PMID- 36590309
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230103
IS  - 1687-8450 (Print)
IS  - 1687-8469 (Electronic)
IS  - 1687-8450 (Linking)
VI  - 2022
DP  - 2022
TI  - circPOLR1C Promotes the Development of Esophageal Cancer by Adsorbing miR-361-3p 
      and Regulating Cancer Cell Apoptosis and Metastasis.
PG  - 9124142
LID - 10.1155/2022/9124142 [doi]
LID - 9124142
AB  - BACKGROUND: The effect of circular RNA-RNA polymerase I and III subunit C 
      (circPOLR1C) on esophageal cancer (EC) has not been reported. Herein, this study 
      is designed to unveil the effect and the regulatory mechanism of circPOLR1C on 
      EC. METHODS: The expression of circPOLR1C in EC tissues and cells was detected by 
      qRT-PCR. Circular structure, stability, and cell localization of circPOLR1C were 
      confirmed by qRT-PCR, RNase R, actinomycin D, and fluorescence in situ 
      hybridization (FISH) assay. Cell function experiments, nude mouse xenograft, lung 
      transplant model, and HE staining were performed to evaluate the effects of 
      CircPOLR1C on EC in vitro and in vivo. A regulatory relationship between 
      miR-361-3p and circPOLR1C was confirmed by qRT-PCR, circRNA in vivo 
      precipitation, RIP, FISH, CircInteractome database, dual-luciferase reporter 
      assay, and immunohistochemistry. Rescue experiments were applied to assess the 
      effects of miR-361-3p and circPOLR1C on EC cells and tissues. Apoptosis- and 
      epithelial-mesenchymal transformation (EMT)-related gene expressions were 
      quantified by qRT-PCR and Western blot. RESULTS: Highly expressed circPOLR1C in 
      EC was related to tumor differentiation and invasion. circPOLR1C, which mainly 
      exists in the cytoplasm, is a stable circular RNA. circPOLR1C silencing inhibited 
      circPOLR1C expression and EC cell malignant function, while circPOLR1C 
      overexpression promoted the growth of transplanted tumors and lung metastasis. 
      The enrichment of miR-361-3p was higher than that of other targeted miRNAs. 
      circPOLR1C adsorbed miR-361-3p to regulate apoptosis- and EMT-related genes and 
      partially reversed the tumor suppressive effect of miR-361-3p, which was lowly 
      expressed in EC tissues. Silencing the target genes of miR-361-3p also inhibited 
      the malignant development of EC cells. CONCLUSION: circPOLR1C adsorbs miR-361-3p 
      and regulates apoptosis- and EMT-related gene expressions to promote the 
      development of EC.
CI  - Copyright (c) 2022 Yong Fang et al.
FAU - Fang, Yong
AU  - Fang Y
AUID- ORCID: 0000-0002-7539-250X
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui 
      District, Shanghai 200032, China.
FAU - Yin, Jun
AU  - Yin J
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui 
      District, Shanghai 200032, China.
FAU - Shen, Yaxing
AU  - Shen Y
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui 
      District, Shanghai 200032, China.
FAU - Wang, Hao
AU  - Wang H
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui 
      District, Shanghai 200032, China.
FAU - Tang, Han
AU  - Tang H
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui 
      District, Shanghai 200032, China.
FAU - Chen, Xiaosang
AU  - Chen X
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui 
      District, Shanghai 200032, China.
LA  - eng
PT  - Journal Article
DEP - 20221223
PL  - Egypt
TA  - J Oncol
JT  - Journal of oncology
JID - 101496537
PMC - PMC9803566
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2023/01/03 06:00
MHDA- 2023/01/03 06:01
PMCR- 2022/12/23
CRDT- 2023/01/02 04:21
PHST- 2022/03/16 00:00 [received]
PHST- 2022/11/22 00:00 [revised]
PHST- 2022/12/01 00:00 [accepted]
PHST- 2023/01/02 04:21 [entrez]
PHST- 2023/01/03 06:00 [pubmed]
PHST- 2023/01/03 06:01 [medline]
PHST- 2022/12/23 00:00 [pmc-release]
AID - 10.1155/2022/9124142 [doi]
PST - epublish
SO  - J Oncol. 2022 Dec 23;2022:9124142. doi: 10.1155/2022/9124142. eCollection 2022.