Function Of LINC00152 Research Articles

LINC00511 promotes lung squamous cell carcinoma proliferation and migration via inhibiting miR-150-5p and activating TADA1.

BackgroundRecently, accumulating data have supported that long non-coding RNAs (lncRNAs) may contribute to tumorigenesis. LncRNA LINC00511 (LINC00511) has been proved to serve as an oncogene in several tumors. However, as a novel lncRNA, the crucial role and potential mechanism of LINC00511 in LUSC is largely unknown.MethodsHere, we performed a differential gene expression analysis of the LINC00511 in LUSC using data from TCGA database. Loss-of-functional assays were used to gain further insights into the latter function of LINC00511 on the malignant phenotypes in vitro. Meanwhile, qRT-PCR, western blot, dual-luciferase reporter, and RIP assays were utilized to highlight the molecular basis of LINC00511 in LUSC.ResultsLINC00511 was upregulated in LUSC tissues in TCGA database compared to adjacent non-tumor counterparts, and its expression level was strongly associated with tumor stage. LINC00511 deficiency significantly suppressed LUSC cell proliferation and migration. Furthermore, mechanistic investigation demonstrated that LINC00511 accelerated LUSC progression partially through its up-regulation of TADA1 via targeting miR-150-5p.Conclusionsour study highlights that LINC00511 facilitates LUSC progression via sequestering miR-150-5p and targeting TADA1, suggesting a need for development of a strategy for therapeutic targeting of LINC00511 in LUSC.

LINC00511 influences cellular proliferation through cyclin-dependent kinases in papillary thyroid carcinoma.

Background: Proverbially, the incidence rate of papillary thyroid carcinoma (PTC) has increased year by year. Many long noncoding RNAs (lncRNAs) have been discovered having a relationship with tumor genesis tightly recently. Thanks to the previous researches, we found long intergenic noncoding RNA 00511 (LINC00511) is overexpressed and acts as an oncogene in non-small-cell lung cancer and breast cancer. However, the biological role and function of LINC00511 are still unclear in PTC.Methods: We got the expression of LINC00511 in PTC tissues and matched adjacent tissues, as well the cell lines (B-CPAP, KTC-1, and KTC-1) by way of quantitative real-time polymerase chain reaction (qRT-PCR). In vitro, we knocked down the LINC00511 with small interfering RNA in PTC cell lines and demonstrated the function of LINC00511 by Cell Counting Kit-8, cell colony formation, Transwell migration, Transwell invasion, apoptosis assays, and cell cycle assays. Then, we discovered several downstream proteins of LINC00511 using Western blotting.Results: We proved that LINC00511's expression in PTC tissues and cell lines is higher than the control. LINC00511 promoted cellular proliferation, migration, invasion, G1/S transition and reduced apoptosis in vitro experiment. Knocked-down of LINC00511 resulted in the reduction of histone methyltransferase enhancer of zeste homolog 2 (EZH2), cyclin-dependent kinase 2 (CDK2) and cyclin-dependent kinase 4 (CDK4).Conclusions: Our results certified the role and function of LINC00511 in PTC, and it could become a novel tumor therapeutic target.

LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.

