Long non-coding RNA LINC01116 accelerates the progression of keloid formation by regulating miR-203/SMAD5 axis

BackgroundEmerging evidence reveals the importance of long non-coding RNAs (lncRNAs) in the development and progression of keloid formation. However, the roles and molecular mechanism of lncRNA LINC01116 in the progression of keloid formation remain largely unknown.MethodsThe expression levels of LINC01116, microRNA-203 (miR-203) and SMAD family member 5 (SMAD5) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell proliferation, migration and invasion were detected by Cell counting Kit-8 (CCK-8) assay and transwell assay. Flow cytometry and western blot assay were used to examine cell apoptosis and extracellular matrix (ECM) production. The interaction between miR-203 and LINC01116 or SMAD5 was predicted by bioinformatics analysis and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) and RNA pull-down assays.ResultsLINC01116 and SMAD5 were upregulated while miR-203 was downregulated in keloid tissues and keloid fibroblasts. LINC01116 knockdown suppressed the proliferation, migration, invasion, and ECM production but induced apoptosis in keloid fibroblasts through enhancing miR-203 and inhibiting SMAD5. Moreover, SMAD5 was identified as a direct target of miR-203 and miR-203 could directly bind to LINC01116. Besides, LINC01116 regulated SMAD5 expression by targeting miR-203.ConclusionDownregulation of LINC01116 inhibited the progression of keloid formation by regulating miR-203/SMAD5 axis, which might provide a novel target for keloid therapy.     

Novel long noncoding RNA LINC02323 promotes cell growth and migration of ovarian cancer via TGF‐β receptor 1 by miR‐1343‐3p

BackgroundThis study was aimed at investigating the effects of long noncoding RNA (lncRNA) LINC02323 in ovarian cancer and its possible mechanism.MethodsMicroarray analysis and QPCR were utilized to identify lncRNA LINC02323 expression in patients with ovarian cancer. MTT assay was used for analysis of ovarian cancer cell proliferation. Western blot was utilized to investigate its possible mechanism.ResultsIn patients with ovarian cancer, lncRNA LINC02323 expression was up‐regulated and miR‐1343‐3p expression was down‐regulated. Over‐expression of lncRNA LINC02323 promoted cell growth and reduced LDH activity levels in vitro model by suppression of miR‐1343‐3p expression. Down‐regulation of lncRNA LINC02323 reduced cell growth and increased LDH activity levels in vitro model by induction of miR‐1343‐3p expression. Over‐expression of miR‐1343‐3p reduced cell growth and reduced LDH activity levels in vitro model by suppression of TGF‐β receptor. Down‐regulation of miR‐1343‐3p promoted cell growth and reduced LDH activity levels in vitro model by induced of TGF‐β receptor.ConclusionOur findings show that Novel long noncoding RNA LINC02323 promotes cell growth of ovarian cancer via TGF‐β receptor 1 by miR‐1343‐3p.     

LINC00346 regulates glycolysis by modulation of glucose transporter 1 in breast cancer cells

Most cancer cells preferentially metabolize glucose by glycolysis rather than oxidative phosphorylation to proliferate efficiently. LncRNAs have been proposed as crucial regulators in pathophysiological processes including cell growth, apoptosis and glucose metabolism. However, little is known regarding the specific role of LINC00346 in regulating glucose metabolism in breast cancer. LINC00346 and miR-148a/b expression in breast cancer cells was detected by qRT-PCR. The relationships between LINC00346, glucose transporter 1 (GLUT1) and miR-148a/b in breast cancer cells were explored by luciferase reporter assay. Cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Glycolysis was detected by measuring the glucose uptake and lactate production. Results showed that LINC00346 was over-expressed while miR-148a/b was low-expressed in breast cancer cells. miR-148a/b were direct targets of LINC00346 in breast cancer cells. LINC00346 knockdown inhibited cell proliferation and glycolysis, and induced apoptosis by upregulating miR-148a/b in breast cancer cells. Furthermore, we found that LINC00346 knockdown repressed GLUT1 expression in breast cancer cells by upregulating miR-148a/b. In conclusion, LINC00346 knockdown suppressed breast cancer cell glycolysis by upregulating miR-148a/b and repressing GLUT1 expression.     

LINC01207 promotes prostate cancer progression by sponging miR-1182 to upregulate AKT3

