scholarly journals LSINCT5 predicts unfavorable prognosis and exerts oncogenic function in osteosarcoma

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Weidong He ◽  
Ming Lu ◽  
Dongbo Xiao
Keyword(s):  
Cell Proliferation ◽  
Overall Survival ◽  
Cancer Progression ◽  
Histological Grade ◽  
Migration And Invasion ◽  
Large Tumor ◽  
Tissue Samples ◽  
Enneking Stage ◽  
Oncogenic Function

AbstractThe dysregulated expression of LSINCT5 (long stress-induced non-coding transcript 5) has been found in various human tumors, and was generally related to cancer progression and unfavorable prognosis. Although the role of LSINCT5 in osteosarcoma was reported not long ago, the sample size of that study was limited. Our study presented more evidence about the clinical significance and biological function of LSINCT5 in osteosarcoma. In our results, we found LSINCT5 expression was increased in osteosarcoma tissue samples and cell lines, and high LSINCT5 expression was associated with advanced Enneking stage, large tumor size, high histological grade and present distant metastasis. Meanwhile, we observed high LSINCT5 expression was correlated with worse overall survival, and high LSINCT5 expression could be an independent poor predictor for overall survival in osteosarcoma cases. Moreover, we found inhibition of LSINCT5 expression suppressed cell proliferation, migration and invasion in vitro, and LSINCT5 overexpression dramatically facilitated cell proliferation, migration and invasion in vitro. In conclusion, our study suggests that LSINCT5 exerts oncogenic function in osteosarcoma cells, and may be a potential predictor for clinical outcome in osteosarcoma patients.

scholarly journals LOXL1-AS1 predicts poor prognosis and promotes cell proliferation, migration, and invasion in osteosarcoma

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Si Chen ◽  
Weiguo Li ◽  
Ai Guo
Keyword(s):  
Cell Proliferation ◽  
Overall Survival ◽  
Poor Prognosis ◽  
Histological Grade ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Loss Of Function ◽  
Osteoblast Cell Line ◽  
Enneking Stage

Abstract lncRNA LOXL1 antisense RNA 1 (lncRNA LOXL1-AS1) was recently found to function as oncogenic lncRNA in glioblastoma, prostate cancer, and medulloblastoma. The role of LOXL1-AS1 in osteosarcoma was still unknown. In our study, we found LOXL1-AS1 expression levels were higher in osteosarcoma tissues and cell lines than normal bone tissues and normal osteoblast cell line, respectively. Moreover, high-expression of LOXL1-AS1 was correlated with Enneking stage, tumor size, distant metastasis, histological grade, and overall survival time in osteosarcoma patients. Furthermore, LOXL1-AS1 overexpression acted as an independent poor predictor for overall survival in osteosarcoma patients. The loss-of-function studies showed knockdown of LOXL1-AS1 dramatically inhibited osteosarcoma cell proliferation, migration, and invasion through suppressing PI3K-AKT pathway. In conclusion, LOXL1-AS1 predicts clinical progression and poor prognosis in osteosarcoma patients and functions as oncogenic lncRNA to regulate cell proliferation, cell cycle, migration, and invasion.

miR-369-3p serves as prognostic factor and regulates cancer progression of hepatocellular carcinoma

2021 ◽  
Author(s):  
Can Chen ◽  
Yi Zong ◽  
Jiaojiao Tang ◽  
Ruisheng Ke ◽  
Lizhi Lv ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Pcr Analysis ◽  
Reverse Transcription Pcr ◽  
Huh7 Cells

Background: The aim of this study was to investigate the role of miR-369-3p in hepatocellular carcinoma (HCC). Materials & methods: The expression levels of miR-369-3p were detected using the quantitative real-time reverse transcription-PCR analysis. The cell counting kit-8 and transwell assays were used to explore the effects of miR-369-3p on cell proliferation, migration and invasion of HCC cells. Results: The miR-369-3p expression was downregulated in HCC tissues and cell lines, in comparison to the normal controls, respectively. In vitro, overexpression of miR-369-3p in Hep 3B and Huh7 cells inhibited cell proliferation, migration and invasion. SOX4 was a direct target of miR-369-3p. Conclusion: Our results suggested that miR-369-3p may be a tumor suppressor in HCC by targeting SOX4.

scholarly journals SPON2 Is Upregulated through Notch Signaling Pathway and Promotes Tumor Progression in Gastric Cancer

