scholarly journals Hsp74, a Potential Bladder Cancer Marker, Has Direct Interaction with Keratin 1

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Ling Chen ◽  
YaRong Wang ◽  
Le Zhao ◽  
Wei Chen ◽  
Chunhui Dong ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Early Diagnosis ◽  
Western Blot ◽  
Cancer Progression ◽  
Molecular Basis ◽  
Direct Interaction ◽  
Molecular Target ◽  
Therapeutic Monitoring ◽  
Diagnosis And Prognosis ◽  
Keratin 1

Early diagnosis and prognosis monitoring are very important for the survival of patients with bladder cancer. To identify candidate biomarkers of bladder cancer, we used a combination of techniques including 2-DE, co-IP, western blot, LC-MS/MS, and immunohistochemistry. Hsp74 was identified with high expression in bladder cancer. The cellular location of expression products of gene Hsp74 showed that they were distributed into cytoplasm and keratin 1 was found to be associated with Hsp74. The results provide a new idea to understand the molecular basis of bladder cancer progression and pinpoint new potential molecular target for early diagnosis and therapeutic monitoring of bladder cancer.

New HSP90 selective inhibitors as therapeutic agents for prostate and bladder cancer.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 285-285 ◽  
Author(s):  
Weiya Liu ◽  
Derek Jensen ◽  
Eugene Lee ◽  
Jessie Gills ◽  
Jeffrey M. Holzbeierlein
Keyword(s):  
Bladder Cancer ◽  
Western Blot ◽  
Protein Degradation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Selective Inhibition ◽  
Client Protein ◽  
Selective Inhibitors ◽  
Oncogenic Pathways ◽  
Bladder Cancer Cells

285 Background: Hsp90 is a molecular chaperone responsible for folding many of the proteins directly associated with cancer progression and consequently, inhibition of the Hsp90 protein folding machinery results in a combinatorial attack on numerous oncogenic pathways. Hsp90 family consist of four isoforms; Hsp90α, Hsp90β, Grp94 and Trap-1. The development of Hsp90 isoform-selective inhibitors represent an alternative approach towards the treatment of cancer that may limit some of the detriments. We demonstrate novel Hsp90 inhibitors, on prostate and bladder cancer cells, which shows both potent antiproliferative effects and specific selectivity for Hsp90β. Methods: PC3MM2, LNCap-LN3, C4-2b, LAPC4 (prostate cancer) and T24, UC3 (bladder cancer) cancer cells were utilized. Cell Titer-Glo luminescent anti-proliferative assay was used to determine the IC50 numbers after 72h treatment. Trypan Blue Cytotoxicity assay was performed for 24h treatment with increasing concentrations of KUNB inhibitors. Effects of KUNB inhibitors on Hsp90’s client protein degradation were investigated by Western Blot. Results: KUNB31 manifested an IC50 of 3.00 µM against UC3 bladder cancer cells, UC3 cells were then evaluated via western blot analyses of known Hsp90α- and Hsp90β-dependent client proteins following treatment with KUNB31 for 24 hours. The data showed that, KUNB31 would not induce the heat shock response like 17AAG, and did cause Hsp90β related protein degradation (CXCR4). Moreover, Hsp27, PKM2, Her2, Hsf-1and Akt all showed degradation to different extent. KUNB105 exhibited potent anti-proliferative in both prostate and bladder cancer cells. IC50 number was determined as 1.24 µM for PC3MM2, 1.18 µM for LNCap-LN3, 1.03 µM for C4-2b, 2.56 µM for LAPC4, 0.20 µM for T24, and 0.30 µM for UC3 cancer cells. Conclusions: KUNB novel Hsp90β selective inhibitors, exhibit potent anti-proliferative and cytotoxic activity along with client protein degradation, without induction of HSR in prostate and bladder cancer cell lines. KUNB compound’s selective inhibition on Hsp90β isomers supports the development of Hsp90-selective inhibitors as a method to overcome the detriments associated with pan-inhibition in cancer treatment.

scholarly journals MiR-10a-5p: A Promising Biomarker for Early Diagnosis and Prognosis Evaluation of Bladder Cancer

2021 ◽  
Vol Volume 13 ◽  
pp. 7841-7850
Author(s):  
Lei Yang ◽  
Hong-Fang Sun ◽  
Lin-Qing Guo ◽  
Hai-Bing Cao
Keyword(s):  
Bladder Cancer ◽  
Early Diagnosis ◽  
Diagnosis And Prognosis ◽  
Prognosis Evaluation

951: TOB1 and ID-1 Two Novel Genes Implicated in Bladder Cancer Progression and Prognosis

2004 ◽  
Vol 171 (4S) ◽  
pp. 252-252
Author(s):  
Paul Perrotte ◽  
Nadia Benachenou ◽  
Pierre I. Karakiewicz ◽  
Myriam Senay ◽  
Fred Saad
Keyword(s):  
Bladder Cancer ◽  
Cancer Progression ◽  
Novel Genes

scholarly journals TYRO3 as a molecular target for growth inhibition and apoptosis induction in bladder cancer

2019 ◽  
Vol 120 (5) ◽  
pp. 555-564 ◽  
Author(s):  
Florent Dufour ◽  
Linda Silina ◽  
Hélène Neyret-Kahn ◽  
Aura Moreno-Vega ◽  
Clémentine Krucker ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Growth Inhibition ◽  
Molecular Target ◽  
Apoptosis Induction

scholarly journals Circulating Cell-Free DNA in Liquid Biopsies as Potential Biomarker for Bladder Cancer: A Review

