scholarly journals LncRNA NRON Inhibits Osteosarcoma Cell Proliferation, Invasion by Regulating MVB12B

2020 ◽  
Author(s):  
Yancheng Liu ◽  
Jingyu Zhang ◽  
Yongqiang Jiao ◽  
Shuwei Ma ◽  
Xinlong Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Noncoding Rna ◽  
Bioinformatics Analysis ◽  
Osteosarcoma Cell ◽  
Potential Therapeutic Target ◽  
Rescue Experiment ◽  
Important Regulator ◽  
Direct Target ◽  
The Relationship

Abstract Aims: Long noncoding RNA have been proved as important regulator in various diseases. NRON was a newly identified tumor-related lncRNA, and previous studies have reported its function in hepatocellular carcinoma and heart failure. However, the function and mechanism of lncRNA NRON in osteosarcoma still unknown. Methods: Cell proliferation, invasion, migration and apoptosis were detected via CCK-8, transwell assay and Western. Bioinformatics analysis was used to predict the potential target of NRON. Rescue experiment was performed to identify the relationship between NRON and MVB12B. Results: The expression of lncRNA NRON was significantly downregulate in osteosarcoma tissues and cell lines. Knockdown of NRON promoted cell proliferation, invasion and EMT. Overexpression of NRON inhibited cell proliferation, invasion and EMT. Bioinformatics analysis predicted that MVB12B was the direct target. The expression of MVB12B was significantly upregulated in osteosarcoma tissues and cell lines. Rescue experiment further confirmed the relationship between NRON and MVB12B. Overexpression of MVB12B completely reversed the function of NRON. Conclusion: Taken together, our results comprehensively analyzed the function of NRON in osteosarcoma and provided possible mechanism that NRON inhibited osteosarcoma development by regulating MVB12B. Thus, our study may offer a potential therapeutic target for treating osteosarcoma.

scholarly journals LncRNA RBM5-AS1 Promotes Osteosarcoma Cell Proliferation, Migration, and Invasion

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Biyong Deng ◽  
Runsang Pan ◽  
Xin Ou ◽  
Taizhe Wang ◽  
Weiguo Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Western Blotting ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Pediatric Age Group ◽  
The Relationship

Purpose. Osteosarcoma (Os) is the most frequent malignant tumor of the bone in the pediatric age group, and accumulating evidences show that lncRNAs play a key role in the development of Os. Thus, we investigated the role of RBM5-AS1 and its molecular mechanism. Methods. The expression of RBM5-AS1 in Os tissues and cell lines was detected by real-time polymerase chain reaction (QPCR). The effect of RBM5-AS1 on the proliferation of Os cells was detected using CCK8 assays and flow cytometry. The effect of RBM5-AS1 on the migration and invasion of Os cells was detected by transwell assays. And we performed QPCR and western blotting assays to investigate the relationship between RBM5-AS1 and RBM5. Finally, western blotting assays were performed to explore the mechanism of RBM5. Results. LncRNA RBM5-AS1 was overexpressed in the Os tissues and cell lines. And lncRNA RBM5-AS1 promoted Os cell proliferation, migration, and invasion in vitro and tumor growth in vivo. LncRNA RBM5-AS1 targets RBM5 in Os cells. Conclusion. To sum up, the results showed that lncRNA RBM5-AS1 promotes cell proliferation, migration, and invasion in Os.

scholarly journals The proliferation and invasion of osteosarcoma are inhibited by miR-101 via targetting ZEB2

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Haopeng Lin ◽  
Xiaodong Zheng ◽  
Ting Lu ◽  
Yang Gu ◽  
Canhao Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Bone Cell ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Direct Target ◽  
Proliferation And Invasion

AbstractHaving a better grasp of the molecular mechanisms underlying carcinogenesis and progression in osteosarcoma would be helpful to find novel therapeutic targets. Different types of cancers have presented abnormal expression of miRNA-101 (miR-101). Nevertheless, we still could not figure out what expression of miR-101 in human osteosarcoma is and its biological function. Thus, we conducted the present study to identify its expression, function, and molecular mechanism in osteosarcoma. We detected the expression of miR-101 in osteosarcoma samples and cell lines. The effects of miR-101 on osteosarcoma cells’ proliferation and invasion were evaluated. Luciferase reporter assay was applied to identify the direct target of miR-101. Compared with adjacent normal specimens and normal bone cell line by using qPCR, the expression levels of miR-101 in osteosarcoma specimens and human osteosarcoma cell lines distinctly decreased. According to function assays, we found that overexpression of miR-101 significantly inhibited the cell proliferation and invasion in osteosarcoma cells. Moreover, we confirmed that zinc finger E-box binding homeobox 2 (ZEB2) was a direct target of miR-101. In addition, overexpression of ZEB2 could rescue the inhibition effect of proliferation and invasion induced by miR-101 in osteosarcoma cells. MiR-101 has been proved to be down-regulated in osteosarcoma and has the ability to suppress osteosarcoma cell proliferation and invasion by directly targetting ZEB2.

