scholarly journals Up-regulated long non-coding RNA ILF3-AS1 indicates poor prognosis of nasopharyngeal carcinoma and promoted cell metastasis

2020 ◽  
Vol 35 (4) ◽  
pp. 61-70
Author(s):  
Xuewen Yang ◽  
Feng Lin ◽  
Feng Gao
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Poor Prognosis ◽  
Tissue Samples ◽  
Small Interference Rna ◽  
Invasion And Migration ◽  
Advanced Tumor ◽  
Bmi1 Expression ◽  
Tumor Node Metastasis Stage ◽  
Novel Target ◽  
And Migration

Background: Long non-coding RNAs (lncRNAs) have been confirmed to participate in the regulation of nasopharyngeal carcinoma. Here, we endeavored to explore the character of lncRNA ILF3-AS1 in the nasopharyngeal carcinoma and its function. Methods: A total of 68 nasopharyngeal carcinoma tissues and adjacent normal nasopharyngeal tissues were collected. Expressions of lncRNA ILF3-AS1 in these tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between the expression level of lncRNA ILF3-AS1 and clinical pathological characteristics was analyzed. Inhibition of lncRNA ILF3-AS1 was done using small interference RNA. Results: lncRNA ILF3-AS1 expression was significantly up-regulated in the 68 nasopharyngeal carcinoma tissue samples compared to their adjacent normal tissue samples. Increased lncRNA ILF3-AS1 level was related to the advanced tumor node metastasis stage and the metastasis of nasopharyngeal carcinoma. Also, increased lncRNA ILF3-AS1 indicated poor prognosis of nasopharyngeal carcinoma patients. Inhibition of lncRNA ILF3-AS1 reduced proliferation, invasion and migration of nasopharyngeal carcinoma cells. MicroRNA-320a (miR-320a) was determined as a direct target for lncRNA ILF3-AS1 in nasopharyngeal carcinoma. Furthermore, lncRNA ILF3-AS1 could sponge miR-320a to promote BMI1 expression. The expression of BMI1 was significantly inhibited by the down-regulation of lncRNA ILF3-AS1. Conclusions: For the first time, we demonstrated that lncRNA ILF3-AS1 was markedly over-expressed in nasopharyngeal carcinoma tissues and cells. Elevated lncRNA ILF3-AS1 expression was correlated with severe cancer stage and poor prognosis. lncRNA ILF3-AS1 could promote proliferation, invasion, and migration of cells, which might indicate a novel target site for the future diagnosis and therapy of nasopharyngeal carcinoma.

scholarly journals Long noncoding RNA UCA1 promotes the proliferation, invasion, and migration of nasopharyngeal carcinoma cells via modulation of miR-145

2018 ◽  
Vol Volume 11 ◽  
pp. 7483-7492 ◽  
Author(s):  
Jing Wu ◽  
Mingyu Du ◽  
Qian Zhang ◽  
Wenjun Zhang ◽  
Yanxin Fan ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Carcinoma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals miR-23a-3p is a Key Regulator of IL-17C-Induced Tumor Angiogenesis in Colorectal Cancer

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1363 ◽  
Author(s):  
Yunna Lee ◽  
Su Jin Kim ◽  
Jieun Choo ◽  
Gwangbeom Heo ◽  
Jin-Wook Yoo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Tumor Angiogenesis ◽  
Ex Vivo ◽  
Underlying Mechanism ◽  
Vegf Receptor ◽  
Invasion And Migration ◽  
Novel Target ◽  
And Migration

