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LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis
Sun, XueFeng; Wang, GuangSuo; Ding, PeiKun; Li, ShiXuan.
  • Sun, XueFeng; The Second Clinical Medical College of Jinan University. Department of Thoracic Surgery. Shenzhen. CN
  • Wang, GuangSuo; The Second Clinical Medical College of Jinan University. Department of Thoracic Surgery. Shenzhen. CN
  • Ding, PeiKun; The Second Clinical Medical College of Jinan University. Department of Thoracic Surgery. Shenzhen. CN
  • Li, ShiXuan; The Second Clinical Medical College of Jinan University. Department of Thoracic Surgery. Shenzhen. CN
Braz. j. med. biol. res ; 53(12): e9317, 2020. graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132508
ABSTRACT
LINC00355 has been reported aberrantly over-expressed and associated with poor prognosis in various types of cancer. However, reports regarding the effect of LINC00355 on lung squamous cell carcinoma (SCC) are rare. This study aimed to explore the function of LINC00355 in the development and progression of lung SCC and reveal the underlying mechanism. The expression and subcellular location of LINC00355 were determined by qRT-PCR and RNA-FISH, respectively. The lung SCC cell growth was analyzed by CCK-8 assay, transwell invasion, wound healing, colony formation, and flow cytometry assays. Reactive oxygen species level was evaluated by DCFH-DA probes. Bioinformatics online websites, luciferase reporter assay, RNA binding protein immunoprecipitation (RIP), and RNA pull-down assays were utilized to investigate the interaction among LINC00355, miR-466, and Ly-1 antibody reactive clone (LYAR). The results showed that LINC00355 was upregulated in lung SCC and was positively associated with poor overall survival in lung SCC patients. LINC00355 was mainly located in the cytoplasm of SCC cells. Additionally, LINC0035 functioned as a competing endogenous RNA (ceRNA) to target miR-466, and LYAR was identified as a direct target of miR-466. LINC00355 expression negatively correlated with miR-466 level, and positively correlated with LYAR level. Mechanistically, knockdown of LINC00355 inhibited cell proliferation, migration and invasion, promoted cell apoptosis in vitro, and suppressed tumor growth in vivo through targeting miR-466, and thus down-regulated LYAR expression. These findings provide a new sight for understanding the molecular mechanism of lung SCC and indicate that LINC00355 may serve as a potential biomarker for the diagnosis and treatment of lung SCC.
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Full text: Available Index: LILACS (Americas) Main subject: Carcinoma, Squamous Cell / RNA, Long Noncoding / Lung Neoplasms Type of study: Prognostic study Limits: Humans Language: English Journal: Braz. j. med. biol. res Year: 2020 Type: Article Institution/Affiliation country: The Second Clinical Medical College of Jinan University/CN

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Full text: Available Index: LILACS (Americas) Main subject: Carcinoma, Squamous Cell / RNA, Long Noncoding / Lung Neoplasms Type of study: Prognostic study Limits: Humans Language: English Journal: Braz. j. med. biol. res Year: 2020 Type: Article Institution/Affiliation country: The Second Clinical Medical College of Jinan University/CN