PMID- 31298337
OWN - NLM
STAT- MEDLINE
DCOM- 20200930
LR  - 20200930
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 13
DP  - 2019 Jul
TI  - MicroRNA-31 inhibits papillary thyroid carcinoma cell biological progression by 
      directly targeting SOX11 and regulating epithelial-to-mesenchymal transition, ERK 
      and Akt signaling pathways.
PG  - 5863-5873
LID - 18329 [pii]
LID - 10.26355/eurrev_201907_18329 [doi]
AB  - OBJECTIVE: The current study aimed to explore the roles of miR-31 and SOX11 in 
      papillary thyroid carcinoma (PTC). PATIENTS AND METHODS: Fifty-four paired human 
      PTC specimens and matched normal thyroid tissues were obtained. Meanwhile, human 
      thyroid epithelial cell Nthy-ori3-1 and PTC cells were cultured. The effects of 
      miR-31 on PTC cell proliferation, invasion and migration were detected by cell 
      proliferation assays and transwell assay, respectively. SOX11 expression in 
      tissue samples was examined by immunohistochemical staining analyses (IHC). The 
      correlation between SOX11 and miR-31 was clarified by Dual-Luciferase reporter 
      assay. The relative mRNA and protein expression were detected by quantitative 
      Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. In addition, the 
      xenograft model experiments were performed. RESULTS: Declined miR-31 expressions 
      were frequently identified in PTC, leading to poorer overall survival (OS) and 
      worse clinicopathologic features of PTC patients. Moreover, functional assays 
      indicated that miR-31 overexpression could notably repress PTC cell 
      proliferation, invasion and migration abilities by regulating the extracellular 
      regulated protein kinases (ERK) and protein kinase B (Akt) signaling pathways and 
      epithelial-mesenchymal transition (EMT). In addition, the results of the 
      Luciferase reporter assay demonstrated that SOX11 was a direct functional target 
      of miR-31 in PTC cells. In vivo, miR-31 restoration significantly suppressed the 
      tumor growth of xenograft PTC models. CONCLUSIONS: Our findings indicated that 
      miR-31 exerted anti-PTC functions via targeting SOX11 and modulating the ERK and 
      Akt signaling pathways and EMT. MiR-31 may potentially serve as a novel biomarker 
      in future therapeutics of PTC.
FAU - Wang, Y
AU  - Wang Y
AD  - Department of Breast and Thyroid Surgery, Liaocheng People's Hospital, Liaocheng, 
      China. xnpuu4w82358@163.com.
FAU - Liu, B-G
AU  - Liu BG
FAU - Zhou, C-X
AU  - Zhou CX
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 (MIRN31 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (SOX11 protein, human)
RN  - 0 (SOXC Transcription Factors)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - *Epithelial-Mesenchymal Transition
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Female
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - MicroRNAs/genetics/*metabolism
MH  - Middle Aged
MH  - Neoplasms, Experimental/metabolism/pathology/surgery
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - SOXC Transcription Factors/genetics/*metabolism
MH  - Signal Transduction
MH  - Thyroid Cancer, Papillary/*metabolism/pathology/surgery
MH  - Thyroid Neoplasms/*metabolism/pathology/surgery
EDAT- 2019/07/13 06:00
MHDA- 2020/10/02 06:00
CRDT- 2019/07/13 06:00
PHST- 2019/07/13 06:00 [entrez]
PHST- 2019/07/13 06:00 [pubmed]
PHST- 2020/10/02 06:00 [medline]
AID - 18329 [pii]
AID - 10.26355/eurrev_201907_18329 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jul;23(13):5863-5873. doi: 
      10.26355/eurrev_201907_18329.