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1439
Author(s):  
Hyeon-Gu Kang ◽  
Won-Jin Kim ◽  
Myung-Giun Noh ◽  
Kyung-Hee Chun ◽  
Seok-Jun Kim
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Notch Signaling Pathway ◽  
Migration And Invasion ◽  
Gene Assay ◽  
Gastric Cancer Progression

Spondin-2 (SPON2) is involved in cancer progression and metastasis of many tumors; however, its role and underlying mechanism in gastric cancer are still obscure. In this study, we investigated the role of SPON2 and related signaling pathway in gastric cancer progression and metastasis. SPON2 expression levels were found to be upregulated in gastric cancer cell lines and patient tissues compared to normal gastric epithelial cells and normal controls. Furthermore, SPON2 silencing was observed to decrease cell proliferation and motility and reduce tumor growth in xenograft mice. Conversely, SPON2 overexpression was found to increase cell proliferation and motility. Subsequently, we focused on regulatory mechanism of SPON2 in gastric cancer. cDNA microarray and in vitro study showed that Notch signaling is significantly correlated to SPON2 expression. Therefore, we confirmed how Notch signaling pathway regulate SPON2 expression using Notch signaling-related transcription factor interaction and reporter gene assay. Additionally, activation of Notch signaling was observed to increase cell proliferation, migration, and invasion through SPON2 expression. Our study demonstrated that Notch signaling-mediated SPON2 upregulation is associated with aggressive progression of gastric cancer. In conclusion, we suggest upregulated SPON2 via Notch signaling as a potential target gene to inhibit gastric cancer progression.

USP44 hypermethylation promotes cell proliferation and metastasis in breast cancer

2020 ◽  
Author(s):  
Xin Chen ◽  
Xiaotang Wu ◽  
Wen Lei
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Cell Behaviors ◽  
Specific Pcr ◽  
Proliferation And Metastasis ◽  
Induced Apoptosis

Aim: The methylation and expression levels of USP44 in breast cancer were investigated and their effects on tumor cells were researched. Materials & Methods: Bioinformatics was employed to identify the target gene from TCGA database. Sodium bisulfite and decitabine were used for DNA modification and demethylation, and methylation-specific PCR and reverse transcriptase PCR were performed to assess USP44 methylation and expression levels. Tumor cell behaviors were assayed via several in vitro experiments. Results: USP44 was hypermethylated, which caused its poor expression in breast cancer, whereas its overexpression significantly suppressed cancer cell proliferation, migration and invasion and induced apoptosis. Conclusion: USP44 negatively functions in cancer progression upon overexpression, indicating its potential as a therapeutic target for clinical treatment of breast cancer.

scholarly journals LINC01224 promotes colorectal cancer progression through targeting miR-485-5p/MYO6 axis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingfeng Gu ◽  
Liang Dong ◽  
Yun Wang ◽  
Wenjia Nie ◽  
Wencong Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Binding Interaction ◽  
Tissue Samples ◽  
Rna Immunoprecipitation ◽  
Colorectal Cancer Progression ◽  
Transcription Factor Yy1

Abstract Background Long noncoding RNAs (lncRNAs) are related to colorectal cancer (CRC) development. However, the role and mechanism of lncRNA LINC01224 in CRC development are largely unknown. Methods LINC01224, Yin Yang 1 (YY1), microRNA (miR)-485-5p, and myosins of class VI (MYO6) levels were examined using quantitative reverse transcription polymerase chain reaction and western blotting. Functional analyses were processed through CCK-8, colony formation, flow cytometry, transwell, and xenograft analyses. Dual-luciferase reporter, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation, and pull-down assays were conducted to analyze the binding interaction. Results LINC01224 abundance was elevated in CRC tissue samples and cell lines. Elevated LINC01224 might indicate the lower 5-year overall survival in 52 CRC patients. LINC01224 was upregulated via the transcription factor YY1. LINC01224 knockdown restrained CRC cell proliferation, migration, and invasion and increased apoptosis. MiR-485-5p was sponged by LINC01224, and miR-485-5p downregulation relieved the influence of LINC01224 interference on CRC progression. MYO6 was targeted via miR-485-5p and regulated via LINC01224/miR-485-5p axis. MiR-485-5p overexpression suppressed CRC cell proliferation, migration, and invasion and facilitated apoptosis. MYO6 upregulation mitigated the role of miR-485-5p. LINC01224 knockdown decreased xenograft tumor growth. Conclusion YY1-induced LINC01224 regulates CRC development via modulating miR-485-5p/MYO6 axis.

