LncRNA SNHG1 contributes to the cisplatin resistance and progression of NSCLC via miR-330-5p/DCLK1 axis.

Long non-coding RNAs (lncRNAs) are involved in the occurrence and progression of multiple cancers, including non-small cell lung cancer (NSCLC). Herein, we explored the exact role and underlying mechanism of lncRNA small nucleolar RNA host gene 1 (SNHG1) in NSCLC. The levels of SNHG1, microRNA-330-5p (miR-330-5p) and doublecortin-like kinase 1 (DCLK1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was carried out to measure the chemoresistance and proliferation of NSCLC cells. The metastasis and apoptosis of NSCLC cells were examined by transwell migration and invasion assays and flow cytometry. Western blot assay was conducted to detect the levels of proliferation-associated proteins and DCLK1. The interaction between miR-330-5p and SNHG1 or DCLK1 was predicted by StarBase and microT_CDS databases. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to validate these interactions. In vivo chemosensitivity experiment was conducted to assess the function of SNHG1 in the chemoresistance of NSCLC in vivo. SNHG1 was dramatically up-regulated in cisplatin (DDP)-resistant NSCLC tissues and cells. SNHG1 promoted the DDP resistance and malignant behaviors of NSCLC cells. SNHG1 functioned through targeting miR-330-5p, and si-SNHG1-mediated effects in NSCLC cells were attenuated by the addition of in-miR-330-5p. DCLK1 messenger RNA (mRNA) could directly bind to miR-330-5p, and miR-330-5p acted as a tumor suppressor in NSCLC through down-regulating DCLK1. SNHG1 silencing elevated the DDP sensitivity of NSCLC cells in vivo. SNHG1 elevated DDP resistance and malignant potential of NSCLC cells through elevating the level of DCLK1 via sponging miR-330-5p.

Ge P ，Cao L ，Zheng M ，Yao Y ，Wang W ，Chen X ... -  《-》

Long non-coding RNA SNHG1 contributes to cisplatin resistance in non-small cell lung cancer by regulating miR-140-5p/Wnt/β-catenin pathway.

Shi SL ，Zhang ZH 《NEOPLASMA》

Circ_PIP5K1A regulates cisplatin resistance and malignant progression in non-small cell lung cancer cells and xenograft murine model via depending on miR-493-5p/ROCK1 axis.

Chemoresistance limits the therapeutic effect of cisplatin (DDP) on non-small cell lung cancer (NSCLC). Circular RNAs (circRNAs) function as important regulators in chemoresistance. This study aimed to explore the regulation of circRNA Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Alpha (circ_PIP5K1A) in DDP resistance. The expression analysis of circ_PIP5K1A, micoRNA-493-5p (miR-493-5p) and Rho Associated Coiled-Coil Containing Protein Kinase 1 (ROCK1) was conducted through reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell sensitivity was determined using 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyl tetrazolium bromide (MTT) assay. Cell proliferation and cell viability were evaluated by colony formation assay and MTT assay, respectively. Cell cycle and apoptosis detection was performed via flow cytometry. Cell motility was examined by transwell migration or invasion assay. Dual-luciferase reporter assay was applied to confirm the target binding. ROCK1 protein level was assayed via Western blot. In vivo assay was carried out using xenograft model in mice. Circ_PIP5K1A level was abnormally increased in DDP-resistant NSCLC tissues and cells. Silencing circ_PIP5K1A reduced DDP resistance, proliferation, cell cycle progression and cell motility in DDP-resistant NSCLC cells. Circ_PIP5K1A directly interacted with miR-493-5p in NSCLC cells. The function of circ_PIP5K1A was dependent on the negative regulation of miR-493-5p. MiR-493-5p directly targeted ROCK1 and circ_PIP5K1A regulated the ROCK1 level via acting as a sponge of miR-493-5p. Overexpression of miR-493-5p inhibited chemoresistance and cancer progression by downregulating ROCK1 expression in DDP-resistant NSCLC cells. Circ_PIP5K1A regulated DDP sensitivity in vivo via the miR-493-5p/ROCK1 axis. These findings suggested that circ_PIP5K1A upregulated the ROCK1 expression to promote DDP resistance and cancer progression in NSCLC by sponging miR-493-5p.

Feng N ，Guo Z ，Wu X ，Tian Y ，Li Y ，Geng Y ，Yu Y ... -  《RESPIRATORY RESEARCH》

LncRNA SNHG1 influences cell proliferation, migration, invasion, and apoptosis of non-small cell lung cancer cells via the miR-361-3p/FRAT1 axis.

Non-small-cell lung cancer (NSCLC) is the most lethal type of cancer. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as crucial regulators in the development of NSCLC. The aim of our study was to explore the molecular mechanism of SNHG1 to enable better treatment for NSCLC patients. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of Small nucleolar RNA host gene 1 (SNHG1), miR-361-3p and frequently rearranged in advanced T-cell lymphomas 1 (FRAT1). The protein level of FRAT1 was measured by western blot assay. Cell proliferation was evaluated by methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells were counted by transwell assay. The relationship between miR-361-3p and SNHG1 or FRAT1 was confirmed by dual-luciferase reporter assay. Our results indicated that SNHG1 and FRAT1 were highly expressed in NSCLC tissues and cells. SNHG1 silencing inhibited proliferation, induced apoptosis and blocked migration and invasion of NSCLC cells. Also, FRAT1 downregulation suppressed proliferation, promoted apoptosis and hindered migration and invasion of NSCLC cells. Further, FRAT1 could recover the effects of SNHG1 silencing on proliferation, apoptosis, migration and invasion of NSCLC cells. SNHG1 sponged miR-361-3p and negatively regulated miR-361-3p expression. Meanwhile, miR-361-3p targeted FRAT1 and inversely modulated FRAT1 expression. In addition, miR-361-3p inhibition abated the effect of SNHG1 knockdown on FRAT1 expression. In conclusion, LncRNA SNHG1 promoted the proliferation, repressed apoptosis and enhanced migration and invasion of NSCLC cells by regulating FRAT1 expression via sponging miR-361-3p.

Li X ，Zheng H 《-》

Upregulation of Long Noncoding RNA (lncRNA) X-Inactive Specific Transcript (XIST) is Associated with Cisplatin Resistance in Non-Small Cell Lung Cancer (NSCLC) by Downregulating MicroRNA-144-3p.

Tian LJ ，Wu YP ，Wang D ，Zhou ZH ，Xue SB ，Zhang DY ，Wei YG ，Liu W ... -  《MEDICAL SCIENCE MONITOR》