Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

Wu, Dongmei; Han, Xin‐Rui; Wen, Xin; Wang, Shan; Wang, Yongjian; Shen, Min; Fan, Shao‐Hua; Zhuang, Juan; Zhang, Zi-Feng; Shan, Qun; Li, Meng‐Qiu; Sun, Chunhui; Lü, Jun; Zheng, Yuxin

doi:10.1159/000492279

Cited by 13 publications

(8 citation statements)

References 45 publications

(48 reference statements)

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“…Low-grade GBM is generally related with neurological dysfunction [3]. Because of the increasing rate of recrudesce, infiltrative rate and limited treatment means, the prognosis of high-grade GBM is still poor [4]. Despite multiple developments in medical and surgical treatments, GBM is still a deadly disease with a high mortality rate [5].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

Chi

Yang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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2020) Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-ABSTRACT Background: Glioblastoma multiforme (GBM) is one of the most prevailing primary brain tumours among adults and most aggressive cancers. Despite multiple developments in medical and surgical treatments, GBM is still a deadly disease with a high mortality rate. Here, this study was performed to investigate the function of circPVT1 on GBM. Methods: CCK-8 and flow cytometry were utilised to estimate viability and apoptosis in both cells. qRT-PCR was performed to determine circPVT1 and miR-199a-5p expression. Western blot was conducted to determine apoptosis, migration and EMT-related proteins levels when silencing circPVT1. Subsequently, these parameters were re-tested after up-regulating miR-199a-5p. Results: CircPVT1 was highly expressed in GBM tissues. Silencing circPVT1 raised two cells apoptosis and reduced viability and migration capacity. Moreover, EGF-induced EMT was repressed by silencing circPVT1. In addition, miR-199a-5p expression was elevated when silencing circPVT1. And silencing circPVT1 exerted above changes via up-regulating miR-199a-5p. Finally, silencing circPVT1 repressed YAP1 and PI3K/AKT pathways via up-regulating miR-199a-5p. Conclusion: Our data suggested that silencing circPVT1 inhibited viability, migration, EGF-induced EMT and promoted apoptosis as well as repressed YAP1 and PI3K/AKT pathways by up-regulating miR-199a-5p. HIGHLIGHTS 1. CircPVT1 expression is highly expressed in GBM tissues; 2. Si-circPVT1 represses migration and promoted apoptosis in U539 and U251 cells; 3. Si-circPVT1 represses migration and promoted apoptosis when elevating miR-199a-5p; 4. Si-circPVT1 represses EGF-induced EMT when increasing miR-199a-5p; 5. Si-circPVT1 suppresses YAP1 and PI3K/AKT pathways by up-regulating miR-199-5p. ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

Chi

Yang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…11 As reported before, LncRNA-LINC01260 was lowered in spinal cord glioma and co-expressed with CARD11 in multiple cancers, such as breast invasive carcinoma and prostate adenocarcinoma. 12,13 In this study, we have demonstrated that LINC01260 was low-expressed in NSCLC patients. However, the role of LINC01260 played in the procedure of NSCLC and the underlying mechanism is still unknown.…”

Section: Introductionmentioning

confidence: 59%

<p>The LINC01260 Functions as a Tumor Suppressor via the miR-562/CYLD/NF-κB Pathway in Non-Small Cell Lung Cancer</p>

