PMID- 35502885
OWN - NLM
STAT- MEDLINE
DCOM- 20220504
LR  - 20220716
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 5
DP  - 2022 May
TI  - Circular RNA CircSHKBP1 accelerates the proliferation, invasion, angiogenesis, 
      and stem cell-like properties via modulation of microR-766-5p/high mobility group 
      AT-hook 2 axis in laryngeal squamous cell carcinoma.
PG  - 11551-11563
LID - 10.1080/21655979.2022.2068922 [doi]
AB  - Laryngeal squamous cell carcinoma (LSCC) is a common malignancy in head and neck. 
      Circular SHKBP1 (circSHKBP) exerts momentous functions in the occurrence of many 
      cancers including LSCC. Thus, we investigated the oncogenic capacities of 
      circSHKBP1 in LSCC, and revealed the underlying mechanism as a competing 
      endogenous RNA. The expression levels of circSHKBP1, miR-766-5p, and high 
      mobility group AT-hook 2 (HMGA2) were examined by quantitative real-time PCR and 
      their influences on the overall survival were measured by Kaplan-Meier method. 
      The correlations between circSHKBP1 and miR-766-5p or HMGA2 were detected by 
      Spearman's rank correlation analysis. In vitro, the influences of 
      circSHKBP1/miR-766-5p/HMGA2 axis on the tumorigenesis of LSCC were examined by 
      CCK-8, transwell, sphere formation, and angiogenesis assays, respectively. 
      circSHKBP1 expression was up-regulated in the LSCC specimens and cell lines. And 
      elevated circSHKBP1 expression was closely linked to poor prognosis. Silencing 
      circSHKBP1 expression restrained cell proliferation, invasion, angiogenesis, stem 
      cell-like properties and tumor growth. We observed that miR-766-5p was 
      down-regulated and negatively correlated to circSHKBP1 in LSCC samples. However, 
      HMGA2 was highly expressed and positively associated with circSHKBP1 in these 
      specimens. Importantly, the levels of circSHKBP1, miR-766-5p, and HMGA2 were 
      closely associated with patients' clinical parameters including lymph nodes 
      metastasis and TNM stages. Mechanistic analysis clarified that circSHKBP1 sponged 
      miR-766-5p to regulate HMGA2, the target of miR-766-5p. Moreover, miR-766-5p 
      inhibition and overexpression of HMGA2 rescued the tumor-suppressing roles of 
      circSHKBP1 downregulation in LSCC. In conclusion, circSHKBP1 accelerated the 
      tumorigenesis of LSCC via modulating HMGA2 by targeting miR-766-5p.
FAU - Chen, Fu
AU  - Chen F
AD  - Department of Radiation Oncology, Eye & ENT Hospital of Fudan University, 
      Shanghai, China.
FAU - Zhang, Haiyan
AU  - Zhang H
AD  - Department of Radiation Oncology, Eye & ENT Hospital of Fudan University, 
      Shanghai, China.
FAU - Wang, Jie
AU  - Wang J
AD  - Department of Radiation Oncology, Eye & ENT Hospital of Fudan University, 
      Shanghai, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (HMGA2 Protein)
RN  - 0 (HMGA2 protein, human)
RN  - 0 (MIRN766 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Circular)
SB  - IM
MH  - Carcinogenesis/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - *HMGA2 Protein/genetics
MH  - Humans
MH  - *Laryngeal Neoplasms/genetics
MH  - *MicroRNAs/genetics
MH  - Neoplasm Invasiveness
MH  - Neoplastic Stem Cells
MH  - Neovascularization, Pathologic
MH  - *RNA, Circular/genetics
MH  - *Squamous Cell Carcinoma of Head and Neck/genetics
PMC - PMC9275975
OTO - NOTNLM
OT  - CircSHKBP1
OT  - HMGA2
OT  - MiR-766-5p
OT  - laryngeal squamous cell carcinoma
OT  - tumorigenesis
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/05/04 06:00
MHDA- 2022/05/06 06:00
PMCR- 2022/05/03
CRDT- 2022/05/03 08:42
PHST- 2022/05/03 08:42 [entrez]
PHST- 2022/05/04 06:00 [pubmed]
PHST- 2022/05/06 06:00 [medline]
PHST- 2022/05/03 00:00 [pmc-release]
AID - 2068922 [pii]
AID - 10.1080/21655979.2022.2068922 [doi]
PST - ppublish
SO  - Bioengineered. 2022 May;13(5):11551-11563. doi: 10.1080/21655979.2022.2068922.