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Showing 4 results for Lncrna
X.n. Yu, Ph.d., M. Wang,
Volume 20, Issue 1 (1-2022)
Abstract
Background: To investigate whether LncRNA LINC01204 affects lung cancer cell apoptosis, migration, invasion and radiosensitivity by regulating miR-214. Materials and Methods: Normal lung cells HBE and lung cancer cells A549 were cultured in-vitro, and pcDNA3.1, pcDNA3.1-LINC01204, pcDNA3.1-LINC01204 and miR-NC, pcDNA3.1-LINC01204 and miR-214 mimics were transfected into A549 cells, respectively. qRT-PCR, flow cytometry, scratch test, and Transwell chamber test, clone formation test, dual luciferase, and Western blot methods were used in this study. Results: Compared with HBE cells, A549 cells had significantly reduced LINC01204 expression level (P<0.05), and significantly increased miR-214 expression level (P<0.05); transfection of pcDNA3.1-LINC01204 could significantly increase apoptosis rate and Cleaved-caspase3, E-cadherin protein levels (P<0.05), reduce migration healing rate, N-cadherin protein levels and cell survival fraction (P<0.05) with sensitization enhancement ratio SER at 1.950, reduce the number of invasive cells (P<0.05). Dual luciferase report experiments confirmed that LINC01204 can bind to miR-214 in a targeted way; co-transfection of pcDNA3.1-LINC01204 and miR-214 mimics can significantly reduce the apoptosis rate and Cleaved-caspase3 and E-cadherin protein levels (P<0.05), improve the migration healing rate, N-cadherin protein level and cell survival fraction (P<0.05) with sensitization enhancement ratio SER at 0.728, increase the number of invasive cells (P<0.05). Conclusion: LINC01204 overexpression can negatively regulate miR-214 expression to promote lung cancer cell apoptosis and inhibit migration and invasion, thereby enhancing radiosensitivity.
Y. Zhou, Y. Bi, M. Wan, N. Xu, Y. Xu, P. Liu, H. Jiang, H. Fang, H. Hu, S. Xu, S. Lan,
Volume 22, Issue 2 (4-2024)
Abstract
Background: Conventional treatments on osteosarcoma (OS) yield limited improvements in metastatic or relapsed cases, necessitating innovative therapeutic strategies. This study's objective is to reveal the role of long non-coding RNAs (lncRNAs) in prognosis and potential molecular pathways of OS. Materials and Methods: This study integrated bioinformatics, statistical analysis, and computational techniques to investigate m6A-related prognostic lncRNA clusters in OS. Consensus clustering and risk analysis were performed on the m6A-related prognostic lncRNAs. Nomogram model was built for survival prediction, and was assessed using survival time receiver operator characteristic (ROC) analysis and decision curves. A competitive endogenous RNA (ceRNA) network was built to explore lncRNA-miRNA (microRNA)-mRNA interactions using the microRNA database and metascape website, followed by functional enrichment analyses. Results: The analysis unveiled three distinct OS clusters, with Cluster 2 exhibiting the highest risk in the immune microenvironment. High risk 7-lncRNA signature demonstrated strong prognostic value in predicting OS overall survival. The ceRNA network highlighted complex interactions among mRNAs, miRNAs and lncRNAs. Functional enrichment analysis indicated that mRNAs within the ceRNA network were linked to many biological functions. Furthermore, 30 differentially expressed genes (DEGs) derived from low-risk and high-risk groups enriched in GO-BP connected to MAGE (melanoma antigen gene) family member A2 (MAGEA2) and MAGEA2B. These DEGs in high risk group were also upregulated in the three KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway. Conclusion: This study disclosed the role of high-risk m6A-associated lncRNAs in prognosis and potential molecular pathways of OS. These findings provided novel insights into OS pathogenesis and potential therapeutic targets, warranting further validation in clinical settings.
A.p. S.e. El Feky, O.s. Zahra, M.n. Salem, M.i. Morsi,
Volume 22, Issue 4 (10-2024)
Abstract
Background: Long non-coding RNAs (LncRNAs) play an important role in the biological and pathological processes of many cancers. LncRNA SChLAP1 and ATB have been shown to be overexpressed in a variety of cancers and may be involved in tumor cell invasion and metastasis. The goal of this study was to investigate the significance of lncRNA ATB and SChLAP1 expression in liquid biopsy of metastatic prostate cancer (PCa) relative to routine investigations. Materials and Methods: urine samples from 65 PCa patients we collected to assess ATB and SChlap1 by realtime PCR, serum samples were collected to assess PSA. Bone scan and clinicopathological data including Gleason sum, clinical stage, tumor size and lymph node involvement were collected. Results: A significant elevation in lncRNA SChLAP1 and ATB expression in bone scan-diagnosed metastatic PCa patients. Both markers were significantly associated with advanced clinical stage, Gleason sum and tumor size. SCHLAP1 expression has high specificity (100%) and moderate sensitivity (68%) at a cutoff point of 2.528. ATB expression has a high sensitivity (93.75%) and specificity (75.76%) at a cutoff value of 4.55. In univariate analysis, Gleason score (> 8), tumor size (> 2), lncRNA ATB express (>4.55), lncRNA SCHAP (>2.53), and PSA (> 35 pg/ml) were independently predictive of a positive bone scan. Only ATB was significant, regardless of the other adjusted factors. Conclusions: Expression levels of LncRNA SCHALP1 and ATB in PCa patients’ urine samples are promising, non-invasive markers that are associated with advanced clinicopathological parameters, including advanced clinical stage, high grade (Gleason sum) and larger tumor size.
M. Huang, M.sc., Y. Peng, Y. Sun, W. Gao, J. Fei, C. Zhou, L. Xie, L. Zhou, W. Wu,
Volume 23, Issue 1 (1-2025)
Abstract
Background: High-intensity focused ultrasound (HIFU) represents a therapeutic medical procedure that operates by inducing ablation and mechanical disruption. Despite its established efficacy, its potential impact on tumor chemotherapy remains uncertain. Long noncoding RNA (lncRNA) MAFA-AS1 facilitated cancer cell proliferation and fostering drug resistance, but the precise significance and functional implications of MAFA-AS1 in the context of ovarian cancer (OC) remain largely unexplored. The objective of this experiment is to further investigate the potential of HIFU in inhibiting the chemotherapy resistance mechanism of OC. Materials and Methods: Five types of human ovarian cancer cells were employed in this study. There were four different groups, namely MAFA-AS1 siRNA, si-NC, pcDNA3.1-HIF-1 (hypoxia-inducible factor-1), and pcDNA3.1-control. Quantitative real-time PCR, cell proliferation assay, apoptosis assay, western blot assay, subcellular fractionation, aerobic glycolysis analysis, RNA immunoprecipitation (RIP), and luciferase reporter assay were conducted for experimentation and validation. Results: Significant upregulation of MAFA-AS1 in OC cells was observed. Through loss-of-function experiments based on HIFU, we unraveled its oncogenic functions in OC. MAFA-AS1 was discovered to bind to HIF-1 mRNA, thereby enhancing its expressed stability. Further investigations revealed an interaction between MAFA-AS1 and fat mass and obesity-associated protein (FTO), positively modulating HIF-1 mRNA stability in an FTO-dependent manner. Importantly, MAFA-AS1 exerts its effects on OC by acting through HIF-1. Conclusion: The study underscores the role of MAFA-AS1 in promoting aerobic glycolysis and chemical resistance in OC by up-regulating HIF-1 expression, suggesting that targeting MAFA-AS1 holds promise as a therapeutic strategy for OC patients undergoing chemotherapy.
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