<p>SP1-Induced Upregulation of lncRNA LINC00514 Promotes Tumor Proliferation and Metastasis in Osteosarcoma by Regulating miR-708</p>

Abstract

Background: Growing studies have suggested the dysregulation of long non-coding RNAs (lncRNAs) in several tumors, including osteosarcoma (OS). However, limited studies report metastasis-associated lncRNAs in OS. Our present study aimed to explore the roles of lncRNA LINC00514 (LINC00514) in OS. Materials and Methods: The LINC00514 expression was measured using qPCR assays in OS tissues and cell lines. The clinical significance of LINC00514 expression in OS patients was analyzed using chi-square test, Kaplan-Meier assays and multivariate analysis. The possible effects of LINC00514 in tumor cellular progression were determined using a series of functional assays. The mechanisms of LINC00514 action were explored through bioinformatics, luciferase reporter assays and RT-PCR assays. The mechanisms involved the upregulation of LINC00514 expression in OS were determined using luciferase reporter and chromatin immunoprecipitation (ChIP) assays. Results: We showed that LINC00514 expressions were distinctly upregulated in both OS tissues and cell lines, especially in advanced cases. High levels of LINC0051 were positively correlated with advanced tumor stages, distant metastasis, and reduced survival of patients with OS. Functional experiments indicated that silencing of LINC00514 suppressed the ability of cell growth, colony formation and metastasis, whereas promoted cell apoptosis in vitro. Mechanistic investigation revealed that LINC00514 could directly bind to miR-708 and effectively serve as a ceRNA for miR-708. In addition, LINC00514 was upregulated by the transcription factor SP1. Conclusion: Our findings revealed SP1-induced upregulation of LINC00514 as an oncogene in OS through competitively binding to miR-708, suggesting that there are potential diagnostic and treatment values of LINC00514 in OS.

LINC00514 promotes lipogenesis and tumor progression in esophageal squamous cell carcinoma by sponging miR‑378a‑5p to enhance SPHK1 expression

“…LINC00514 was reported to be involved in the development and progression of neuroendocrine prostate cancer. Mi et al ( 38 ) found that the expression of LINC00514 was markedly upregulated in osteosarcoma tissues and cells, and high levels of LINC00514 were positively associated with advanced tumor stages, distant metastasis and reduced overall survival of patients. Another study on osteosarcoma confirmed that LINC00514 was upregulated in osteosarcoma tissues and cells, and an increased LINC00514 level was associated with tumor size, TNM stage and distant metastasis.…”

“…Yu et al ( 18 ) verified that LINC00514 knockdown suppressed cell proliferation in vitro and in vivo , as well as colony formation, migration and invasion in osteosarcoma. LINC00514 functioned as a ceRNA by directly absorbing miR-708-5p, and consequently promoting cell proliferation ( 38 ). In addition, LINC00514 downregulation suppressed the proliferation, migration and invasion of papillary thyroid cancer cells, which was achieved by sponging miR-204-3p to increase the expression of cell division cycle 23 ( 19 ).…”

LINC00514 promotes gastric cancer cell growth and EMT progression via miR-204-3p/KRAS

“…Yu et al [ 29 ] illustrated that LINC00514 enhanced osteosarcoma development by sponging miR-708/URGCP. Mi et al [ 30 ] also noted that SP1-influenced LINC00514 overexpression induced metastasis and growth by modulating miR-708 in osteosarcoma. Until now, the roles of LINC00514 in gastric tumor are undefined and need to be studied.…”

The COX10-AS1/miR-641/E2F6 Feedback Loop Is Involved in the Progression of Glioma

“…Initially, researchers found that the expression of many lncRNAs was dysregulated in a variety of tumours, including gliomas and that the expression levels of some lncRNAs could be used as prognostic indicators (10,11). With further studies, researchers have found that lncRNAs can affect tumour progression by their involvement in a variety of cellular processes, such as proliferation, migration, invasion, autophagy, and epithelial-mesenchymal transition (EMT) (12)(13)(14). COX10 antisense RNA 1 (COX10-AS1) is a non-coding transcript located on chromosome 17 (14029292-14069458, complement).…”