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Proteomic analysis of the invasiveness of human bladder cancer cells

ABSTRACT: To identification of key drivers involved in the development of muscle invasive bladder cancer, which displays poor prognosis, we isolated one subpopulation of human 5637 bladder cancer cells with highly invasiveness and the other subpopulation of 5637 cells with low invasiveness by Transwell method. Through proteomic analysis, differentially expressed proteins were displayed.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: zhu sam

LAB HEAD: Zhou Hu

PROVIDER: PXD007709 | Pride | 2018-03-15

REPOSITORIES: Pride

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			Action	DRS
	20170516_ZHW_HRM_2_1_TMT6_F01.raw	Raw
	20170516_ZHW_HRM_2_1_TMT6_F02.raw	Raw
	20170516_ZHW_HRM_2_1_TMT6_F03.raw	Raw
	20170516_ZHW_HRM_2_1_TMT6_F04.raw	Raw
	20170516_ZHW_HRM_2_1_TMT6_F05.raw	Raw

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Publications

Wnt7a activates canonical Wnt signaling, promotes bladder cancer cell invasion, and is suppressed by miR-370-3p.

Huang Xiaojing X Zhu Hongwen H Gao Zemin Z Li Junzun J Zhuang Junlong J Dong Yu Y Shen Bing B Li Meiqian M Zhou Hu H Guo Hongqian H Huang Ruimin R Yan Jun J

The Journal of biological chemistry 20180316 18

Once urinary bladder cancer (UBC) develops into muscle-invasive bladder cancer, its mortality rate increases dramatically. However, the molecular mechanisms of UBC invasion and metastasis remain largely unknown. Herein, using 5637 UBC cells, we generated two sublines with low (5637 NMI) and high (5637 HMI) invasive capabilities. Mass spectrum analyses revealed that the Wnt family protein Wnt7a is more highly expressed in 5637 HMI cells than in 5637 NMI cells. We also found that increased Wnt7a e ...[more]

PMID: 29549123

Similar Datasets

Proteomic analysis of the invasiveness of human bladder cancer cells

Project description:To identification of key drivers involved in the development of muscle invasive bladder cancer, which displays poor prognosis, we isolated one subpopulation of human 5637 bladder cancer cells with highly invasiveness and the other subpopulation of 5637 cells with low invasiveness by Transwell method. Through proteomic analysis, differentially expressed proteins were displayed.

2018-08-27 | MSV000082854 | MassIVE

Muscular invasiveness in bladder cancer

Project description:Patients with bladder cancer need frequent controls over long follow-up time due to high recurrence rate and risk of conversion to muscle invasive cancer with poor prognosis. We identified cancer-related molecular signatures in apparently healthy bladder in patients with subsequent muscular invasiveness during follow-up. Global proteomics of the normal tissue biopsies revealed specific proteome fingerprints in these patients prior to subsequent muscular invasiveness. In these presumed normal samples, we detected modulations of proteins previously associated with different cancer types. This study indicates that analyzing apparently healthy tissue of a cancer-invaded organ may predict disease progression.

2018-10-26 | PXD010260 | Pride

miR-193 inhibits bladder cancer progression by targeting N-myc

Project description:Growing evidence has indicated that miR-193 is involved in the initiation and progression of malignancy, such as bladder cancer, hepatocellular carcinoma, renal cell carcinoma, and colorectal cancer. Nevertheless, the mechanisms of miR-193 in the development of metastatic bladder cancer remains unknown. In the current study, we clarified the association of miR-193/N-myc was implicated in cancer metastasis. miR-193 expression increased in metastatic bladder cancer biopsies compared to the primary cases. Moreover, the elevation of miR-193 was correlated with the invasiveness, lymph node metastasis, and advanced stages of bladder cancer significantly. Downregulation of miR-193 by shRNA hampered proliferation and migration while inducing cell apoptosis. Furthermore, miR-193 sponged N-myc and diminished miR-103 expression. Overexpression of miR-193 released oncogene N-myc expression, leading to the promotion of cell proliferation and migration. Besides, knockout of miR-193 suppressed tumor growth in the human T24 mice models. Briefly, the present findings suggested that miR-193-N-myc were novel promising pathways for conquering bladder cancer progression.

2021-01-13 | GSE164682 | GEO

Gene differential expressions between cell subpopulations with high invasiveness (invaded) and low invasiveness (non-invaded) in human lung cancer H460 cell line

Project description:Cell populations with different invasiveness were isolated and collected with cell culture inserts of Boyden-type cell invasion chambers coated with 1xBME (base membrane extract). Cells that invaded to bottom chamber were collected as cell population with high-invasiveness , and cells that remained in the insert chamber were collected as cell population with low-invasiveness. The selection with Boyden-type cell invasion chambers was repeated six times, and cells with high invasiveness were terms as H-INV subline, and cells with low invasiveness were termed as L-INV subline. Microarray analysis was performed with Illumina HumanHT-12 v4 Expression BeadChips

2015-07-15 | GSE68916 | GEO

Characterization and therapeutic targeting of the miR-21/PPP2R2A/ERK molecular circuit in bladder cancer

Project description:MicroRNAs play an important role in the pathogenesis of different types of cancer including bladder cancer. MiR-21 has been identified to have an oncogenic function, while its inhibition suppresses tumor growth. Here, we followed an integrated bioinformatics and molecular analyses to identify the molecular mediators of miR-21 oncogenic function in bladder cancer and evaluate the therapeutic potential of a chemically-modified miR-21 inhibitor in bladder xenografts. MiR-21 expression was found to up-regulated in human bladder cancers relative to normal tissues and miR-21 inhibition suppressed bladder cancer cell properties, including growth, invasiveness and anchorage-independence. Intravenous administration of an antisense oligonucleotide against miR-21 harboring locked-nucleic-acid (LNA-miR-21) modifications blocked bladder tumor growth in vivo. Transcriptomic analysis of 28 bladder cancer cell lines revealed a gene signature that negatively correlated with miR-21 expression levels. Bioinformatics and 3’UTR luciferase assay analyses revealed a direct interaction between miR-21 the 3’UTR of PPP2R2A gene. Inhibition of PPP2R2A expression induced bladder cancer growth, suggesting its tumor suppressor function. Gene profiling followed by IPA network analysis revealed that PPP2R2A regulates the ERK1/2 molecular network. Taken together, PPP2R2A is the functional mediator of miR-21 oncogenic activity on bladder cancer and LNA-miR-21 could have a therapeutic potential in bladder cancer patients.

