scholarly journals TSLC1 inhibits bladder cancer cells proliferation and promotes apoptosis by targeting miR-125b

2020 ◽  
Author(s):  
Jun Zhu ◽  
Rui Hu ◽  
NingJing Ou ◽  
Zhen Liang ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Line ◽  
Migration And Invasion ◽  
P53 Expression ◽  
Transwell Migration Assay ◽  
Migration Assay ◽  
Bladder Cancer Cells ◽  
Cancer Tissues ◽  
The Relationship

Abstract Backgroud: The aim of this study was to investigate the relationship between the expression of tumor suppressor in lung cancer-1 (TSLC1) and miRNA-125b in bladder cancer (BC) pathogenesis. Methods: The expression of miRNA-125b,TSLC1 and p53 in BC cell line was detected by real-time quantitative RT-PCR (RT-qPCR) or western blot. Transwell migration assay was used in the in vitro migration and invison anssay. TSLC1 and p53 expression was evaluated by immunohistochemistric staining in bladder cancer tissues. Results: We showed that the expression of miRNA-125b was significantly decreased in BC cell line(T24) transfection of miR-125b inhibitor.Knockdown of miRNA-125b promoted the growth and metastasis of T24 cells,while overexpression of miRNA-125b had the opposite effects. Furthermore,TSLC1 was significantly positive correlated with miRNA-125b expression and negative correlated with p53 expression in T24 cells.TSLC1 transfection increased the expression of miRNA-125b,and inhibited BC cell migration and invasion in vitro,and promoted apoptosis. The expression of TSLC1 and p53 was opposite in bladder cancer tissues. Conclusions: Our data provided strong evidence that TSLC1 inhibited tumorigenesis and development of BC through up-regulating tumor-suppressive miRNA-125b.

scholarly journals miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells

2018 ◽  
Vol 51 (2) ◽  
pp. 513-527 ◽  
Author(s):  
Junfeng Zhang ◽  
Longsheng Wang ◽  
Shiyu Mao ◽  
Mengnan Liu ◽  
Wentao Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Methylation Status ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

Background/Aims: Increasing evidence showed that miR-1-3p plays a major role in malignant tumor progression. However, the specific biological function of miR-1-3p in bladder cancer is yet unknown. Methods: The expression levels of miR-1-3p in bladder cancer tissues and cell lines were examined by qRT-PCR. Bisulfite sequencing PCR was used for DNA methylation analysis. The target of miR-1-3p was validated by a dual luciferase reporter assay, and the effects of miR-1-3p on phenotypic changes in bladder cancer cells were investigated in vitro and in vivo. Results: The expression of miR-1-3p in bladder cancer cells was downregulated as compared to normal SV-HUC-1 cells. Also, the expression of miR-1-3p was significantly lower in bladder cancer tissues than the corresponding non-cancerous tissues. The methylation status of CpG islands was involved in the regulation of miR-1-3p expression. miR-1-3p inhibited the bladder cancer cell proliferation, migration, and invasion by directly targeting the 3’-UTR of glutaminase. It also exerted an anti-tumor effect by negatively regulating the glutaminase in a xenograft mouse model. Furthermore, GLS depletion resulted in the prolonged expression of γH2AX. Conclusion: Taken together, these results demonstrated that miR-1-3p acts as a tumor suppressor via regulation of glutaminase expression in bladder cancer progression, and miR-1-3p might represent a novel therapeutic target for the treatment of bladder cancer.

scholarly journals Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling

2020 ◽  
Vol 7 ◽  
Author(s):  
Changshui Zhuang ◽  
Ying Liu ◽  
Shengqiang Fu ◽  
Chaobo Yuan ◽  
Jingwen Luo ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Line ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Pathological Process ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion

A subset of long non-coding RNAs (lncRNAs), categorized as miRNA-host gene lncRNAs (lnc-miRHGs), is processed to produce miRNAs and involved in cancer progression. This work aimed to investigate the influences and the molecular mechanisms of lnc-miRHGs MIR497HG in bladder cancer (BCa). The miR-497 and miR-195 were derived from MIR497HG. We identified that lnc-miRHG MIR497HG and two harbored miRNAs, miR-497 and miR-195, were downregulated in BCa by analyzing The Cancer Genome Atlas and our dataset. Silencing of MIR497HG by CRISPR/Cas13d in BCa cell line 5637 promoted cell growth, migration, and invasion in vitro. Conversely, overexpression of MIR497HG suppressed cell progression in BCa cell line T24. MiR-497/miR-195 mimics rescued significantly the oncogenic roles of knockdown of MIR497HG by CRISPR/Cas13d in BCa. Mechanistically, miR-497 and miR-195 co-ordinately suppressed multiple key components in Hippo/Yap and transforming growth factor β signaling and particularly attenuated the interaction between Yap and Smad3. In addition, E2F4 was proven to be critical for silencing MIR497HG transcription in BCa cells. In short, we propose for the first time to reveal the function and mechanisms of MIR497HG in BCa. Blocking the pathological process may be a potential strategy for the treatment of BCa.