scholarly journals Knockdown of Long Noncoding RNA CAT104 Inhibits the Proliferation, Migration, and Invasion of Human Osteosarcoma Cells by Regulating MicroRNA-381

2018 ◽  
Vol 27 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Bo Xia ◽  
Lei Wang ◽  
Li Feng ◽  
Baofang Tian ◽  
Yuanjie Tan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Inhibitory Effects ◽  
Human Osteosarcoma Cells ◽  
E Box ◽  
Direct Target Gene ◽  
Direct Target

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. This study aimed to explore the effects of long noncoding RNA CAT104 and microRNA-381 (miR-381) on osteosarcoma cell proliferation, migration, invasion, and apoptosis, as well as the underlying potential mechanism. We found that CAT104 was highly expressed in osteosarcoma MG63 and OS-732 cells. Knockdown of CAT104 significantly inhibited OS-732 cell proliferation, migration, and invasion, but promoted cell apoptosis. CAT104 regulated the expression of miR-381, and miR-381 participated in the effects of CAT104 on OS-732 cells. Zinc finger E-box-binding homeobox 1 (ZEB1) was a direct target gene of miR-381, which was involved in the regulatory roles of miR-381 in OS-732 cell proliferation, migration, invasion, and apoptosis, as well as c-Jun N-terminal kinase (JNK) and Wnt/β-catenin pathways. In conclusion, our research verified that suppression of CAT104 exerted significant inhibitory effects on osteosarcoma cell proliferation, migration, and invasion by regulating the expression of miR-381 and downstream ZEB1, as well as JNK and Wnt/β-catenin pathways.

scholarly journals MiR-125b Functions as a Tumor Suppressor and Enhances Chemosensitivity to Cisplatin in Osteosarcoma

2016 ◽  
Vol 15 (6) ◽  
pp. NP105-NP112 ◽  
Author(s):  
Fei Wang ◽  
Dapeng Yu ◽  
Zhen Liu ◽  
Ruijie Wang ◽  
Yan Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Cell Lines ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Human Osteosarcoma ◽  
Translational Level

MicroRNAs are highly conserved noncoding RNA that negatively modulate protein expression at a posttranscriptional and/or translational level and are deeply involved in the pathogenesis of several types of cancers. To date, the potential microRNAs regulating the growth and progression of osteosarcoma are not fully identified yet. Previous reports have shown differentially expressed miR-125b in osteosarcoma. However, the role of miR-125b in human osteosarcoma has not been totally illuminated. In this study, we have shown that miR-125b was downregulated in human osteosarcoma tissues compared to the adjacent tissues and effects as a tumor suppressor in vitro. We found that stable overexpression of miR-125b in osteosarcoma cell lines U2OS and MG-63 inhibited cell proliferation, migration, and invasion. Our data also verified that Bcl-2 is the target of miR-125b. Meanwhile, we showed that Bcl-2 was inversely correlated with miR-125b in osteosarcoma tissues. More importantly, we proved that miR-125b increased the chemosensitivity of osteosarcoma cell lines to cisplatin by targeting Bcl-2. In conclusion, our data demonstrate that miR-125b is a tumor suppressor and support its potential application for the treatment of osteosarcoma in the future.

XIST: A Meaningful Long Noncoding RNA in NSCLC Process

2020 ◽  
Vol 26 ◽  
Author(s):  
Yujie Shen ◽  
Yexiang Lin ◽  
Kai Liu ◽  
Jinlan Chen ◽  
Juanjuan Zhong ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Critical Role ◽  
Biological Functions ◽  
Potential Therapeutic Target ◽  
Considerable Evidence ◽  
Lncrna Xist ◽  
Nsclc Patients ◽  
The Relationship

Background: A number of studies have proposed that lncRNA XIST plays a role in the development and chemosensitivity of NSCLC. Besides, XIST may become a potential therapeutic target for NSCLC patients. The aim of this review is to reveal the biological functions and exact mechanisms of XIST in NSCLC. Methods: In this review, relevant researches involving in the relationship between XIST and NSCLC are collected through systematic retrieval of PubMed Results: XIST is an oncogene in NSCLC and is abnormally upregulated in NSCLC tissues. Considerable evidence has shown that XIST exerts a critical role in the proliferation, invasion, migration, apoptosis and chemosensitivity of NSCLC cells. XIST mainly functions as a ceRNA in NSCLC process, while XIST also functions at transcriptional levels. Conclusion: LncRNA XIST has potential to become a novel biomolecular marker of NSCLC and a therapeutic target for NSCLC.