MicroRNAs (miRNAs) have emerged as key players in tumor angiogenesis. Interleukin-17C (IL-17C) was identified to promote colorectal cancer (CRC) progression. Therefore, we aimed to investigate the effect of IL-17C on tumor angiogenesis, the involvement of miR-23a-3p in IL-17C signaling, and the direct target gene of miR-23a-3p in CRC. In vitro and ex vivo angiogenesis, a mouse xenograft experiment, and immunostaining were performed to test the effect of IL-17C on tumor angiogenesis. ELISA, quantitative real time PCR, and gene silencing were used to uncover the underlying mechanism. IL-17C induced angiogenesis of intestinal endothelial cells, subsequently enhancing cell invasion and migration of DLD-1 cells. IL-17C-stimulated DLD-1 cells produced vascular endothelial growth factor (VEGF) to enhance angiogenesis. Moreover, IL-17C markedly accelerated xenograft tumor growth, which was manifested by substantially reduced tumor growth when treated with the VEGF receptor 2 inhibitor Ki8751. Accordingly, Ki8751 suppressed the expression of IL-17C-stimulated PECAM and VE-cadherin in xenografts. Furthermore, IL-17C activated STAT3 to increase the expression of miR-23a-3p that suppressed semaphorin 6D (SEMA6D) expression, thereby permitting VEGF production. Taken together, our study demonstrates that IL-17C promotes tumor angiogenesis through VEGF production via a STAT3/miR-23a-3p/SEMA6D axis, suggesting its potential as a novel target for anti-CRC therapy.

scholarly journals Long Noncoding RNA HOXB-AS1 Is Upregulated in Endometrial Carcinoma and Sponged miR-149-3p to Upregulate Wnt10b

2020 ◽  
Vol 19 ◽  
pp. 153303382096746
Author(s):  
Da Liu ◽  
Min Qiu ◽  
Lili Jiang ◽  
Kuiran Liu
Keyword(s):  
Endometrial Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Competing Endogenous Rna ◽  
Tissue Samples ◽  
Invasion And Migration ◽  
Underlying Mechanisms ◽  
And Migration ◽  
Oncogenic Function

The functions of Long noncoding RNA (lncRNA) HOXB-AS1 have been investigated in glioblastoma and multiple myeloma. However, the role of lncRNA HOXB-AS1 in endometrial carcinoma (EC) remains largely unknown. This study investigated the underlying mechanisms of the lncRNA HOXB-AS1 on the progression of EC. In this study, We found that HOXB-AS1 expression was significantly upregulated in EC tissue samples and was associated with shorter survival time. Furthermore, upregulation of HOXB-AS1 promoted proliferation, invasion, and migration of EC cell. HOXB-AS1 and Wnt10b directly bound to miR-149-3p. HOXB-AS1 increased the expression of Wnt10b by binding to miR-149-3p. We further verified the upregulation of β-catenin, cyclin D1, and c-myc induced by HOXB-AS1. In conclusion, our results indicated that HOXB-AS1 exerted oncogenic function as competing endogenous RNA (ceRNA) of miR-149-3p to release Wnt10b and activated Wnt/β-catenin pathway.

scholarly journals Stimulation of TLR4 by LMW-HA Induces Metastasis in Human Papillary Thyroid Carcinoma through CXCR7

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Shipeng Dang ◽  
Yongde Peng ◽  
Lei Ye ◽  
Yanan Wang ◽  
Zhongqing Qian ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Thyroid Tissue ◽  
Tissue Samples ◽  
Normal Tissues ◽  
Cell Proliferation And Migration ◽  
Novel Target ◽  
And Migration ◽  
Tissues Expression ◽  
Stimulation Of ◽  
Proliferation And Migration

In inflammatory sites, high molecular weight hyaluronan fragments are degraded into lower molecular weight hyaluronan fragments (LMW-HA) to regulate immune responses. However, the function of LMW-HA in PTC progression remains to be elucidated. In this study, we found that receptor of LMW-HA, TLR4, was aberrantly overexpressed in PTC tissues and cell line W3. Exposure of W3 cells to LMW-HA promoted cell proliferation and migration via TLR4. Knockdown of TLR4 has provided evidence that TLR4 is essential for LMW-HA-induced CXCR7 expression, which is responsible for LMW-HA-induced proliferation and migration of W3 cells. In tumor-bearing adult nude mice, stimulation of LMW-HA on W3 cells promotes CXCR7 expression in tumor masses (P=0.002) and tumor growth (P<0.001). To further confirm our findings, we investigated the clinicopathologic significance of TLR4 and CXCR7 expression using immumohistochemistry in 135 human PTC tissues and 56 normal thyroid tissue samples. Higher rates of TLR4 (53%) and CXCR7 (24%) expression were found in PTC tissues than in normal tissues. Expression of TLR4 or CXCR7 is associated with tumor size and lymph node metastasis. Therefore, LMW-HA may contribute to the development of PTC via TLR4/CXCR7 pathway, which may be a novel target for PTC immunomodulatory therapy.

