retinoblastoma initiation and 
      progression, and aberrant expression of miR-613 had been reported in various
      types of cancer. However, the role and mechanism of its function in
      retinoblastoma are still unclear. In this study, we found that miR-613 was
      downregulated in retinoblastoma tissues and cell lines. Overexpression of miR-613
      suppressed retinoblastoma cell proliferation, migration, and invasion and induced
      cell cycle arrest in vitro. Additionally, overexpressed miR-613 also inhibited
      tumor formation of retinoblastoma cells in vivo. We further identified E2F5 as a 
      direct target of miR-613. Reintroduction of E2F5 without 3'-untranslated region
      reversed the inhibitory effects of miR-613 on cell proliferation and invasion.
      Our data collectively indicate that miR-613 functions as a tumor suppressor in
      retinoblastoma through downregulating E2F5, supporting the targeting of the novel
      miR-613/E2F5 axis as a potentially effective therapeutic approach for
      retinoblastoma.
FAU - Zhang, Yiting
AU  - Zhang Y
AD  - 1 Department of Ophthalmology, Medical School of Nanjing University, Jinling
      Hospital, Nanjing, China.
FAU - Zhu, Xinyue
AU  - Zhu X
AD  - 1 Department of Ophthalmology, Medical School of Nanjing University, Jinling
      Hospital, Nanjing, China.
FAU - Zhu, Xiaomin
AU  - Zhu X
AD  - 2 Department of Ophthalmology, Jinling Hospital, Nanjing, China.
FAU - Wu, Yan
AU  - Wu Y
AD  - 2 Department of Ophthalmology, Jinling Hospital, Nanjing, China.
FAU - Liu, Yajun
AU  - Liu Y
AD  - 1 Department of Ophthalmology, Medical School of Nanjing University, Jinling
      Hospital, Nanjing, China.
FAU - Yao, Borui
AU  - Yao B
AD  - 1 Department of Ophthalmology, Medical School of Nanjing University, Jinling
      Hospital, Nanjing, China.
FAU - Huang, Zhenping
AU  - Huang Z
AD  - 1 Department of Ophthalmology, Medical School of Nanjing University, Jinling
      Hospital, Nanjing, 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 (E2F5 Transcription Factor)
RN  - 0 (E2F5 protein, human)
RN  - 0 (MIRN613 microRNA, human)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Apoptosis/genetics
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/*genetics
MH  - E2F5 Transcription Factor/*biosynthesis/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, Tumor Suppressor
MH  - Humans
MH  - MicroRNAs/biosynthesis/*genetics
MH  - Neoplasm Invasiveness/genetics/pathology
MH  - Retinoblastoma/*genetics/pathology
OTO - NOTNLM
OT  - E2F5
OT  - Retinoblastoma
OT  - miR-613
EDAT- 2017/03/30 06:00
MHDA- 2017/04/08 06:00
CRDT- 2017/03/30 06:00
AID - 10.1177/1010428317691674 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Mar;39(3):1010428317691674. doi: 10.1177/1010428317691674.

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