scholarly journals LncRNA SNHG15 contributes to doxorubicin resistance of osteosarcoma cells through targeting the miR-381-3p/GFRA1 axis

2020 ◽  
Vol 15 (1) ◽  
pp. 871-883
Author(s):  
Jinshan Zhang ◽  
Dan Rao ◽  
Haibo Ma ◽  
Defeng Kong ◽  
Xiaoming Xu ◽  
...  
Keyword(s):  
Cell Lines ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Inhibitory Effect ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells

AbstractBackgroundOsteosarcoma is a common primary malignant bone cancer. Long noncoding RNA small nucleolar RNA host gene 15 (SNHG15) has been reported to play an oncogenic role in many cancers. Nevertheless, the role of SNHG15 in the doxorubicin (DXR) resistance of osteosarcoma cells has not been fully addressed.MethodsCell Counting Kit-8 assay was conducted to measure the half-maximal inhibitory concentration value of DXR in osteosarcoma cells. Western blotting was carried out to examine the levels of autophagy-related proteins and GDNF family receptor alpha-1 (GFRA1). Quantitative reverse transcription-polymerase chain reaction was performed to determine the levels of SNHG15, miR-381-3p, and GFRA1. The proliferation of osteosarcoma cells was measured by MTT assay. The binding sites between miR-381-3p and SNHG15 or GFRA1 were predicted by Starbase bioinformatics software, and the interaction was confirmed by dual-luciferase reporter assay. Murine xenograft model was established to validate the function of SNHG15 in vivo.ResultsAutophagy inhibitor 3-methyladenine sensitized DXR-resistant osteosarcoma cell lines to DXR. SNHG15 was upregulated in DXR-resistant osteosarcoma tissues and cell lines. SNHG15 knockdown inhibited the proliferation, DXR resistance, and autophagy of osteosarcoma cells. MiR-381-3p was a direct target of SNHG15, and GFRA1 bound to miR-381-3p in osteosarcoma cells. SNHG15 contributed to DXR resistance through the miR-381-3p/GFRA1 axis in vitro. SNHG15 depletion contributed to the inhibitory effect of DXR on osteosarcoma tumor growth through the miR-381-3p/GFRA1 axis in vivo.ConclusionsSNHG15 enhanced the DXR resistance of osteosarcoma cells through elevating the autophagy via targeting the miR-381-3p/GFRA1 axis. Restoration of miR-381-3p expression might be an underlying therapeutic strategy to overcome the DXR resistance of osteosarcoma.

scholarly journals Rhotekin 2 silencing inhibits proliferation and induces apoptosis in human osteosarcoma cells

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Xiong Wang ◽  
Lei Zhang ◽  
Wenji Wang ◽  
Yuchen Wang ◽  
Ye Chen ◽  
...  
Keyword(s):  
Cell Lines ◽  
Phase Cell ◽  
Osteosarcoma Cell ◽  
Cyclin Dependent Kinase ◽  
Potential Therapeutic Target ◽  
Human Osteosarcoma ◽  
Cycle Arrest ◽  
Human Osteosarcoma Cells ◽  
Human Osteosarcoma Cell ◽  
Induced Apoptosis

Human osteosarcoma is the most frequent primary malignant of bone, and often occurs in adolescents. However, molecular mechanism of this disease remains unclear. In the present study, we found that the level of Rhotekin 2 (RTKN2) was up-regulated in osteosarcoma tissues and cell lines. In addition, silencing of RTKN2 of human osteosarcoma cell lines U2OS, inhibited proliferation, and induced G1 phase cell cycle arrest via reducing the level of the cyclin-dependent kinase 2 (CDK2). Furthermore, RTKN2 knockdown in the U2OS cells induced apoptosis by increasing the level of Bax and decreasing the level of Bcl2. These results suggested that RTKN2 is involved in the progression of human osteosarcoma, and may be a potential therapeutic target.

scholarly journals LncRNA IDH1-AS1 links the functions of c-Myc and HIF1α via IDH1 to regulate the Warburg effect

2018 ◽  
Vol 115 (7) ◽  
pp. E1465-E1474 ◽  
Author(s):  
Shaoxun Xiang ◽  
Hao Gu ◽  
Lei Jin ◽  
Rick F. Thorne ◽  
Xu Dong Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Enzymatic Activity ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Warburg Effect ◽  
Noncoding Rna ◽  
Ros Production ◽  
Xenograft Growth ◽  
The Relationship ◽  
The Warburg Effect