scholarly journals LINC00675 is a prognostic factor and regulates cell proliferation, migration and invasion in glioma

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Zhibing Li ◽  
Yijian Li ◽  
Qibai Wang
Keyword(s):  
Cell Proliferation ◽  
Cancer Colorectal ◽  
Tumor Promoter ◽  
Migration And Invasion ◽  
Large Tumor ◽  
Who Grade ◽  
Protein Expressions ◽  
Glioma Cell Proliferation ◽  
Expression Status

LINC00675 has been suggested to be dysregulated in gastric cancer, colorectal cancer and pancreatic cancer. However, the expression status and biological function of LINC00675 in glioma were still unknown. Thus, we reported LINC00675 was overexpressed in glioma tissues and cell lines, and positively associated with advanced WHO grade, large tumor size and poor prognosis. Moreover, univariate and multivariate analyses suggested that high-expression of LINC00675 was an independent unfavorable prognostic predictor for glioma. In addition, levels of LINC00675 expression were positively correlated with TRIP6 mRNA and protein expressions. The in vitro experiment showed that silencing of LINC00675 inhibits glioma cell proliferation, migration and invasion through regulating TRIP6. In conclusion, LINC00675 acts as a tumor promoter in glioma progression.

scholarly journals CircNOL10 suppresses breast cancer progression by sponging miR-767-5p to regulate SOCS2/JAK/STAT signaling

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Fang Wang ◽  
Xiaochun Wang ◽  
Jingruo Li ◽  
Pengwei Lv ◽  
Mingli Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Cytokine Signaling

Abstract Background Circular RNAs (circRNAs) have caught increasing attentions and interests for their important involvement in cancer initiation and progression. This study aims to investigate the biological functions of circNOL10 and its potential molecular mechanisms in breast cancer (BC). Materials and methods qRT-PCR and western blot assays were performed to measure the expression of related genes. CCK-8, colony formation, flow cytomerty and transwell assays were used to assess cell proliferation, cell cycle, migration and invasion. RNA pull-down, luciferase reporter and RIP assays were applied to address the potential regulatory mechanism of circNOL10. Results CircNOL10 was down-regulated in BC tissues and cells. Low expression of circNOL10 was associated with larger tumor size, advanced TNM stage, lymph node metastasis and unfavorable prognosis. Overexpression of circNOL10 inhibited cell proliferation, migration, invasion and EMT in vitro and slowed xenograft tumor growth in vivo. Mechanistically, circNOL10 could act as a molecular sponge for miR-767-5p, leading to the up-regulation of suppressors of cytokine signaling 2 (SOCS2) and inactivation of JAK2/STAT5 pathway. Moreover, circNOL10-mediated suppression of malignant phenotypes was attenuated by miR-767-5p. Similar to circNOL10, enforced expression of SOCS2 also resulted in the suppression of cell proliferation and metastasis. Furthermore, knockdown of SOCS2 reversed the tumor-suppressive effect induced by circNOL10. Conclusions CircNOL10 repressed BC development via inactivation of JAK2/STAT5 signaling by regulating miR-767-5p/SOCS2 axis. Our findings offer the possibility of exploiting circNOL10 as a therapeutic and prognostic target for BC patients.

scholarly journals Circular RNA circ-ZKSCAN1 inhibits bladder cancer progression through miR-1178-3p/p21 axis and acts as a prognostic factor of recurrence

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Junming Bi ◽  
Hongwei Liu ◽  
Wei Dong ◽  
Weibin Xie ◽  
Qingqing He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Progression ◽  
Tumor Grade ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Rank Test ◽  
Circular Rnas