scholarly journals Upregulated Vav2 in gastric cancer tissues promotes tumor invasion and metastasis

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769839 ◽  
Author(s):  
Bi-bo Tan ◽  
Yong Li ◽  
Li-qiao Fan ◽  
Qun Zhao ◽  
Qing-wei Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Activity ◽  
Migration And Invasion ◽  
Invasion And Metastasis ◽  
Clinical Value ◽  
Gastric Cancer Cells ◽  
Positive Rate ◽  
Cancer Tissues ◽  
The Relationship

Several studies have proved that Vav2 gene is associated with the carcinogenesis of some tumors, but the relationship between Vav2 gene and gastric cancer remains unclear. Purpose of this study is to detect the expression of Vav2 protein in gastric cancer tissues and to evaluate the clinical value of Vav2. Furthermore, both effect of Vav2 gene on invasion and metastasis of gastric cancer cells and its mechanism are investigated in vitro. Results showed that positive rate of Vav2 protein was significantly higher in gastric cancer tissues than in adjacent tissues and notably higher in metastatic lymph nodes than in gastric cancer tissues. Results of western blot were consistent with immunohistochemistry. Expression of Vav2 protein in gastric cancer tissues was related to degree of tumor differentiation, lymph node metastasis, and clinical stages. Inhibition of endogenous Vav2 in BGC823 cells led to significantly decreased cell activity, migration, and invasion ability in vitro, and expression of Rac1, MMP-2, and MMP-9 decreased, whereas expression of TIMP-1 increased. We concluded that Vav2 might promote invasion and metastasis of gastric cancer by regulating some invasion and metastasis-related genes.

scholarly journals LPS Upregulated VEGFR-3 Expression Promote Migration and Invasion in Colorectal Cancer via a Mechanism of Increased NF-κB Binding to the Promoter of VEGFR-3

2016 ◽  
Vol 39 (5) ◽  
pp. 1665-1678 ◽  
Author(s):  
Guangwei Zhu ◽  
Qiang Huang ◽  
Wei Zheng ◽  
Yongjian Huang ◽  
Jin Hua ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Neutralizing Antibody ◽  
High Expression ◽  
Migration And Invasion ◽  
Colorectal Cancer Cells ◽  
Cancer Tissues ◽  
The Relationship

Background and Aim: Lipopolysaccharide(LPS) could promote the progression of colorectal cancer, but the specific regulatory mechanisms are largely unknown. So, this study aim to clarify the mechanisms that LPS upregulated VEGFR-3, which promotes colorectal cancer cells migration and invasion with a mechanism of increased NF-κB bind to the promoter of VEGFR-3. Methods: The present study examined the VEGFR-3 expression in colorectal cancer tissues and analyzed the relationship between the VEGFR-3 expression with clinical parameters. PCR, Western blot, CCK-8, colone formation assay, and Transwell assay detected that LPS promoted the migration and invasion and the role of VEGFR-3 in the process of colorectal carcinoma in vitro. Used the methods of promoter analysis, EMSA assay and ChIP assay to explore the mechanisms LPS increased the expression of VEGFR-3. Results: VEGFR-3 was significantly high expression in the colorectal cancer tissues. And the high expression was associated with the TNM stage and lymph node metastasis of colorectal cancer. LPS could promote the migration and invasion, which could be blocked by the neutralizing antibody IgG of VEGFR-3. And found that -159 nt to +65 nt was the crucial region of VEGFR-3 promoter. And detected that the NF-κB was important transcription factor for the VEGFR-3 promoter. And LPS could increase NF-κB binding to VEGFR-3 promoter and upregulated the expression of VEGFR-3 to exert biological functions. Conclusion: We have elucidated the relationship between LPS and the VEGFR-3 expression and revealed that VEGFR-3 play very important role in the process of LPS promoting the migration and invasion of colorectal cancer cells. Further illuminated the mechanism that LPS upregulated VEGFR-3 expression via increased NF-κB bind to the promoter of VEGFR-3.