Lung cancer is a malignant tumor with extremely high morbidity and mortality. Recent studies have identified the vital role of LINC00511 (lncRNAs) in the development and progression of non-small cell lung cancer (NSCLC). In this research, we aim to explore the biological function of LINC00511 in the development and metastasis of NSCLC. LINC00511 expression in 57 paired NSCLC patients' tissues and matched normal tissues were detected by Real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation assay, colony formation assay and transwell assay were conducted to observe the biological behavior changes of NSCLC cells through the influence of LINC00511. In addition, dual-luciferase reporter gene assay, RNA immunoprecipitation assay (RIP) and, chromatin immunoprecipitation (ChIP) were performed to discover the potential targets of LINC00511 in NSCLC cells. LINC00511 was highly expressed in NSCLC tissues and cell lines compared with controls. LINC00511 expression was positively correlated with tumor size, tumor stage, lymph node metastasis and distant metastasis, but negatively correlated with overall survival (OS) of NSCLC patients. Receiver Operating Characteristic (ROC) curves suggested that LINC00511 could be an effective indicator to distinguish NSCLC patients from normal people. Cell counting kit-8 (CCK-8), flow cytometry and transwell assay showed that knockdown of LINC00511 in A549 cells decreased viability, accelerated apoptosis and inhibited invasive and migratory abilities. Overexpression of LINC00511 in PC9 cells obtained the opposite biological effects. Chromatin fractionation predicted that LINC00511 was mainly distributed in the nucleus. RIP and ChIP assay showed that LINC00551 directly bound to lysine-specific demethylase 1 (LSD1) and enhancer of zeste homolog 2 (EZH2). It inhibited expressions of LATS2 and KLF2 by binding to their promoter regions. LINC00511 is upregulated in NSCLC tissues and cell lines. It is closely related to tumor size, tumor stage, lymph node metastasis and, distant metastasis of NSCLC patients. Knockdown of LINC00511 attenuates proliferative, migratory and invasive capacities, but induces apoptosis of NSCLC cells. LATS2 and KLF2 are target genes of LINC00511, which are regulated by LINC00511 through binding to EZH2 and LSD1, thus influencing the progression of NSCLC.

Upregulation of long noncoding RNA LINC00152 promotes proliferation and metastasis of esophageal squamous cell carcinoma.

Purpose: Esophageal cancer is a major cause of cancer-related mortality worldwide. The long noncoding RNA LINC00152 has been confirmed to play an oncogenic role in many cancers. However, the expression pattern and function of LINC00152 in human esophageal squamous cell carcinoma (ESCC) remain unclear. Materials and methods: We evaluated LINC00152 expression in ESCC by qPCR and in situ hybridization. Proliferation, apoptosis, cell cycle, migration and invasion were examined in ESCC cells knocked down for LINC00152 knockdown by siRNA. Furthermore, an mRNA microarray was performed in ESCC cells with LINC00152 knockdown. Results: LINC00152 was significantly upregulated in human ESCC clinical samples (P<0.001) and cell lines (P=0.008), and LINC00152 overexpression was related to lymphatic metastasis (P=0.03) and advanced pTNM classification (P=0.005). Furthermore, ESCC patients with LINC00152 overexpression had significantly shorter overall survival (P=0.007), and LINC00152 overexpression was an independent risk factor for overall survival of ESCC patients. LINC00152 knockdown inhibited the proliferation, migration and invasion of ESCC cells in vitro. In addition, mechanistic investigations through mRNA array and immunoblot analyses demonstrated that LINC00152 regulated the expression of several cell cycle-related proteins and SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) interactions in vesicular transport pathway proteins. Conclusion: Our research indicated that LINC00152 exhibits oncogenic functions in ESCC and may represent a potential new target for ESCC therapy.

Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis

BackgroundEmerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism.MethodsThe lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding.ResultsLINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription.ConclusionIn conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them.

Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa-miR-29b-3p in pancreatic ductal adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC. Linc00511 levels in PDAC tissue specimens and cell lines were examined by quantitative real‐time PCR. Corresponding adjacent non‐neoplastic tissues were used as controls. The function of linc00511 in PDAC cell lines was determined by RNA interference approach in vitro and in vivo. Fluorescence in situ hybridization (FISH) was used to characterize linc00511 expression in PDAC cells. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were obtained from bioinformatic analysis, luciferase assays and RIP assays. The association between the linc00511/hsa‐miR29b‐3p axis and VEGFA was verified by Western blotting assay. Immunohistochemistry was performed to evaluate the expression of VEGFA in PDAC samples. The aberrant up‐regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. Mechanistically, linc00511 could up‐regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa‐miR‐29b‐3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. Linc00511 is a novel lncRNA that plays a significant regulatory role in the pathogenesis and progression of PDAC. Thus, Linc00511 represents a new prognostic biomarker to predict clinical outcome of PDAC patients after surgery and may serve as a potential therapeutic target for PDAC treatment.