Downregulation of lncRNA SNHG12 reversed IGF1R-induced osteosarcoma metastasis and proliferation by targeting miR-195-5p

Xu, Nuo; Xu, Jun; Zuo, Zhuan; Liu, Yang; Yan, Feng; Han, Chen

doi:10.1016/j.gene.2019.144145

Cited by 28 publications

(20 citation statements)

References 27 publications

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“…LncRNAs have drawn increasing attention in recent years owing to their roles in tumorigenesis [18,29,30]. An increasing number of studies have illustrated that lncRNAs play important roles in OS progression, providing an insight into OS pathogenesis [31][32][33]. Hence, lncRNAs are potential diagnostic and therapeutic targets for OS.…”

Section: Discussionmentioning

confidence: 99%

LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression

et al. 2020

Aging

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Long intergenic nonprotein-coding RNA 00514 (LINC00514) is upregulated in papillary thyroid cancer and contributes to its aggressiveness. In this study, we thoroughly explored the expression profile, specific functions, and relevant molecular mechanism of LINC00514 in osteosarcoma (OS). Herein, LINC00514 was significantly upregulated in OS tissues and cells, and increased LINC00514 expression was closely correlated with tumor size, TNM stage, and distant metastasis. OS patients with high LINC00514 expression had shorter overall survival than those with low LINC00514 expression. LINC00514 interference inhibited OS cell proliferation, colony formation, migration, and invasion in vitro but promoted cell apoptosis and G0/G1 cell cycle arrest. LINC00514 downregulation hindered OS tumor growth in vivo. Mechanistically, LINC00514 functioned as a competing endogenous RNA by directly interacting with microRNA-708-5p (miR-708) and consequently increasing the expression of upregulator of cell proliferation (URGCP). Both miR-708 knockdown and URGCP restoration partially neutralized anticancer activities of LINC00514 silencing in OS cells. LINC00514 increases URGCP expression by acting as a competing endogenous RNA for miR-708, thus exerting oncogenic roles in OS progression. In conclusion, the LINC00514/miR-708/URGCP pathway may be a promising target for drug discovery in the future.

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Section: Discussionmentioning

confidence: 99%

LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression

et al. 2020

Aging

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“…For example, lncRNA SNHG12 regulates the metastasis and growth of osteosarcoma by targeting the miR-195-5p/IGF1R axis. 7 As a vital miRNA, miR-410-3p serves whether as an oncogene or tumor suppressor gene in different tumors. 8 Nevertheless, the function of the lncRNA-mediated miR-410-3p in tumors remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

<p>LINC00680 Promotes the Progression of Non-Small Cell Lung Cancer and Functions as a Sponge of miR-410-3p to Enhance HMGB1 Expression</p>

Wang

Li²,

Zheng³

et al. 2020

OTT

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Purpose: LINC00680 was reported to be involved in various cancers through multiple mechanisms. Therefore, we intended to investigate its role in the progression of non-small cell lung cancer (NSCLC). Materials and Methods: Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was used to test LINC00680 in NSCLC tissue and cell lines. Subsequently, A549 and H1299 cells were transfected with LINC00680 overexpressing plasmids and their proliferation and colony formation and apoptosis was tested by Transwell assay and flow cytometry. In addition, xenograft tumor experiments in nude mice also affirmed. Meanwhile, we predicted that miR-410-3p, LINC00680 and high-mobility group protein box 1(HMGB1) relationship by Starbase, dual-luciferase reporter and RIP assay. Finally, the carcinogenic effects of LINC00680 were reversed by ethyl pyruvate (EP), a specific inhibitor of HMGB1. Results: LINC00680 was upregulated in NSCLC and was closely related to the malignancy and poor prognosis of NSCLC patients. LINC00680 promoted proliferation and colony formation and inhibited apoptosis of A549 and H1299 cells. In addition, overexpressing LINC00680 accelerated the growth of NSCLC cells in xenograft tumor experiments in nude mice also affirmed. Meanwhile, high-mobility group protein box 1(HMGB1) was astoundingly amplified in NSCLC and was negatively regulated by miR-410-3p. Further, HMGB1 acted as a downstream target of miR-410-3p, upregulating miR-410-3p to attenuate HMGB1, while LINC00680 strengthened the expression of HMGB1 in A549 and H1299 cells. Discussion: Thus, these results indicated that LINC00680 was cancerogenic in NSCLC by upregulating HMGB1 via sponging miR-410-3p.

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“…21 SNHG12 targeted miR-195-5p to promote growth and metastasis in osteosarcoma. 22 And lncRNA AC114812.8 initiates proliferation, migration and invasion of bladder tumor cells by modulating miR-371b-5p/FUT4 pathway. 23 Besides, lncRNA AB074169 suppress thyroid cancer growth by affecting CDKN1a expression.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA PSMA3-AS1 Promotes Lung Cancer Growth and Invasion via Sponging MiR-4504</p>

Zhu

2020

CMAR

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Background: Long noncoding RNAs (lncRNAs) have close correlation with tumorigenesis. And how lncRNAs participate in lung cancer require investigation in-depth. The aim of this study was to determine the role of lncRNA PSMA3-AS1 in lung cancer progression. Methods: PSMA3-AS1 expression was analyzed via qRT-PCR. Kaplan-Meier method was used to analyze survival rate based on PSMA3-AS1 value. Proliferation was measured via CCK8 and colony formation assays. Transwell assay was utilized to examine migration and invasion. Luciferase reporter assay and RNA pulldown assay were utilized to analyze the interaction between PSMA3-AS1 and miR-4504. Results: PSMA3-AS1 expression was upregulated in lung cancer tissues and cell lines. PSMA3-AS1 expression was positively correlated with clinical stage and metastasis. PSMA3-AS1 overexpression predicted a poor prognosis in lung cancer patients. PSMA3-AS1 knockdown suppressed proliferation, migration and invasion of lung cancer cells. Through bioinformatics analysis, PSMA3-AS1 was predicted to sponge miR-4504. MiR-4504 expression was inhibited by PSMA3-AS1. And inhibition of miR-4504 reversed the effects of PSMA3-AS1 depletion. Conclusion: PSMA3-AS1 promotes the tumorigenesis of lung cancer through inhibiting miR-4504.

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Downregulation of lncRNA SNHG12 reversed IGF1R-induced osteosarcoma metastasis and proliferation by targeting miR-195-5p

Cited by 28 publications

References 27 publications

LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression

LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression

<p>LINC00680 Promotes the Progression of Non-Small Cell Lung Cancer and Functions as a Sponge of miR-410-3p to Enhance HMGB1 Expression</p>

<p>LncRNA PSMA3-AS1 Promotes Lung Cancer Growth and Invasion via Sponging MiR-4504</p>

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