scholarly journals Circular RNA circGLIS3 promotes bladder cancer proliferation via the miR-1273f/SKP1/Cyclin D1 axis

2021 ◽  
Author(s):  
Shuilian Wu ◽  
Jialei Yang ◽  
Haotian Xu ◽  
Xin Wang ◽  
Ruirui Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cyclin D1 ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Multiple Tumor ◽  
Bladder Cancer Cells

AbstractExtensive research confirmed that circRNA can play a regulatory role in various stages of tumors by interacting with various molecules. Identifying the differentially expressed circRNA in bladder cancer and exploring its regulatory mechanism on bladder cancer progression are urgent. In this study, we screened out a circRNA-circGLIS3 with a significant upregulation trend in both bladder cancer tissues and cells. Bioinformatics prediction results showed that circGLIS3 may be involved in multiple tumor-related pathways. Function gain and loss experiments verified circGLIS3 can affect the proliferation, migration, and invasion of bladder cancer cells in vitro. Moreover, silencing circGLIS3 inhibited bladder cancer cell growth in vivo. Subsequent research results indicated circGLIS3 regulated the expression of cyclin D1, a cell cycle–related protein, and cell cycle progression. Mechanically, circGLIS3 upregulates the expression of SKP1 by adsorbing miR-1273f and then promotes cyclin D1 expression, ultimately promoting the proliferation of bladder cancer cells. In summary, our study indicates that circGLIS3 plays an oncogene role in the development of bladder cancer and has potential to be a candidate for bladder cancer. Graphical abstract

scholarly journals EGFR-AS1 Promotes Bladder Cancer Progression by Upregulating EGFR

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Anbang Wang ◽  
Aimin Jiang ◽  
Xinxin Gan ◽  
Zheng Wang ◽  
Jinming Huang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Diagnostic Marker ◽  
Bladder Cancer Cells ◽  
The Relationship ◽  
Proliferation And Invasion

Long noncoding RNAs play an essential role in bladder cancer progression. The role of long noncoding RNA EGFR-AS1 in bladder cancer needs further study. We used clinical specimens to analyze the relationship between EGFR-AS1 and bladder cancer patients’ characteristics. The functional experiments and mechanism studies were performed using qRT-PCR, transwell assay, survival analysis, and correlation analysis. We found that high expression of EGFR-AS1 was nearly related to aggressive bladder cancer and indicated poor prognosis for patients. The functional experiments in vivo and in vitro suggested that EGFR-AS1 promoted the proliferation and invasion of bladder cancer cells. Mechanically, EGFR-AS1 promoted the expression of EGFR by inhibiting the degradation of EGFR mRNA, thereby promoting the metastasis of bladder cancer. In addition, EGFR-AS1/EGFR may be involved in the immune-related pathways of bladder cancer. These studies indicate that the EGFR-AS1/EGFR pathway may be a potential diagnostic marker and therapeutic target for bladder cancer.

scholarly journals Methylation regulation of MUC6 correlates with metastasis of gastric cancer

2020 ◽  
Author(s):  
Ding Shi ◽  
Xiaoxia Xi
Keyword(s):  
Cell Lines ◽  
Promoter Region ◽  
Quantitative Polymerase Chain Reaction ◽  
Migration And Invasion ◽  
Sgc7901 Cell ◽  
Transwell Migration Assay ◽  
Migration Assay ◽  
Normal Tissues ◽  
Polymerase Chain ◽  
Cancer Tissues

Abstract Background: The aim of this study was to investigate the mechanism of the downregulation of MUC6 and its influence on GC metastasis.Methods: The expression of MUC6 was examined in cancer tissues and their corresponding adjacent normal tissues in 40 gastric adenocarcinoma patients. The investigation of methylation level of MUC6 promoter region in gastric cell lines and gastric specimen tissues was performed through immunohistochemistry and/or quantitative polymerase chain reaction (qPCR)s. MUC6 was knocked down in GES-1 cell lines and overexpressed in SGC7901 cell lines; the effects of MUC6 knockdown and overexpression on cell migration and invasion were examined using Transwell migration assay. The effects of demethylation and methylation on MUC6 expression were examined using Western blot, qPCR, or double luciferase report experiment.Results: The expression of MUC6 in GC tissues was significantly lower than that in normal paracancerous tissues. While the cells migration and invasion abilities were decreased significantly after overexpression of MUC6, these abilities increased significantly after the knocking down of MUC6. The methylation levels of MUC6 in GC tissues and GC cell lines (MGC803, MKN45, AGS, SGC7901, and BGC823) were significantly higher than those in paracancerous tissues and gastric epithelial cells. The promoter methylation could significantly reduce the binding of MUC6 promoter region to the related transcription factors. The expression of MUC6 increased with the concentration of demethylated drugs and the time of action.Conclusion: The expression of MUC6 was regulated by methylation of its promoter, and this methylation of MUC6 promoter may lead to significant downregulation of MUC6 in GC and promote the metastasis of GC.

