Downregulation of circLPAR3 inhibits tumor progression and glycolysis by liberating miR‐144‐3p and upregulating LPCAT1 in oral squamous cell carcinoma. Issue 2 (11th March 2022)

• Record Type: Journal Article
• Authors: Su, Zhijian; Pan, Chao; Xie, Honghui; Ning, Yanyang; Li, Shuangjiang; Xiao, Haibo
• Is Part Of: Laryngoscope investigative otolaryngology. Volume 7:Issue 2(2022)
• Page Start: 425
• Page End: 436
• Publication Date: 2022-03-11
• Subjects: circLPAR3 -- LPCAT1 -- miR‐144‐3p -- OSCC; Otolaryngology -- Periodicals; Laryngoscopy -- Periodicals; Otolaryngology; Otolaryngology; Periodicals; Periodicals; 617.51
• DOI: 10.1002/lio2.771
• Languages: English
• ISSNs: 2378-8038

Abstract

Abstract: Background: Increasing evidence demonstrated the important roles of circular RNAs (circRNAs) in human cancer progression, including oral squamous cell carcinoma (OSCC). The study intentions were to explore the role and molecular mechanism of hsa_circ_0004390 (circLPAR3) in OSCC progression. Methods: Expression of circLPAR3 in collected samples and cultured cell lines was detected with real‐time quantitative reverse transcription‐polymerase chain reaction (RT‐qPCR). Loss‐of‐function experiments were performed to determine the effect of circLPAR3 silencing on OSCC cell proliferation, migration, invasion, apoptosis, angiopoiesis, and glycolysis. The sponge function of circLPAR3 was predicted by bioinformatics analysis and validated by the dual‐luciferase reporter and RNA pull‐down assays. In vivo experiments were conducted to validate the function of circLPAR3. Results: A marked increase in circLPAR3 expression was observed in OSCC samples and cell lines. Furthermore, circLPAR3 could distinguish OSCC samples from paired non‐tumor samples, and patients with high circLPAR3 expression had a poor prognosis. Furthermore, circLPAR3 inhibition decreased OSCC growth in xenograft mouse models. Moreover, circLPAR3 silencing repressed cell proliferation, migration, invasion, angiopoiesis, glycolysis, and induced cell apoptosis in OSCC cells in vitro. Mechanically, circLPAR3 sponged miR‐144‐3p to prohibit the inhibiting effect of miR‐144‐3p on LPCAT1, thus promoting OSCC progression. Conclusion: CircLPAR3 exerted a tumor‐promoting effect on OSCC growth through elevating LPCAT1 expression via functioning as a miR‐144‐3p sponge. This study supports the possible role of circLPAR3 in the diagnosis, prognosis, and treatment of OSCC. Abstract :