<i>LINC00968</i> functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

Liu, Gang; Yuan, Dongtang; Sun, Peng; Liu, Weidong; Wu, Pengfei; Liu, Huan; Yu, Guangyang

doi:10.1002/jcp.26624

Cited by 37 publications

(36 citation statements)

References 30 publications

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“…Previous studied showed that LINC00968 acted crucial roles in the development of nonsmall cell lung cancer and osteosarcoma . For example, Wang et al identified that LINC00968 expression level was upregulated in nonsmall cell lung cancer tissues and cells.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00968 promotes endothelial cell proliferation and migration via regulating miR‐9‐3p expression

Zhao

Zhang

Wang

2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) have been showed to play a crucial role in pathogenesis and development of cardiovascular diseases. Our study aimed to study the expression and functional role of lncRNA LINC00968 in the development of coronary artery disease (CAD). We showed that the LINC00968 expression level was upregulated in the CAD tissues compared with normal arterial tissues. In addition, we showed that the expression level of LINC00968 was upregulated by oxidized low‐density lipoprotein (oxLDL) treatment in endothelial cell. Ectopic expression of LINC00968 regulated the proliferation and migration of endothelial cell. Moreover, we showed that overexpression of LINC00968 inhibited miR‐9‐3p expression in an endothelial cell. Furthermore, we demonstrated that the miR‐9‐3p expression was downregulated in the CAD samples compared with normal arterial tissues and the expression level of miR‐9‐3p was downregulated by oxLDL treatment in endothelial cell. Finally, we showed that ectopic expression of LINC00968 promoted endothelial cell proliferation and migration partly through regulating miR‐9‐3p expression. These results suggested that LINC00968 plays a crucial role in the progression of the CAD.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00968 promotes endothelial cell proliferation and migration via regulating miR‐9‐3p expression

Zhao

Zhang

Wang

2018

J of Cellular Biochemistry

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“…The PI3K/Akt pathway is frequently hyperactivated in osteosarcoma, and contributes to disease initiation and development (37). Moreover, inhibition of this pathway via small compounds is a potential therapeutic approach for osteosarcoma (38). Previous studies have shown that Wilms' tumor 1 knockdown in MG-63 cells results in deregulation of cell cycle proteins and downregulation of the PI3K/AKT pathway (39,40).…”

Section: Discussionmentioning

confidence: 99%

Wnt/β‑catenin signaling modulates piperine‑mediated antitumor effects on human osteosarcoma cells

Yang

et al. 2020

Mol Med Report

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The plant extract piperine is used as a traditional Chinese medicine due to its anti-inflammatory effects and efficacy against numerous types of cancer. The aim of the present study was to investigate the antitumor mechanism of piperine in human osteosarcoma U2OS and 143B cell lines. The effects of piperine on cell apoptosis and invasion of human osteosarcoma cells were assessed using flow cytometry and Transwell assays. Moreover, western blotting was used to measure the effects of piperine on the protein expression levels of the metastasis markers matrix metalloproteinase-2 (MMP-2) and vascular endothelial growth factor (VEGF). In addition, the involvement of the Wnt/β-catenin signaling pathway in modulating the effects of piperine was examined via western blot analysis. The results of MTT and Transwell invasion assays indicated that piperine treatment dose-dependently reduced U2OS and 143B cell viability and invasion. Furthermore, a significant reduction was identified in MMP-2, VEGF, glycogen synthase kinase-3β and β-catenin protein expression levels, as well as the expression levels of their target proteins cyclooxygenase-2, cyclin D1 and c-myc, in U2OS cells after piperine treatment. In addition, similar results were observed in 143B cells. Therefore, the present study demonstrated the efficacy of piperine in osteosarcoma, and identified that the Wnt/β-catenin signaling pathway may modulate the antitumor effects of piperine on human U2OS and 143B cells.

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“…LINC00968 was rst identi ed by Hui et al in 2015, and the following researches demonstrated its diverse role in different human cancers. LINC00968 inhibited the progression of breast cancer yet acted as an oncogene in epithelial ovarian cancer and osteosarcoma [8][9][10]12]. Here in our study, we investigated the exact role of LINC00968 in the progression of LUAD.…”

Section: Discussionmentioning

confidence: 99%

“…Although increasing evidences revealed that lncRNAs are involved in numerous human diseases, cancer included, full understanding of their exact molecular mechanisms is still far beyond completion [7]. Long intergenic non-protein coding RNA 968 (LINC00968) is reported to be dysregulated in several human cancers including breast cancer, osteosarcoma, and epithelial ovarian cancer [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC00968 inhibits lung adenocarcinoma progression through sponging miR-22-5p and further restoring CDC14A

Bian

Zhang

et al. 2020

Preprint

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Background: Lung adenocarcinoma (LUAD) is a high aggressive human cancer which usually diagnosed at advanced stages. Accumulating evidences indicate that long noncoding RNAs (lncRNAs) are crucial participants in LUAD progression. Methods: The mRNA levels of LINC00968, miR-22-5p and cell division cycle 14A (CDC14A) were measured using quantitative real-time PCR. Cell proliferation was evaluated using cell counting kit-8 and flow cytometry. Cell migration and cell invasion were assessed by wound healing and transwell assay, respectively. The interactions between LINC00968 and miR-22-5p were validated by RNA immunoprecipitation, RNA pull down and luciferase reporter assay. Results: We found that lncRNA LINC00968 was significantly down-regulated in LUAD tissues and cell lines. LINC00968 level was positively correlated to survival rate, and negatively correlated to tumor node metastasis stage, tumor size and lymph node metastasis of LUAD patients. LINC00968 over-expression in LUAD cells inhibited cell proliferation and induced cell cycle arrest at G1 phase. LINC00968 over-expression also suppressed migration, invasion and epithelial mesenchymal transition (EMT) as evidenced by elevated E-cadherin, decreased N-cadherin, TWIST and SNAIL levels. We further validated that LINC00968 localized in cytoplasma and acted as an upstream of microRNA miR-22-5p, which was up-regulated in LUAD tissues and cell lines. Besides, elevated miR-22-5p expression abolished the effect of LINC00968 over-expression on LUAD progression including in vivo tumor growth. In addition, we first validated that cell division cycle 14A (CDC14A), which was down-regulated in LUAD tissues, was a downstream target of miR-22-5p. We over-expressed CDC14A in LUAD cells and miR-22-5p induced LUAD progression was partially reversed. Conclusion: our study demonstrated that LINC00968 inhibited proliferation, migration and invasion of LUAD by sponging miR-22-5p and further restoring CDC14A. This novel regulatory network might provide us with promising diagnostic and therapeutic target in LUAD treatment.

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LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

Cited by 37 publications

References 30 publications

Long noncoding RNA LINC00968 promotes endothelial cell proliferation and migration via regulating miR‐9‐3p expression

Long noncoding RNA LINC00968 promotes endothelial cell proliferation and migration via regulating miR‐9‐3p expression

Wnt/β‑catenin signaling modulates piperine‑mediated antitumor effects on human osteosarcoma cells

Long noncoding RNA LINC00968 inhibits lung adenocarcinoma progression through sponging miR-22-5p and further restoring CDC14A

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