Abstract
The lncRNA small nucleolar host gene 3 (SNHG3) was discovered to play an important role in the occurrence and development of lung adenocarcinoma (LUAD). However, the underlying molecular mechanism of SNHG3 in LUAD remains unclear. In the present study, SNHG3 expression levels in LUAD tissues and cell lines were analyzed using reverse transcription-quantitative PCR. The effects of SNHG3 on the proliferation, apoptosis, migration, and invasion of LUAD cells were determined using Cell Counting Kit-8, colony formation, flow cytometry, wound healing, and Transwell chamber assays, respectively. The specific underlying mechanism of SNHG3 in LUAD was investigated using bioinformatics analysis and a dual luciferase reporter assay. The results revealed that SNHG3 expression levels were downregulated in LUAD tissues and cell lines. Functionally, SNHG3 overexpression suppressed the proliferation, migration, and invasion of LUAD cells, while promoting apoptosis. Mechanistically, microRNA- (miR-) 890 was identified as a potential target of SNHG3, and its expression was negatively regulated by SNHG3. Notably, SNHG3 was found to promote LUAD progression by targeting miR-890. In conclusion, the findings of the present study revealed that lncRNA SNHG3 promoted the occurrence and progression of LUAD by regulating miR-890 expression.
Highlights
Lung cancer is a common type of cancer with high incidence and mortality rates worldwide [1]
Similar to the patient studies, small nucleolar host gene 3 (SNHG3) expression levels were found to be markedly downregulated in Lung adenocarcinoma (LUAD) cell lines (A549, H1299, and H1975) compared with 16HBE cells (Figure 1(c)). e expression levels of SNHG3 were downregulated to the greatest extent in A549 and H1299 cells; these two cell lines were selected for use in subsequent experiments. ese results indicated that SNHG3 expression levels may be significantly downregulated in LUAD tissues and cells
The Long noncoding RNAs (lncRNAs) SNHG3 was discovered to serve as a competing endogenous RNA to regulate the progression of various cancer types [18,19,20]
Summary
Lung cancer is a common type of cancer with high incidence and mortality rates worldwide [1]. Non-small-cell lung cancer (NSCLC) represents ∼85% of all lung cancer types and has a mortality rate of ∼50%. Lung adenocarcinoma (LUAD), a leading cause of cancer-related mortality, accounts for ∼40% of NSCLCs and has a 5-year survival rate of only 15% [2]. For more than half a century, even with the significant progress and development made in molecular biology, oncology, and medicinal technology, the treatment of LUAD has been and remains ineffective [5]. A large number of molecular biology studies have focused on investigating the mechanisms underlying LUAD, the exact molecular mechanism of LUAD remains unclear
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