2018-04-19 | GSE97782 | GEO

Intestinal ablation of CKIalpha highlights invasiveness control

Project description:Wnt signaling, which drives the rapid self-renewal of the gut epithelium is causally associated with intestinal neoplasia. Here we show that CKIalpha is a activation depends on p53 and p21Waf1/Cip1: CKIα ablation provokes activation of p53 and p21, which assume a pivotal role in suppressing invasive cancer. Dual loss of CKIalpha and either p53 or p21 results in rapid, rampant malignant signature denoted p53supinv (p53-suppressed invasiveness) that is conditionally induction of invasiveness. Like invasiveness control, the transcriptional suppression of p53supinv genes is largely mediated by p21, independently of cell cycle control, representing a novel tumor suppressor function of wild-type p53.

2010-10-23 | GSE24760 | GEO

Intestinal ablation of CKIalpha highlights invasiveness control

Project description:Wnt signaling, which drives the rapid self-renewal of the gut epithelium is causally associated with intestinal neoplasia. Here we show that CKIalpha is a activation depends on p53 and p21Waf1/Cip1: CKIÎ± ablation provokes activation of p53 and p21, which assume a pivotal role in suppressing invasive cancer. Dual loss of CKIalpha and either p53 or p21 results in rapid, rampant malignant signature denoted p53supinv (p53-suppressed invasiveness) that is conditionally induction of invasiveness. Like invasiveness control, the transcriptional suppression of p53supinv genes is largely mediated by p21, independently of cell cycle control, representing a novel tumor suppressor function of wild-type p53. 13 arrays of mice entrocytes herto or homozygot for gut specific KO of CKI alpha. Crossed with p53 or p21 KO mice.

2010-10-23 | E-GEOD-24760 | biostudies-arrayexpress

Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (mRNA)

Project description:Background: Circular RNAs (circRNAs), a subclass of noncoding RNAs, have been reported to be involved in the progression of various diseases. However, the exact role of circRIMS1, also termed hsa_circ_0132246, in human bladder cancer remains to be discovered. Methods: By performing RNA-seq comparing bladder cell lines and normal uroepithelial cells, circRIMS1 was selected as the research object. We further verified by qRT-PCR that circRIMS1 was upregulated in bladder cancer tissue and cell lines. Proliferation, colony formation, Transwell migration, Matrigel invasion, apoptosis, western blotting and in vivo tumorigenesis and metastasis assays were utilized to evaluate the roles of circRIMS1, miR-433-3p and CCAR1. For mechanistic investigation, RNA pull-down, fluorescence in situ hybridization (FISH) and luciferase reporter assay confirmed the binding of circRIMS1 with miR-433-3p. Results: CircRIMS1 was significantly upregulated in bladder cancer and circRIMS1 expression was associated with the pathological stage and histological grade of bladder cancer. Inhibition of circRIMS1 suppressed the proliferation, migration and invasion of bladder cancer cells in vitro and in vivo, while overexpression of circRIMS1 exerted the opposite effects. Moreover, the circRIMS1/miR-433-3p/CCAR1 regulatory axis was confirmed to be responsible for the biological functions of circRIMS1. Conclusions: CircRIMS1 acts as a tumor promoter in bladder cancer to enhance tumor growth, migration and invasion via the miR-433-3p/CCAR1 regulatory axis, which provides a new therapeutic target and a novel biomarker in bladder cancer. Keywords: CircRIMS1, Bladder cancer, miR-433-3p, CCAR1, Progression, Metastasis

2020-05-09 | GSE150143 | GEO

Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (circRNA)

2020-05-09 | GSE150142 | GEO

Human bladder cancer cell line mRNA-seq

Project description:Circular RNAs (circRNAs) have been increasingly indicated to be important participants in the development and progression of various malignant tumors. Our previous studies found that hundreds of circRNAs were aberrantly expressed in bladder cancer (BC) by high-throughput sequencing and we have confirmed that the downregulated circRNAs circHIPK3, BCRC3 and circNR3C1 played inhibitory roles in BC progression. However, the role of these upregulated circRNAs remain to be clarified. In this study, we analyzed circRNA high-throughout sequencing from human tissues and focused on the upregulated circRNAs and identified a novel circular RNA, hsa_circ_0001361 (also named bladder cancer upregulated circRNA-1, BCUC-1), as a new candidate circRNA derived from FNDC3B gene. The expression levels of circRNA and miRNAs in BC tissues and cells were detected by qRT-PCR. Transwell migration, Matrigel invasion, CCK-8, EdU, cell cycle and in vivo tumor metastasis assays were preformed to evaluate the effects of circ0001361 on BC cells. Transcriptome analysis was performed to find the potential genes that could be regulated by BCUC-1. Luciferase reporter, RNA pull-down and fluorescence in situ hybridization (FISH) assays were applied to verify the interaction between BCUC-1 and miR-491-5p.

2019-09-06 | GSE136919 | GEO

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