scholarly journals MicroRNA-517c Functions as a Tumor Suppressor in Hepatocellular Carcinoma via Downregulation of KPNA2 and Inhibition of PI3K/AKT Pathway

2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Limin Ma ◽  
Changming Tao ◽  
Yingying Zhang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Epithelial To Mesenchymal Transition ◽  
Clinical Analysis ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Tissue Samples ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Objective. Hepatocellular carcinoma (HCC) is a kind of solid and highly aggressive malignant tumor with poor prognosis. MicroRNA (miRNA/miR) has been confirmed to be involved in HCC development. The current study focused on the functions and mechanisms of miR-517c in HCC. Methods. Expressions of miR-517c and Karyopherin α2 (KPNA2) mRNA in HCC cell lines and tissue samples were examined using quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was conducted for detections of epithelial-to-mesenchymal transition (EMT) and PI3K/AKT markers. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and Transwell assays were utilized to investigate the influence of miR-517c on HCC cell proliferation, invasion, and migration. TargetScan and luciferase reporter assay were performed to search for the potential target gene of miR-517c. Results. We demonstrated that miR-517c expressions were decreased in HCC tissues and cells. Moreover, the clinical analysis showed that decreased miR-517c expressions in HCC tissues correlated with shorter overall survival and malignant clinicopathologic features of HCC patients. MTT assay showed that miR-517c upregulation prominently repressed HCC cell proliferation. In addition, miR-517c restoration could significantly suppress HCC cell invasion and migration as demonstrated by Transwell assays. We also found that miR-517c directly targeted KPNA2 and regulated the PI3K/AKT pathway and EMT, exerting prohibitory functions in HCC. Conclusion. Taken together, this study stated that miR-517c inhibited HCC progression via regulating the PI3K/AKT pathway and EMT and targeting KPNA2 in HCC, providing a novel insight into HCC treatment.

scholarly journals A Novel Circular RNA CircRFX3 Serves as a Sponge for MicroRNA-587 in Promoting Glioblastoma Progression via Regulating PDIA3

2021 ◽  
Vol 9 ◽  
Author(s):  
Tong Li ◽  
Jianguo Xu ◽  
Yi Liu
Keyword(s):  
Circular Rna ◽  
Molecular Therapy ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Competing Endogenous Rna ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Downstream Target ◽  
Novel Target ◽  
And Migration

An increasing number of studies have indicated that circular RNAs (circRNAs) participate in the progression of numerous tumors. However, the functions of circRNAs in glioblastoma (GBM) remain largely unknown. In this study, we focused on a novel circRNA (hsa_circRFX3_003) that was spliced from RFX3, which we named circRFX3. We confirmed that the expression of circRFX3 was substantially increased in GBM cell lines and clinical GBM tissues. The results of a series of overexpression and knockdown assays indicated that circRFX3 could boost the proliferation, invasion, and migration of GBM cells. By performing dual-luciferase reporter gene and RNA pull-down assays, we verified that circRFX3 could sponge microRNA-587 (miR-587) to exercise its function as a competing endogenous RNA (ceRNA) in the development of GBM. In addition, PDIA3 was proven to be a downstream target of miR-587 and to regulate the Wnt/β-catenin pathway. In conclusion, circRFX3 could act as a cancer-promoting circRNA to boost the development of GBM and regulate the miR-587/PDIA3/β-catenin axis. This study might provide a novel target for the treatment of GBM with molecular therapy.

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