775: Cell Culture Proteome Identifies CXCL 1 as a Secreted Marker and Mediator for the Tumor Invasion of Bladder Cancer

2007 ◽  
Vol 177 (4S) ◽  
pp. 260-260 ◽  
Author(s):  
Hiroaki Kawanishi ◽  
Yoshiyuki Matsui ◽  
Toshinari Yamasaki ◽  
Takeshi Takahashi ◽  
Hiroyuki Nishiyama ◽  
...  
Keyword(s):  
Cell Culture ◽  
Bladder Cancer ◽  
Tumor Invasion

scholarly journals Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis

2020 ◽  
Vol 11 (12) ◽  
Author(s):  
Weiting Kang ◽  
Qiang Wang ◽  
Yun Dai ◽  
Hanbo Wang ◽  
Muwen Wang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Invasion ◽  
Chromosome 21 ◽  
Expression Level ◽  
Migration And Invasion ◽  
Preoperative Treatment ◽  
Predictive Values ◽  
Mesenchymal Transition ◽  
Regulatory Pathways ◽  
T Stage

AbstractApart from being potential prognostic biomarkers and therapeutic targets, long non-coding RNAs (lncRNAs) modulate the development and progression of multiple cancers. PlncRNA-1 is a newly discovered lncRNA that exhibits the above properties through multiple regulatory pathways. However, the clinical significance and molecular mechanisms of PlncRNA-1 in bladder cancer have not been established. PlncRNA-1 was found to be overexpressed in 71.43% of bladder cancer tissues. Moreover, the expression level correlated with tumor invasion, T stage, age, and number of tumors, but not with gender, recurrent status, preoperative treatment, pathological grade, and tumor size. The expression level of PlncRNA-1 can, to a certain extent, be used as a predictor of the degree of tumor invasion and T stage among BC patients. Inhibiting PlncRNA-1 expression impaired the proliferation, migration, and invasion of T24 and 5637 bladder cancer cells in vitro and in vivo. Specifically, PlncRNA-1 promoter in BC tissues was found to be hypomethylated at position 131 (36157603 on chromosome 21). PlncRNA-1 promoter hypomethylation induces the overexpression of PlncRNA-1. In addition, PlncRNA-1 modulated the expression of smad3 and has-miR-136-5p (miR-136). Conversely, miR-136 regulated the expression of PlncRNA-1 and smad3. PlncRNA-1 mimics competitive endogenous RNA (ceRNA) in its regulation of smad3 expression by binding miR-136. Rescue analysis further revealed that modulation of miR-136 could reverse the expression of smad3 and epithelial–mesenchymal transition (EMT) marker proteins impaired by PlncRNA-1. In summary, PlncRNA-1 has important clinical predictive values and is involved in the post-transcriptional regulation of smad3. The PlncRNA-1/miR-136/smad3 axis provides insights into the regulatory mechanism of BC, thus may serve as a potential therapeutic target and prognostic biomarker for cancer.

scholarly journals Secreted CXCL1 Is a Potential Mediator and Marker of the Tumor Invasion of Bladder Cancer

2008 ◽  
Vol 14 (9) ◽  
pp. 2579-2587 ◽  
Author(s):  
Hiroaki Kawanishi ◽  
Yoshiyuki Matsui ◽  
Masaaki Ito ◽  
Jun Watanabe ◽  
Takeshi Takahashi ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Invasion ◽  
Potential Mediator

Association of stromal lymphocyte infiltration with tumor invasion depth and high-grade T1 bladder cancer.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 488-488 ◽  
Author(s):  
Mathieu Rouanne ◽  
Reem Betari ◽  
Camélia Radulescu ◽  
Nicolas Signolle ◽  
Yves Allory ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Invasion ◽  
Mononuclear Cells ◽  
Cox Model ◽  
Tumor Infiltrating Lymphocytes ◽  
High Grade ◽  
Invasion Depth ◽  
Bcg Therapy ◽  
Variant Histology ◽  
Tumor Invasion Depth