The oncoprotein c-Myc plays an important role in regulating glycolysis under normoxia; yet, in cancer cells, HIF1α, which is essential for driving glycolysis under hypoxia, is often up-regulated even in the presence of oxygen. The relationship between these two major regulators of the Warburg effect remains to be fully defined. Here we demonstrate that regulation of a long noncoding RNA (lncRNA), named IDH1-AS1, enables c-Myc to collaborate with HIF1α in activating the Warburg effect under normoxia. c-Myc transcriptionally repressed IDH1-AS1, which, upon expression, promoted homodimerization of IDH1 and thus enhanced its enzymatic activity. This resulted in increased α-KG and decreased ROS production and subsequent HIF1α down-regulation, leading to attenuation of glycolysis. Hence, c-Myc repression of IDH1-AS1 promotes activation of the Warburg effect by HIF1α. As such, IDH1-AS1 overexpression inhibited cell proliferation, whereas silencing of IDH1-AS1 promoted cell proliferation and cancer xenograft growth. Restoring IDH1-AS1 expression may therefore represent a potential metabolic approach for cancer treatment.

scholarly journals MiR-520b/e Regulates Proliferation and Migration by Simultaneously Targeting EGFR in Gastric Cancer

2016 ◽  
Vol 40 (6) ◽  
pp. 1303-1315 ◽  
Author(s):  
Shuang Li ◽  
Haiyang Zhang ◽  
Tao Ning ◽  
Xinyi Wang ◽  
Rui Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Cell Lines ◽  
Growth Factor Receptor ◽  
Over Expression ◽  
Epidermal Growth ◽  
And Migration ◽  
The Relationship ◽  
Proliferation And Migration

Background: MicroRNAs (miRNAs) have been demonstrated to play a crucial role in tumorigenesis. Previous studies have shown that miR-520b/e acts as a tumor suppressor in several tumors. Other studies indicated that epidermal growth factor receptor (EGFR) is highly expressed in many tumors, and involved in the development of tumors, such as cell proliferation, migration, angiogenesis and apoptosis. However, the correlation of miRNAs and EGFR in gastric cancer (GC) has not been adequately investigated. Our aim was to explore the relationship. Methods: The expression levels of EGFR and miR-520b/e were examined by RT-PCR and Western blot. We also investigated the relationship between EGFR and miR-520b/e in GC cell lines by relevant experiments. Results: In this study, we found that miR-520b/e inhibits the protein expression of EGFR by directly binding with the 3'-untranslated region (3'-UTR). And it was shown that the down-regulation of miR-520b/e promotes cell proliferation and migration by negative regulation of the EGFR pathway, while over-expression of miR-520b/e inhibits these properties. In addition, the biological function of EGFR in GC cell lines was validated by silencing and over-expression assays respectively. Conclusions: Taken together, our results demonstrate that miR-520b/e acts as a tumor suppressor by regulating EGFR in GC, and provide a novel marker and insight for the potential therapeutic target of GC.

The Effect of miR-155 on the Regulation of Hyperplasia of Middle Membrane of Blood Vessel in Rat Hypertension Model

2019 ◽  
Vol 9 (7) ◽  
pp. 982-987
Author(s):  
Xiaoying Wang ◽  
Yanke Hao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bioinformatics Analysis ◽  
Luciferase Assay ◽  
Ki 67 ◽  
Vsmc Proliferation ◽  
Tunica Media ◽  
Proliferation And Apoptosis ◽  
The Relationship

Vascular smooth muscle cell (VSMC) abnormal proliferation is related to hypertension. P27 can arrest cell cycle and its downregulation is associated with hypertension. miR-155 plays a regulatory role in VSMC proliferation, while its relationship with hypertension is still unclear. Bioinformatics analysis reveals a relationship between p27 mRNA and miR-155. The present study explores miR-155's role in p27 expression, VSMC proliferation and apoptosis, as well as in the pathogenesis of hypertension. Dual luciferase assay verified the relationship between miR-155 and p27. miR155, p27, α-SMA, and Ki-67 expressions in the thoracic aorta media of rat hypertension model were detected. VSMCs were cultured in vitro and grouped into, anti-miR-NC, anti-miR-155, pIRES2-blank, pIRES2-p27, and anti-miR-155 + pIRES2-p27 groups followed by analysis of cell cycle by flow cytometry and cell proliferation by EdU staining. Hypertension rats were randomly divided into antagomir-155 and antagomir-control. Caudal artery systolic and diastolic pressures were measured. miR-155 suppressed p27 expression. miR-155 and Ki-67 expressions were significantly enhanced, while p27 and α-SMA levels were reduced in the tunica media from hypertension rats compared with control. Downregulation of miR-155 and/or upregulation of p27 obviously declined cell proliferation and arrested cell cycle in G1 phase. Antagomir-155 injection significantly decreased systolic and diastolic pressures, elevated p27 and α-SMA expressions in media, and reduced the thickness of tunica media. miR-155 enhances VSMC proliferation via regulating p27. miR-155 enhancement was related to hypertension. miR-155 plays a therapeutic effect in hypertension.

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