Long non-coding RNA transmembrane and coiled-coil domain family 1 antisense RNA 1 (TMCC1-AS1) has been frequently reported to be associated with prognosis in patients with liver cancer (LC). However, the biological role of TMCC1-AS1 in LC in vitro remains unclear. The expression levels of TMCC1-AS1 in primary tumor tissues and LC cell lines were determined using reverse transcription-quantitative PCR. The associations between TMCC1-AS1 expression and the clinicopathological factors of patients with LC were statistically analyzed using the χ 2 test. The role of TMCC1-AS1 in LC prognosis was assessed using Kaplan-Meier curves and proportional hazards model (Cox) analysis. Cell proliferation was determined by Cell Counting Kit-8 and colony formation assays. Transwell assays were performed to determine migration and invasion. TMCC1-AS1 expression was found to be significantly upregulated in LC tissues and cell lines compared with the corresponding controls. High TMCC1-AS1 expression was associated with advanced TNM stage and lymph node metastasis. Furthermore, high TMCC1-AS1 expression predicted poor survival in patients with LC. Knockdown of TMCC1-AS1 significantly inhibited the proliferation, migration and invasion of HepG2 and SNU-182 cells, while overexpression of TMCC1-AS1 had the opposite effect in HepG2 and SNU-182 cells. At the molecular level, downregulation of TMCC1-AS1 expression resulted in increased E-cadherin expression and decreased proliferating cell nuclear antigen, Ki67, N-cadherin and Vimentin expression in HepG2 cells. Overexpression of TMCC1-AS1 had the opposite effects on these factors in SNU-182 cells. In conclusion, the present findings indicated that TMCC1-AS1 might be considered as a novel oncogene, which promotes cell proliferation and migration, and may be a potential therapeutic target for LC.

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Neutrophil gelatinase-associated lipocalin (NGAL), also called lipocalin 2, is considered a promising biomarker for acute and chronic kidney injuries. Several studies have demonstrated that its levels increase in plasma and urine in diabetic nephropathy (DN), and its urine concentration increases upon kidney function deterioration. However, its role in DN progression remains unclear. The current study used in vitro gene expression knockdown in human proximal tubular cell line human kidney (HK)2 to investigate the role of NGAL in oxidation and extracellular matrix secretion under high-glucose (HG) incubation. In addition, type 1 diabetes was induced in vivo in knockout NGAL-/and wild-type mice in order to investigate role of NGAL in the progression of DN. The results demonstrated that NGAL knockdown in HK2 cells significantly increased oxidative stress under HG stimulation tested by flow cytometry, and increased the secretion of interleukin-6, fibronectin (FN) and collagen IV examined by ELISA. Western blotting demonstrated that the phosphorylation of Smad2/3 also increased in HK2 cells under transforming growth factor-β1 stimulation. In vivo experiments demonstrated that diabetic NGAL-/mice showed deteriorated renal function compared with that of diabetic wild-type mice. Histopathological analysis suggests that diabetic NGAL-/mice had more serious glomerulosclerosis and tubular vascular degeneration than wild-type mice. Immunohistochemistry suggested that the absence of NGAL lead to increased FN deposition in glomeruli in a mouse model of DN. In conclusion, NGAL appears to have renal protective effects by slowing down the progression of DN, and its effect may be associated with a reduction in oxidation, fibrosis and inflammation.