scholarly journals CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a

2018 ◽  
Vol 46 (4) ◽  
pp. 1606-1616 ◽  
Author(s):  
Peng Li ◽  
Xiao Yang ◽  
Wenbo Yuan ◽  
Chengdi Yang ◽  
Xiaolei Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Rna Binding ◽  
Bioinformatic Analysis ◽  
Biological Behaviour ◽  
Invasion And Migration ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

Background/Aims: CircRNAs regulate gene expression in different malignancies. However, the role of Cdr1as in the tumourigenesis of bladder cancer and its potential mechanisms remain unknown. Methods: qRT-PCR was used to detect Cdr1as and target miRNA expression in bladder cancer tissues and cell lines. Biological functional experiments were performed to detect the effects of Cdr1as on the biological behaviour of bladder cancer cells in vivo and in vitro. Bioinformatic analysis was utilised to predict potential miRNA target sites on Cdr1as. Ago2 RNA binding protein immunoprecipitation assay, RNA antisense purification assay, biotin pull down assay and RNA FISH were performed to detect the interaction between Cdr1as and target miRNAs. Western blot was used to determine the expression level of p21 in bladder cancer cells. Results: Cdr1as was significantly down-regulated in bladder cancer tissues compared with adjacent normal tissues. Overexpression of Cdr1as inhibited the proliferation, invasion and migration of bladder cancer cells in vitro and slowed down tumour growth in vivo. Cdr1as sponged multiple miRNAs in bladder cancer. Moreover, Cdr1as directly bound to miR-135a and inhibited its activity in bladder cancer. Conclusion: Cdr1as is down-regulated and sponges multiple miRNAs in bladder cancer. It exerts anti-oncogenic functions by sponging microRNA-135a.

scholarly journals Fe-doped chrysotile nanotubes containing siRNAs to silence SPAG5 to treat bladder cancer

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jianye Liu ◽  
Yi Zhang ◽  
Hongliang Zeng ◽  
Long Wang ◽  
Qun Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Migration And Invasion ◽  
Outer Diameter ◽  
Antitumor Effects ◽  
Bladder Cancer Cells ◽  
Specific Uptake ◽  
Inner Diameter

Abstract Background For certain human cancers, sperm associated antigen 5 (SPAG5) exerts important functions for their development and progression. However, whether RNA interference (RNAi) targeting SPAG5 has antitumor effects has not been determined clinically. Results The results indicated that Fe-doped chrysotile nanotubes (FeSiNTs) with a relatively uniform outer diameter (15–25 nm) and inner diameter (7–8 nm), and a length of several hundred nanometers, which delivered an siRNA against the SPAG5 oncogene (siSPAG5) efficiently. The nanomaterials were designed to prolong the half-life of siSPAG5 in blood, increase tumor cell-specific uptake, and maximize the efficiency of SPAG5 silencing. In vitro, FeSiNTs carrying siSPAG5 inhibited the growth, migration, and invasion of bladder cancer cells. In vivo, the FeSiNTs inhibited growth and metastasis in three models of bladder tumors (a tail vein injection lung metastatic model, an in-situ bladder cancer model, and a subcutaneous model) with no obvious toxicities. Mechanistically, we showed that FeSiNTs/siSPAG5 repressed PI3K/AKT/mTOR signaling, which suppressed the growth and progression of tumor cells. Conclusions The results highlight that FeSiNTs/siSPAG5 caused no activation of the innate immune response nor any systemic toxicity, indicating the possible therapeutic utility of FeSiNTs/siSPAG5 to deliver siSPAG5 to treat bladder cancer. Graphic abstract

scholarly journals Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Jun Li ◽  
Yan Li ◽  
Fandong Meng ◽  
Liye Fu ◽  
Chuize Kong
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which were mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation of linc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition, and apoptosis increase might be regulated through suppressing the activities of Wnt/β-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/β-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer.

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