Objective: LRRC59 (leucine-rich repeat-containing protein 59) is a ribosome-binding protein which also interacts with the fibroblast growth factor. limited investigation reveals the possibility of LRRC59 role in aggressive phenotype of breast cancer. However, if LRRC59 contribute to the development of lung cancer is still unclear.
Materials and Methods: In this study, a software-based survival analysis TCGA online (GEPIA2) was used to estimate the prognostic value LRRC59 mRNA expression levels for lung cancer. Cells Counting Kit-8 assay, colony-forming assay, cell cycle analysis, and transwell test used to assess the biological function LRRC59 in lung cancer cells. Then, 94 lung adenocarcinoma (LUAD) patient tissue were collected to test the level LRRC59 expression by tissue microarray (TMA) based immunohistochemical staining (IHC). Kaplan-Meier univariate and multivariate Cox regression analysis was performed to evaluate the prognostic value of protein expression in LUAD LRRC59.
Results: High Level of LRRC59 mRNA was significantly associated with poorer survival for lung adenocarcinoma, but not for lung squamous cell carcinoma. ShRNA knockdown of LRRC59 by apparently inhibiting cell proliferation and colony formation in both H1299 and A549 cells. G1 / S phase arrest caused by depletion LRRC59 observed in A549 and H1299 cells. In addition, silencing LRRC59 decreased migrative cells and invasive ability. In addition, the TMA-based IHC showed that it was highly expressed in LRRC59 LUAD network and closely associated with lymph node metastasis (P <0.001), TNM stage (P <0.001), and histological differentiation (P = 0.007). Further multivariate analysis showed that excessive LRRC59 an independent prognostic factor in LUAD.
Conclusion: LRRC59 can serve as novel biomarkers and therapeutic targets for clinical practice LUAD.
Overexpression of LRRC59 Is Associated with Poor Prognosis and Promotes Cell Proliferation and Invasion in Lung Adenocarcinoma
LncRNA MIR4435-2HG inhibit the progression of osteoarthritis through sponges mir-510-3p
Osteoarthritis (OA) is a joint disorder diarthrodial which can have several causes. Long non-coding RNA (lncRNAs) participated in several diseases, including OA. Recently reported that microRNA lncRNA 4435-2HG (MIR4435-2HG) is downregulated in OA tissue; However, the biological role during the progression of OA MIR4435-2HG still unclear. In this study, interleukin (IL) -1β used to build an in vitro model of OA. protein expression of matrix metallopeptidase (MMP) 1, MMP13, collagen II, interleukin (IL) -17A, p65, phosphorylated (p) -p65, IκB and p-IκB in CHON-001 cells were detected by western blotting.
Gene expression of IL-17A, and miR-510-3p MIR4435-2HG network or CHON-001 cells was measured by reverse transcription-quantitative PCR and western blotting, respectively. Cells Counting Kit-8 assay and immunofluorescence staining were used to investigate cell proliferation, and cell apoptosis was detected by flow cytometry. The relationship between MIR4435-2HG, miR-510-3p and IL-17A was investigated using a dual luciferase assay report. MIR4435-2HG and excess miR-510-3p CHON-transfected into 001 cells.
The results show that excess miR4435-2HG significantly increase proliferation and inhibit apoptosis CHON-001 cells. In addition, miR-510-3p identified as a downstream target MIR4435-2HG, and miR-510-3p directly targeted IL-17A. The results of this study indicate that MIR4435-2HG can mediate the development of OA by disabling NF-kB signaling pathway.
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