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Long non‑coding RNA SNHG3 promotes the development of non‑small cell lung cancer via the miR‑1343‑3p/NFIX pathway.

ABSTRACT: The aim of the present study was to identify the function of long non‑coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) and examine its effects on non‑small cell lung cancer (NSCLC). A series of in vitro experiments were employed to evaluate the effects of SNHG3 on the progression of NSCLC, including Cell Counting Kit‑8, 5‑Ethynyl‑2'‑deoxyuridine, flow cytometry, wound healing, Transwell, western blotting and reverse transcription‑quantitative PCR assays. Bioinformatics analyses and a luciferase reporter assay were performed to identify the target gene of SNHG3 and microRNA (miR)‑1343‑3p. Finally, recuse experiments were conducted to verify the effect of SNHG3 and its target gene on proliferation, apoptosis, migration and invasion. The findings indicated that lncRNA SNHG3 was highly expressed in NSCLC tissues and cell lines. Knockdown of lncRNA SNHG3 inhibited cell proliferation, migration and invasion, and accelerated cell apoptosis in NSCLC cell lines. The results of the bioinformatics analysis and the luciferase reporter assay indicated that lncRNA SNHG3 directly bound to miR‑1343‑3p and that it could downregulate the expression levels of miR‑1343‑3p to promote the progression of NSCLC. Rescue experiments indicated that lncRNA SNHG3 increased nuclear factor IX (NFIX) expression by sequestering miR‑1343‑3p in NSCLC. These results suggested that the SNHG3/miR‑1343‑3p/NFIX axis may serve as a novel prognostic biomarker and therapeutic target for NSCLC.

SUBMITTER: Zhao L

PROVIDER: S-EPMC8208627 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundWe have previously developed a unique metastasis-associated signature consisting of six long non-coding RNAs (lncRNAs), including a novel lncRNA, namely LINC02323. In the present study, we aimed to investigate the underlying roles of LINC02323 in the migration, invasion and TGF-β-induced epithelial-mesenchymal transition (EMT) of lung adenocarcinoma (LUAD) cells.MethodsThe distribution of LINC02323 was detected by the nuclear-plasma separation experiment. Cell proliferation was assessd by MTT assay, and cell migration and invation were detected by transwell assays. EMT was detected by RT-qPCR and western blotting. Interaction between miRNA and LINC02323 was predicted by starBase v2.0 and confirmed by the double luciferase reporting system.ResultsLINC02323 was distributed in the cytoplasm and nucleus. The overexpression or deletion of LINC02323 did not affect the proliferation of LUAD cells, while significantly affected the migration and invasion of LUAD cells. TGF-β-induced EMT process was significantly affected by both RNA interference (RNAi) and overexpression of LINC02323. The predicted results showed that there were binding sites between LINC02323 and miR-1343-3p. The expression of LINC02323 was found to be negatively correlated with miR-1343-3p in LUAD by analyzing The Cancer Genome Atlas (TCGA) database. The double luciferase reporting system, RT-qPCR and western blotting experiments confirmed that LINC02323 could bind to miR-1343-3p, which bound to TGF-β receptor 1 (TGFBR1). Inhibition of miR-1343-3p reversed LINC02323 silencing-mediated suppression of migration, invasion and EMT.ConclusionsLINC02323 acts as a competing endogenous RNA (ceRNA), which sponged miR-1343-3p to upregulate the TGFBR1 expression and promote the EMT and metastasis in LUAD.Key pointsSIGNIFICANT FINDINGS OF THE STUDY: LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma.What this study addsLINC02323 is a key molecule in the process of invasion and metastasis of LUAD and might be used as a potential target in metastatic cancer.

Project description:Long non-coding RNAs (lncRNAs) are important biological factors that contribute to the initiation and progression of different types of cancer, including gastric, bladder and colorectal cancer. Small nucleolar RNA host gene 3 (SNHG3) has been implicated in prostate cancer (PCa) progression. However, the expression pattern and function of SNHG3 in PCa remain unclear, impeding the development of novel treatment strategies for this cancer. The present study aimed to investigate a combination of molecular and biochemical approaches to determine the role of SNHG3 in patients at different stages of disease, and elucidate the pathway by which SNHG3 affects PCa progression. A Cell Counting Kit-8 assay was used to assess cell proliferation. Transwell assays were used to analyze cell migration and invasion. Reverse transcription-quantitative PCR and western blotting were used to evaluate the expression levels of RNAs and proteins, respectively. The results demonstrated that SNHG3 expression was upregulated in PCa tissues downloaded from The Cancer Genome Atlas database, which was associated with poor prognosis. Furthermore, cell proliferation, migration and invasion were significantly inhibited following SNHG3 knockdown in vitro, the effects of which were reversed following overexpression of SNHG3 in PCa cells. Bioinformatic analysis revealed that microRNA (miRNA/miR)-1827 was a downstream target of SNHG3. The direct interaction between SNHG3 and miR-1827 was validated via the dual-luciferase reporter and RNA immunoprecipitation assays. Pearson's correlation analysis demonstrated that SNHG3 expression was negatively correlated with miR-1827 expression at different stages of PCa. Furthermore, rescue assays indicated that cotransfection with small interfering-SNHG3 and miR-1827 inhibitor reversed the effects of SNHG3 knockdown on cell proliferation, migration and invasion. In addition, SNHG3 knockdown in vivo suppressed tumor growth. Notably, lncRNA SNHG3 promoted PCa progression through miR-1827 via the Wnt/AKT/mTOR pathway. Taken together, the results of the present study suggest that SNHG3 promotes PCa progression by sponging miR-1827, indicating that SNHG3 may be a promising diagnostic and therapeutic target of PCa.

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Long non‑coding RNA SNHG3 promotes the development of non‑small cell lung cancer via the miR‑1343‑3p/NFIX pathway.

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