NRIP1 aggravates lung injury caused by Pseudomonas aeruginosa in mice by increasing PIAS1 ubiquitination.

Recently, evidence has shown that nuclear receptor interacting protein 1 (NRIP1) is involved in acute lung injury (ALI) progression, but the specific mechanism remains unclear. Pseudomonas aeruginosa (PA)-treated TC-1 cells were transfected with pcDNA-NRIP1 or si-NRIP1, and we found that overexpression of NRIP1 inhibited cell viability and promoted cell apoptosis and secretion of inflammatory factors, and transfection of si-NRIP1 reversed these effects. Furthermore, online bioinformatics analysis and co-immunoprecipitation assay results indicated that NRIP1 could bind to Ubiquitin Conjugating Enzyme E2I (UBE2I), and promoted UBE2I expression. Next, the PA-treated TC-1 cells were transfected with si-NRIP1 alone or together with pcDNA-UBE2I, and we observed that transfection with si-NRIP1 inhibited UBE2I expression, promoted cell viability, and reduced cell apoptosis and inflammatory factor secretion, which could be reversed by UBE2I overexpression. Moreover, UBE2I could bind to protein inhibitor of activated signal transducer and activators of transcription 1 (PIAS1). Overexpression of NRIP1 promoted UBE2I expression and inhibited PIAS1 expression, and NRIP1 promoted PIAS1 ubiquitination and degradation by UBE2I. The PA-treated TC-1 cells were transfected with si-UBE2I alone or together with si-PIAS1, and the results indicated that transfection of si-UBE2I had the same effect as transfection of si-NRIP1. Finally, our in vivo findings indicated that the expression of NRIP1 and UBE2I was decreased, and PIAS1 expression was increased, in the lung tissues of mice with NRIP1 knocked-down, and the inflammatory infiltration in the lung tissue was reduced. In conclusion, our study demonstrates that NRIP1 aggravates PA-induced lung injury in mice by promoting PIAS1 ubiquitination.

lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressor miR-615-5p.

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In the present study, we investigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P<0.0001). The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2, and SHMT2 Moreover, miR-615-5p mimic could antagonize the promoting effect of Gm15290 on cell proliferation and invasion.

LncRNA Gm15290 Promotes Cell Proliferation and Invasion in Non-Small Cell Lung Cancer Through Directly Interacting With and Suppressing the Tumor Suppressor miR-615-5p.

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In this study, weinvestigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly upregulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells, and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion, and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNAhybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P < 0.0001). The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2 and SHMT2. Moreover, miR-615-5p mimic could antagonize the promoting effect of Gm15290 on cell proliferation and invasion.

Extraction, characterization of a Ginseng fruits polysaccharide and its immune modulating activities in rats with Lewis lung carcinoma.

In this study, one polysaccharide (GFP1), with an average molecular weight of 1.4 × 10(5)Da, was isolated from Ginseng fruits. GFP1 was composed of galactose, glucose, rhamnose, and arabinose in a molar ratio of 6.1:2.0:1.1:3.2, and had a backbone mainly consisting of (1 → 6)-linked-Galp, (1 → 3,6)-linked-Galp and (1 → 3,6)-linked-Glcp residues, which was terminated with terminal (1 →)-linked-Araf or -Rhap attached to O-3 position of (1 → 3,6)-linked-Galp and (1 → 3,6)-linked-Glcp. We also evaluated the effect of GFP1 on anti-tumor immune response in Lewis lung carcinoma (LLC)-bearing mouse model and explored the possible mechanism. GPF1 could significantly inhibit tumor growth and lung metastasis in vivo, increase the relative spleen and thymus weight, promote ConA or LPS-induced spleen lymphocytes proliferation, elevate the activities of NK cell in spleen, and increase the serum concentration of interleukin-2 (IL-2) and interferon-γ (IFN-γ), as well as the ratio of CD4(+)/CD8(+) in LLC-bearing mice. All these findings implied that GFP1 could effectively inhibit tumor growth and lung metastasis via activating immune function and provide insights into the mechanism of GFP1 in the prevention and treatment of lung cancer.