Abstract Background Circular RNAs (circRNAs) represent a subclass of regulatory RNAs that have been shown to have significant regulatory roles in cancer progression. However, the biological functions of circRNAs in bladder cancer (BCa) are largely unknown. Methods Cell invasion models were established, and invasion-related circRNAs were detected by qPCR. Using above method, circ-ZKSCAN1 was picked out for further study. Circ-ZKSCAN1 expression and survival analyses were performed through qPCR. The survival curves were generated by the Kaplan-Meier method, and the log-rank test was used to assess the significance. Cell proliferation, migration and invasion were examined to investigate the function of circ-ZKSCAN1. Tumorigenesis in nude mice was assessed to determine the effect of circ-ZKSCAN1 in bladder cancer. Biotin-coupled probe pull-down assays, FISH and luciferase reporter assays were conducted to confirm the relationship between circ-ZKSCAN1 and microRNA. RNA-seq revealed different molecular changes in downstream genes. Results Here, we found that circ-ZKSCAN1 was downregulated in BCa tissues and cell lines. Circ-ZKSCAN1 levels were associated with survival, tumor grade, pathological T stage and tumor recurrence. Overexpressed circ-ZKSCAN1 inhibits cell proliferation, migration, invasion and metastasis in vitro and in vivo. Mechanistically, we demonstrated that circ-ZKSCAN1 upregulated p21 expression by sponging miR-1178-3p, which suppressed the aggressive biological behaviors in bladder cancer. Conclusions These results reveal that Circ-ZKSCAN1 acts as a tumor suppressor via a novel circ-ZKSCAN1/miR-1178-3p/p21 axis, which have the important role in the proliferation, migration and invasion ablitities of BCa cells and provide a novel perspective on circRNAs in BCa progression.

scholarly journals PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

2018 ◽  
Vol 49 (2) ◽  
pp. 696-705 ◽  
Author(s):  
Jing Zhu ◽  
Hua Hu ◽  
Jing Wang ◽  
Ying Yang ◽  
Ping Yi
Keyword(s):  
Cell Proliferation ◽  
Critical Role ◽  
Figo Stage ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
High Rate ◽  
Biological Behavior ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Large Tumor

Background/Aims: Ovarian cancer (OC) is the most lethal gynecologic malignancy, mainly due to the advanced stage at diagnosis in most patients and high rate of relapse. Thus, it is still essential to elucidate the underlying mechanisms and explore the diagnostic and therapeutic targets of OC. Recent studies have revealed that proline-rich protein 11 (PRR11) is dysregulated in different cancers, participating in their initiation and progression; however, it remains unclear whether PRR11 is involved in OC. Methods: Immunohistochemical staining, quantitative reverse transcription PCR, and western blotting were performed to evaluate PRR11 expression in OC tissues and cells. The relationship between PRR11 expression and the clinicopathologic data of patients were analyzed. We upregulated and downregulated PRR11 expression using a PRR11 overexpression vector and PRR11-specifc small interfering RNA, respectively, to further clarify its role in the malignant biological behavior of OC in vitro. Results: Overexpression of PRR11 in OC tissues and cells significantly correlated with advanced FIGO stage, lymph node metastasis, and large tumor size. Downregulation of PRR11 inhibited cell proliferation and prevented the invasion and migration of HO-8910 OC cells, whereas opposite results were observed in Caov3 cells upon PRR11 upregulation. Further analyses showed that PRR11 positively regulated cell proliferation-related proteins, including c-myc and cyclin D1, and increased and decreased the expression of matrix metalloproteinase 2 and tissue inhibitor of metalloproteinase 2, respectively. Additionally, our preliminary results demonstrated that PRR11 expression was mediated by the phosphoinositide 3-kinase/AKT/β-catenin signaling pathway. Conclusion: The results of this study provide evidence that PRR11 plays a critical role in the progression and metastasis of OC, and as such, may serve as a potential prognostic and therapeutic target in OC.

scholarly journals LncRNA BDNF-AS is associated with the malignant status and regulates cell proliferation and apoptosis in osteosarcoma

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Qiang Huang ◽  
Jiao Yang ◽  
Xin He ◽  
Shuyan Shi ◽  
Shuxing Xing
Keyword(s):  
Cell Proliferation ◽  
Large Tumor ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Enneking Stage ◽  
And Function ◽  
Long Non Coding Rna ◽  
Expression Status ◽  
Low Expression

Long non-coding RNA (LncRNA) brain-derived neurotrophic factor antisense (BDNF-AS) has been found to be down-regulated and function in a tumor suppressive role in human cancers. However, the expression status and function of BDNF-AS is still unknown in osteosarcoma (OS). In our study, BDNF-AS expression was found to be decreased in OS tissues and cells. Moreover, BDNF-AS low expression was correlated with advanced Enneking stage, large tumor size and poor prognosis in OS patients. The multivariate analysis suggested low expression of BDNF-AS was an independent unfavorable prognostic factor for overall survival in OS patients. The in vitro studies indicated that BDNF-AS overexpression inhibits OS cell proliferation and promotes cell apoptosis through regulating cleaved caspase-3. In conclusion, BDNF-AS serves as a tumor suppressive lncRNA in OS.

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