488 Background: Morphological assessment of tumor-infiltrating lymphocytes (TIL) has been shown to provide prognostic and potentially predictive significance in many different tumor types. Large studies investigating TIL in urothelial carcinoma are lacking. We investigated in a homogenous population of patients with high-grade T1 (HGT1) bladder cancer the association of TIL with clinico-pathological parameters and clinical outcomes. Methods: Pretreatment index tumors were collected between 2000 and 2015 from 147 patients with primary high-grade cT1N0M0 bladder cancer. The density of stromal TIL was evaluated using hematoxylin and eosin (H&E)-based staining on whole tissue sections. Stromal TIL density was scored as percentage of stromal area infiltrated by mononuclear cells. Inter-reader assessment and stromal TIL correlation with a subset of CD3+ stained sections were evaluated. The main endpoint was correlation with overall survival (OS). Hazard ratios (HRs) and 95% CIs associated with stromal TIL were estimated through a multivariable Cox model. Results: Median follow-up was 8.2 years (6.1-9.5). Induction BCG therapy was followed by 126 patients (86%). Recurrence and progression were respectively observed in 67 patients (46%) and 40 patients (27%). Stromal TIL density was high (≥10%) in 82 tumors (56%). The overall agreement was good between the two readers (κ = 0.75). Correlation between stromal TIL density analyzed on H&E-sections and CD3+ IHC staining was high (ρ = 0.71, p < 1.10-5). Stromal TIL were positively associated with variant histology (p = 0.01) and tumor invasion depth (p = 0.03). For the OS analysis, intense (≥10%) vs. non-intense ( < 10%) stromal TIL unadjusted HR (95% CI, p) was 1.30 (0.75-2.24, p = 0.34) and adjusted HR was 1.25 (0.72-2.16, p = 0.43). Conclusions: Density of stromal TIL was associated with tumor invasion depth and variant histology, but not with prognosis of patients with HGT1 bladder cancer. These data suggest that tumor progression is associated with an increased adaptive immune response but other factors may influence outcome of patients. Characterization of TIL subpopulations may be required to identify immune-related prognostic factors.

Green tea polyphenol suppresses tumor invasion and angiogenesis in N-butyl-(-4-hydroxybutyl) nitrosamine-induced bladder cancer

2010 ◽  
Vol 34 (3) ◽  
pp. 350-354 ◽  
Author(s):  
Yuji Sagara ◽  
Yasuyoshi Miyata ◽  
Koichiro Nomata ◽  
Tomayoshi Hayashi ◽  
Hiroshi Kanetake
Keyword(s):  
Bladder Cancer ◽  
Green Tea ◽  
Tumor Invasion ◽  
Tea Polyphenol ◽  
Green Tea Polyphenol

scholarly journals Downregulation of Ral GTPase-activating protein promotes tumor invasion and metastasis of bladder cancer

Oncogene ◽  
2012 ◽  
Vol 32 (7) ◽  
pp. 894-902 ◽  
Author(s):  
R Saito ◽  
R Shirakawa ◽  
H Nishiyama ◽  
T Kobayashi ◽  
M Kawato ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Invasion ◽  
Gtpase Activating Protein ◽  
Invasion And Metastasis ◽  
Ral Gtpase

scholarly journals 3-D Cell Culture System for Studying Invasion and Evaluating Therapeutics in Bladder Cancer

10.3791/58345 ◽  
2018 ◽  
Author(s):  
Yin Wang ◽  
Mark L. Day ◽  
Diane M. Simeone ◽  
Phillip L. Palmbos
Keyword(s):  
Cell Culture ◽  
Bladder Cancer ◽  
Culture System ◽  
Cell Culture System ◽  
D Cell

scholarly journals Metastasis-associated C4.4A, a GPI-anchored protein cleaved by ADAM10 and ADAM17

2008 ◽  
Vol 389 (8) ◽  
Author(s):  
Cary W. Esselens ◽  
Jordi Malapeira ◽  
Núria Colomé ◽  
Marcia Moss ◽  
Francesc Canals ◽  
...  
Keyword(s):  
Amino Acids ◽  
Cell Culture ◽  
Stable Isotope ◽  
Tumor Progression ◽  
Tumor Invasion ◽  
Isotope Labeling ◽  
Matrix Metalloproteases ◽  
Metabolic Labeling ◽  
Mcf7 Cells ◽  
Proteomic Identification

Abstract Metalloproteases play a complex role in tumor progression. While the activity of some ADAM, ADAMTS and matrix metalloproteases (MMPs) seems to be protumorigenic, the activity of others seems to prevent tumor progression. The identification of the array of substrates of a given metalloprotease (degradome) seems an adequate approach to predict the effect of the inhibition of a metalloprotease in tumors. Here, we present the proteomic identification of a novel substrate for ADAM10 and -17. We used SILAC (Stable Isotope Labeling by Amino acids in Cell culture), a proteomic technique based on the differential metabolic labeling of cells in different conditions. This was applied to MCF7 cells derived from an invasive mammary tumor, and the same cells expressing shRNAs that knock down ADAM10 or -17. Following this approach, we have identified C4.4A as a substrate to both metalloproteases. Since C4.4A is likely involved in tumor invasion, these results indicate that the cleavage of C4.4A by ADAM10 and ADAM17 contributes to tumor progression.

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