Background: Non-small cell lung cancer (NSCLC) is a great threat to human health and the biology of the NSCLC still remains largely unknown. Aberrantly expressed long non-coding RNA (lncRNA) Small nucleolar RNA host gene 6 (SNHG6) was involved in the tumorigenesis and progression of various cancers. The aim of this study is to investigate the roles of SNHG6 in NSCLC.
Methods: qRT-PCR and Western blot assays were applied to detect gene expressions. Cell proliferation and migration assays were used to analyze the gene functions. Luciferase reporter assay, RNA Immunoprecipitation assay and Chromatin immunoprecipitation assay were performed to investigate the molecular mechanism.
Results: We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR-944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9.
Conclusion: Our study illustrates that SNHG6 is an oncogene in NSCLC and involved in NSCLC tumorigenesis by regulating ETS1 signaling via miR-944 and miR-181d-5p.
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http://dx.doi.org/10.2147/OTT.S235336 | DOI Listing |
Appl Biochem Biotechnol
January 2025
Department of Neurosurgery, General Medical 300 Hospital, No. 420 Huanghe Road, Guiyang City, 550006, Guizhou Province, China.
Spinal cord injury (SCI) is one of the devastating neurological disorders that leads to a loss of motor and sensory functions. Long non-coding RNA small nucleolar RNA host gene 6 (lncRNA SNHG6) plays a crucial role in inflammatory regulation across various diseases. This study investigates the role of SNHG6 in SCI development and its underlying regulatory mechanisms.
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University, 1-7-1, Sakamoto, Nagasaki 852-8588, Japan.
Although osteoclasts play crucial roles in the skeletal system, the mechanisms that underlie oxidative stress during osteoclastogenesis remain unclear. The transcription factor Nrf2 and its suppressor, Keap1, function as central mediators of oxidative stress. To further elucidate the function of Nrf2/Keap1-mediated oxidative stress regulation in osteoclastogenesis, DNA microarray analysis was conducted in this study using wild-type (WT), knockout ( KO), and knockout ( KO) osteoclasts.
View Article and Find Full Text PDFMol Biol (Mosk)
December 2024
Laboratory of Functional Genomics, Research Centre for Medical Genetics, Moscow, 115522 Russia.
Long non-coding RNAs (lncRNAs) are involved in many cellular processes while displaying high tissue specificity. In contrast, protein-coding genes, including the category of housekeeping ones, exhibit broad expression patterns. The aim of this study was to highlight the functional importance of widely expressed lncRNAs.
View Article and Find Full Text PDFMol Biol (Mosk)
December 2024
Institute of General Pathology and Pathophysiology, Moscow, 125315 Russia.
Ovarian cancer (OC) develops asymptomatically and escapes diagnosis until advanced stages, the feature contributing to a higher mortality rate. New prospects of OC diagnosis and treatment have been opened in studies of the gene regulation mechanisms that involve long noncoding RNAs (lncRNAs) and identification of the lncRNA genes that are inhibited via methylation of the promoter region. A set of 122 samples of primary OC tumors was examined by methylation specific real-time PCR to assess the methylation level of the lncRNA genes PLUT, SNHG1, SNHG6, SNHG12, and TINCR.
View Article and Find Full Text PDFDig Dis Sci
December 2024
Translational Research Institute, Henan University, Kaifeng, People's Republic of China.
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