Chen¹,

Lei²,

Lin³

et al. 2020

OTT

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Recently, long noncoding RNAs (lncRNAs) have been identified as novel and potential therapeutic targets in various cancer types. Nonetheless, the levels and biological effects of lncRNAs in non-small cell lung cancer (NSCLC) remain largely unknown. In this study, we aimed to identify the effects of lncRNA-LINC01260 throughout the progression of NSCLC and explore the underlying mechanism. Methods: Quantitative real-time PCR (qRT-PCR) and Western blot were performed to measure LINC01260, miR-562, and CYLD expression and protein levels. Luciferase reporter assay was employed to investigate the relationship between LINC01260 and miR-562, and miR-562 and CYLD, respectively. The viability and migration of cells were evaluated using CCK-8, colony formation, and transwell assays. The effects of LINC01260 were identified through tumorigenesis in vivo. ELISA was performed to detect the activity of NF-κB and p65 expression. Results: In NSCLC tissues and cell lines, LINC01260 expression was downregulated, which corresponded to a lower survival rate of patients with NSCLC. Knockdown of LINC01260 accelerated the proliferation, colony formation, and migration of NSCLC cells. Moreover, downregulation of LINC01260 inhibited apoptosis of NSCLC cells by regulating the expression of Bcl-2 and Bax proteins in vitro. In vivo, the downregulation of LINC01260 promoted tumor growth. miR-562 was identified as the target gene of LINC01260, which was upregulated in NSCLC tumors. Furthermore, CYLD was identified as the target gene of miR-562. The effects of LINC01260 were exerted by regulating CYLD via sponging miR-562. ELISA confirmed that the upregulation of CYLD inhibited NF-κB activity; however, the co-transfection of sh-LINC01260 partly reversed the inhibition. Additionally, CYLD reduced p65 expression; however, downregulation of LINC01260 slightly increased the expression level. Conclusion: This study revealed a novel LINC01260/miR-562/CYLD/NF-κB pathway in the pathogenesis of NSCLC and suggested a potential therapeutic target for NSCLC.

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“…Previous studies have been reported that many genes participated in the COPD progression, containing microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) [9]. LncRNA, a cluster of RNA transcripts with more than 200 nucleotides in length, were participated in mediating multiple cell physiological progress, including cell proliferation, apoptosis and migration [10]. In recent years, Li et al found that lncRNA HEIH affected triple-negative breast cancer cells growth and apoptosis through regulating miR-4458/SOCS1 axis [11].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis

Gui

et al. 2020

Med Sci Monit

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Background:Chronic obstructive pulmonary disease (COPD), a general airway disease, is featured by progressive and chronic immunoreaction in the lung. Increasing evidences have showed that cigarette smoking is the main reason in the COPD progression, and human pulmonary microvascular endothelial cell (HPMEC) apoptosis often be observed in COPD, while its pathogenesis is not yet fully described. Upregulation of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) was observed in COPD patients, but the specific mechanism of lncRNA MEG3 in COPD remains unknown. The objective of this research was to explore the role of lncRNA MEG3 in cigarette smoke extract (CSE)-induced HPMECs. Material/Methods:HPMECs were induced by a series of concentrations of CSE (0%, 0.1%, 1%, and 10%). Then cell apoptosis was analyzed by flow cytometry. Cell apoptosis related proteins were tested using western blot assay. Finally, we applied knockdown and over-expression system to explore the lncRNA MEG3 functions in CSE-induced HPMECs. Results:Our results indicated that various concentrations of CSE (0%, 0.1%, 1%, and 10%) significantly promoted cell apoptosis, augmented caspase-3 activity, upregulated Bax expression, decreased Bcl-2 expression, and enhanced lncRNA MEG3 level in HPMECs. LncRNA MEG3-plasmid transfection resulted in the upregulation of lncRNA MEG3, more apoptotic HPMECs, and higher caspase-3 activity. While lncRNA MEG3 knockdown presented the opposite effects. Further investigation suggested that all the effects of CSE treatment on HPMECs were markedly reversed by lncRNA MEG3-shRNA (short hairpin RNA). Conclusions:Our study illustrated a protective effect of lncRNA MEG3-shRNA on CSE-induced HPMECs, indicting lncRNA MEG3 can be a new therapeutic approach for COPD treatment.

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Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

Cited by 13 publications

References 45 publications

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

<p>The LINC01260 Functions as a Tumor Suppressor via the miR-562/CYLD/NF-κB Pathway in Non-Small Cell Lung Cancer</p>

Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis

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