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Upregulated LINC00565 Accelerates Ovarian Cancer Progression By Targeting GAS6.

ABSTRACT: Background:Long noncoding RNAs (lncRNAs) have been identified to participate in tumorigenesis. However, the underlying mechanisms of differentially expressed lncRNAs engaged in diseases remain indistinct and need further exploration. Methods:Raw data files downloaded from TCGA and GEO dataset were used to analyze the differentially expressed lncRNAs and LINC00565 was picked out as the potential oncogene. qRT-PCR was used to analyze the LINC00565 level in ovarian tissues and cell lines. Subsequently, the selected ovarian tumor cells were then transfected with LINC00565 siRNA by Lipofectamine 2000 and the cell cycle was detected by flow cytometry. Effect of LINC00565 on tumor growth and cell cycle was verified by tumor formation assay in nude mice. The mechanism of LINC00565 involving in cell cycle regulation was further explored by Western blot. Results:In this research, we discovered that LINC00565, a novel lncRNA, was highly expressed in ovarian cancer (OC). LINC00565 expression level was negatively associated with outcomes of OC patients. Further analysis showed that LINC00565 expression was closely correlated to tumor size, FIGO stage, but not related to other clinical features. In vitro experiments indicated that knockdown of LINC00565 significantly inhibited proliferative, invasive and migratory abilities of ovarian cancer cells. Besides, knockdown of LINC00565 can induce cell cycle arrest in G0/G1 phase. In addition, in vivo assay showed that low expression of LINC00565 inhibited the growth of OC. Further study found that LINC00565 knockdown markedly downregulated the protein expressions of CyclinD1, CyclinE1 and CDK4, but upregulated the expression of P16 and P21. Subsequently, we confirmed that LINC00565 promoted the progression of OC via upregulating GAS6, which has been confirmed to promote tumor progression. Conclusion:In summary, our study firstly reported that the LINC00565 functioned as an oncogene to promote the progression of OC by interacting with GAS6.

SUBMITTER: Gong M

PROVIDER: S-EPMC6875503 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Upregulated LINC00565 Accelerates Ovarian Cancer Progression By Targeting GAS6.

Gong Mi M Luo Chengyan C Meng Huangyang H Li Siyue S Nie Sipei S Jiang Yi Y Wan Yicong Y Li Huijian H Cheng Wenjun W

OncoTargets and therapy 20191120

<h4>Background</h4>Long noncoding RNAs (lncRNAs) have been identified to participate in tumorigenesis. However, the underlying mechanisms of differentially expressed lncRNAs engaged in diseases remain indistinct and need further exploration.<h4>Methods</h4>Raw data files downloaded from TCGA and GEO dataset were used to analyze the differentially expressed lncRNAs and LINC00565 was picked out as the potential oncogene. qRT-PCR was used to analyze the LINC00565 level in ovarian tissues and cell l ...[more]

PMID: 31819497

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Project description:PurposeTo explore the relationship between retinoic acid receptor gamma (RARG) and ovarian cancer (OC) cell proliferation and the prognosis of patients.MethodsThe transcriptome and clinical information of 379 OC and 88 normal ovarian samples were downloaded from the Cancer Genome Atlas (TCGA) database and the Genotype Tissue Expression (GTEx) database. We compared the mRNA level of RARG between ovrian normal and tumor tissues with the Wilcoxon rank sum test.The R package "limma" was used to analyze the differences in RARG expression between different clinical subgroups. Kaplan-Meier analysis was applied to evaluate the correlation between RARG and prognosis of patients. A nomogram was established to predict the effect of RARG on prognosis of OC patients. Immunohistochemistry and qRT-PCR experiments were conducted to determine the differential expression of RARG between ovarian normal and tumor tissues. Finally, we altered RARG expression using specific siRNA and lentiviral expression vectors to explore the function of RARG by CCK-8, cell cycle, colony formation, and xenograft assays in nude mice.ResultsRARG was highly expressed in ovarian tumors and was an independent predictor of poor overall survival outcomes. Subgroup analysis showed the high expression of RARG was related to FIGO stage III-IV (P=0.027), overall survival time <5 years (P=0.013) and dead status (P=0.041). The Kaplan-Meier curve indicated that patients with high RARG expression level had poor prognosis. The area under the curve (AUC) of RAGR expression for predicting patient survival rates at 1, 5 and 9 years were 0.659, 0.616 and 0.627, respectively. The GSEA enrichment analysis revealed that RARG was involved in ovarian cancer progression through multiple pathways. In cellular experiments in vitro, downregulation of RARG expression significantly suppressed the proliferation and colony formation capacity of OC cells. In cellular experiments in vivo, knockdown of RARG significantly reduced tumor growth in nude mice, decreased expression levels of Ki-67 and proliferation cell nuclear antigen (PCNA).ConclusionsHigh expression of RARG could promote OC cell proliferation and was an independent predictor of poor prognosis. RARG might work as a potential molecular target and biomarker for individualized diagnosis and treatment in OC patients.

Project description:Background:Thyroid cancer is an endocrine malignancy that is growing in incidence worldwide. Despite progress in diagnostics and treatment of thyroid cancer, prognosis remains poor. Emerging research has shown that circular RNAs (circRNAs) have crucial regulatory roles in cancers. However, the possible functions and mechanisms of hsa_circ_0011385 remain undetermined. Materials and methods:Expression levels of hsa_circ_0011385 and miR-361-3p were evaluated by qRT-PCR assay. The interaction between hsa_circ_0011385 and miR-361-3p was verified by dual-luciferase reporter assay. Effects of hsa_circ_0011385 or miR-361-3p on cell viability, proliferation, cell cycle, apoptosis, migration and invasion were confirmed by cell counting kit-8 (CCK-8), carboxyfluoresceinsuccinimidyl ester (CFSE), flow cytometry, and Transwell assays in vitro. The effect of hsa_circ_0011385 on thyroid cancer progression was also determined by in vivo tumor formation assay. Target genes of miR-361-3p were predicted by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and the expression of apoptosis- and metastasis-related proteins were assessed by Western blot assay. Results:Hsa_circ_0011385 upregulated in thyroid cancer; hsa_circ_0011385 knockdown inhibited thyroid cancer cell proliferation, migration and invasion, and promoted cell cycle arrest and apoptosis. In addition, hsa_circ_0011385 could negatively regulate miR-361-3p by functioning as a sponge. Hsa_circ_0011385 promoted thyroid cancer cell proliferation, migration and invasion and suppressed cell cycle arrest and apoptosis by targeting miR-361-3p in vitro. We also found that hsa_circ_0011385 knockdown dramatically inhibited thyroid cancer growth in vivo. Furthermore, hsa_circ_0011385 regulated expression of apoptosis and metastasis-related proteins in thyroid cancer. Conclusions:Hsa_circ_0011385facilitated thyroid cancer cell proliferation, invasion and migration, and inhibited thyroid cancer cell cycle arrest and apoptosis by targeting miR-361-3p, suggesting that the hsa_circ_0011385/miR-361-3p axis might be a promising therapeutic target for thyroid cancer.

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Upregulated LINC00565 Accelerates Ovarian Cancer Progression By Targeting GAS6.

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Upregulated LINC00565 Accelerates Ovarian Cancer Progression By Targeting GAS6.

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