Prostate cancer (PC) is recognized as a common malignancy in male patients. Long non-coding RNA (lncRNA) has been implicated in the development of PC. Recently, long intergenic non-protein coding RNA 1207 (LINC01207) has been reported to regulate the carcinogenesis of multiple cancer types. However, its role in the progression of PC remains to be determined. The aim of the present study was to investigate the expression profile, clinicopathological implication and molecular mechanism of action of LINC01207 in the progression of PC. LINC01207 expression levels were compared between PC tumor and paired normal tissue samples from The Cancer Genome Atlas. The expression of LINC01207 was further analyzed in PC cell lines and a normal prostatic cell line. The role of LINC01207 in proliferation, migration and invasion of PC cells was examined using small interfering RNA-mediated silencing. Western blot analysis was used to investigate the changes in protein levels underlying the mechanism of action of LINC01207. The role of LINC01207 in tumorigenesis was evaluated in a xenograft model. LINC01207 was upregulated in PC tumor samples from TCGA data compared with paired normal tissue. LINC01207 expression was significantly increased in PC cells and tumor tissues compared with in normal prostate cells (RWPE1) and normal prostate tissues, respectively. Furthermore, LINC01207 silencing inhibited PC cell proliferation and colony formation and induced apoptosis. Mechanistic experiments showed that LINC01207 promoted carcinogenesis by sponging miR-1182 to regulate the protein levels of AKT3 in PC cell lines. Thus, the findings of the present study indicated that LINC01207 might play a role in the tumorigenesis of PC and may serve as a therapeutic target for PC treatment.     

A novel lncRNA-LINC01116 regulates tumorigenesis of glioma by targeting VEGFA

Brain glioma is the most common malignant tumor of the central nervous system, and one of the leading causes of death in patients with intracranial tumors. The clinical outcome of glioma is usually poor due to abundant vascularity, fast growth and susceptibility of invasion to normal brain tissues. Our microarray study showed that lncRNA-LINC01116 was significantly upregulated in glioma tissues and played an important role in cell proliferation, cycle, migration, invasion and angiogenesis. In addition, vascular endothelial growth factor (VEGFA) may be the major target genes in the downstream of lncRNA-LINC01116. Dual luciferase assay showed that LINC01116 and VEGFA both contained a miR-31-5p binding site, and LINC01116 could regulate the expression of VEGFA through competitive absorption of miR-31-5p. RNA immunoprecipitation indicated that LINC01116 and VEGFA were present in the miR-31-5p-RISC complex, and biotinylated miR-31-5p pull-down assay suggested that there was a competitive relationship between LINC01116 and VEGFA to bind with miR-31-5p. Collectively, our study has identified a novel lncRNA-LINC01116 and clarified the role and mechanism of LINC01116 in the tumorigenesis of glioma. LINC01116 may prove to be a potential target for the clinical diagnosis and treatment of glioma.     

Clinical Significance of CA-199 and LINC01197 in Pancreatic Cancer

This study aimed to explore the expression and clinical significance of LINC01197 in the serum of patients with pancreatic cancer (PC). Methods: A total of 50 PC patients (patient group) treated in our hospital from March 2012 to April 2014 were collected, and another 50 healthy people (normal group) were collected for physical examination. The expression of LINC01197 in the serum of the two groups was detected by qRT-PCR method, and the expression of CA-199 in serum was detected by Roche automatic biochemistry. The expression and diagnostic values of CA-199 and LINC01197 in PC were analyzed, and the relationship between LINC01197 and the prognosis of PC patients was observed. Results: The expression of CA-199 in the patient group was significantly higher than in the normal group (p < 0.001). The area under the curve was 0.791 and 0.944, respectively. The incidence rate of Phases III + IV, lymphatic invasion, and distant metastasis in patients with low expression of LINC01197 is significantly higher than that in patients with high expression and has higher diagnostic value. With the progress of clinical staging, the expression of TNM gradually decreased and there were differences between groups (p < 0.001). Sperman test analysis found that the decreased TNM staging of LINC01197 gradually increased (r = – 0.816, p < 0.001), and the area under the curve of LINC01197 distinguishing phase I and phase II + phase III + phase IV was 0.930. The 1-year survival rate and 5- year survival rate of patients in low expression group are lower than those in the high expression group (P1 year = 0.037, P5 year = 0.014). Distant metastasis is an independent prognostic factor for PC patients to survive for 1 to 5 years. Differentiation, TNM staging, and LINC01197 are independent prognostic factors for PC patients to survive for 5 years. Conclusion: The low expression of LINC01197 in PC patients indicates poor prognosis of patients and is expected to be a potential diagnostic and prognostic indicator of PC.     

LncRNA LINC00261下调miR-620表达调控鼻咽癌放射敏感性实验研究

目的:探讨LINC00261对鼻咽癌放射敏感性影响及其作用机制。方法:用qRT-PCR检测放射敏感、放射抵抗鼻咽癌组织中miR-620和LINC00261的相对表达水平。采用0、2、4、6、8 Gy 60Coγ射线照射鼻咽癌细胞系6-10B、HNE-3细胞后,qRT-PCR法检测miR-620和LINC0...     

长链非编码RNA LINC00641通过微小RNA-181d-5p靶向真核细胞翻译起始因子4A2抑制宫颈癌细胞增殖的研究

目的 观察长链非编码RNA(LncRNA)LINC00641(LINC00641)在宫颈癌细胞中的表达特征,探讨LINC00641通过微小RNA-181 d-5p(miR-181 d-5p)/真核细胞翻译起始因子4A2(EIF4A2)对宫颈癌细胞增殖的调节作用.方法 选择宫颈癌Hela细胞株,建立空白对照组,构建转染p...