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1448
Author(s):  
Raquel Herranz ◽  
Julia Oto ◽  
Emma Plana ◽  
Álvaro Fernández-Pardo ◽  
Fernando Cana ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Progression ◽  
Specific Treatment ◽  
Predictive Biomarkers ◽  
Liquid Biopsies ◽  
Cell Free Dna ◽  
Specific Patient ◽  
Free Dna ◽  
Potential Biomarker ◽  
Cancer Types

Bladder cancer (BC) is among the most frequent cancer types in the world and is the most lethal urological malignancy. Presently, diagnostic and follow-up methods for BC are expensive and invasive. Thus, the identification of novel predictive biomarkers for diagnosis, progression, and prognosis of BC is of paramount importance. To date, several studies have evidenced that cell-free DNA (cfDNA) found in liquid biopsies such as blood and urine may play a role in the particular scenario of urologic tumors, and its analysis may improve BC diagnosis report about cancer progression or even evaluate the effectiveness of a specific treatment or anticipate whether a treatment would be useful for a specific patient depending on the tumor characteristics. In the present review, we have summarized the up-to-date studies evaluating the value of cfDNA as potential diagnostic, prognostic, or monitoring biomarker for BC in several biofluids.

scholarly journals FTO modifies the m6A level of MALAT and promotes bladder cancer progression

2021 ◽  
Vol 11 (2) ◽  
Author(s):  
Le Tao ◽  
Xingyu Mu ◽  
Haige Chen ◽  
Di Jin ◽  
Ruiyun Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Progression

scholarly journals Intratumoral CD103+ CD8+ T cells predict response to PD-L1 blockade

2021 ◽  
Vol 9 (4) ◽  
pp. e002231
Author(s):  
Romain Banchereau ◽  
Avantika S. Chitre ◽  
Alexis Scherl ◽  
Thomas D. Wu ◽  
Namrata S. Patil ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Clinical Trials ◽  
Cancer Progression ◽  
Cd8 T Cells ◽  
Clonal Expansion ◽  
T Cell Response ◽  
High Dimensional ◽  
Cancer Clinical Trials ◽  
Complex Phenotype ◽  
Cytotoxic Proteins

BackgroundCD8+ tissue-resident memory T (TRM) cells, marked by CD103 (ITGAE) expression, are thought to actively suppress cancer progression, leading to the hypothesis that their presence in tumors may predict response to immunotherapy.MethodsHere, we test this by combining high-dimensional single-cell modalities with bulk tumor transcriptomics from 1868 patients enrolled in lung and bladder cancer clinical trials of atezolizumab (anti-programmed cell death ligand 1 (PD-L1)).ResultsITGAE was identified as the most significantly upregulated gene in inflamed tumors. Tumor CD103+ CD8+ TRM cells exhibited a complex phenotype defined by the expression of checkpoint regulators, cytotoxic proteins, and increased clonal expansion.ConclusionsOur analyses indeed demonstrate that the presence of CD103+ CD8+ TRM cells, quantified by tracking intratumoral CD103 expression, can predict treatment outcome, suggesting that patients who respond to PD-1/PD-L1 blockade are those who exhibit an ongoing antitumor T-cell response.

scholarly journals Hypoxia promotes the metastasis of pancreatic cancer through regulating NOX4/KDM5A-mediated histone methylation modification changes in a HIF1A-independent manner

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Hongzhen Li ◽  
Chunyan Peng ◽  
Chenhui Zhu ◽  
Shuang Nie ◽  
Xuetian Qian ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Nadph Oxidase ◽  
Western Blot ◽  
Cancer Progression ◽  
Histone Methylation ◽  
Invasion And Metastasis ◽  
Independent Manner ◽  
Nadph Oxidase 4

Abstract Background Hypoxia is a characteristic of the tumor microenvironments within pancreatic cancer (PC), which has been linked to its malignancy. Recently, hypoxia has been reported to regulate the activity of important carcinogenic pathways by changing the status of histone modification. NOX4, a member of NADPH oxidase (NOX), has been found to be activated by hypoxia and promote cancer progression in several cancers. But whether it is involved in the epigenetic changes of tumor cells induced by hypoxia is still unclear, and its biological roles in PC also need to be explored. Methods A hypoxic-related gene signature and its associated pathways in PC were identified by analyzing the pancreatic cancer gene expression data from GEO and TCGA database. Candidate downstream gene (NOX4), responding to hypoxia, was validated by RT-PCR and western blot. Then, we evaluated the relationship between NOX4 expression and clinicopathologic parameters in 56 PC patients from our center. In vitro and in vivo assays were preformed to explore the phenotype of NOX4 in PC. Immunofluorescence, western blot and chromatin immunoprecipitation assays were further applied to search for a detailed mechanism. Results We quantified hypoxia and developed a hypoxia signature, which was associated with worse prognosis and elevated malignant potential in PC. Furthermore, we found that NADPH oxidase 4 (NOX4), which was induced by hypoxia and upregulated in PC in a HIF1A-independent manner, caused inactivation of lysine demethylase 5A (KDM5A), increased the methylation modification of histone H3 and regulated the transcription of EMT-associated gene_ snail family transcriptional repressor 1 (SNAIL1). This served to promote the invasion and metastasis of PC. NOX4 deficiency repressed hypoxia-induced EMT, reduced expression of H3K4ME3 and impaired the invasion and metastasis of PC cells; however, knockdown of KDM5A reversed the poor expression of H3KEME3 induced by NOX4 deficiency, thereby promoting EMT. Conclusions This study highlights the prognostic role of hypoxia-related genes in PC and strong correlation with EMT pathway. Our results also creatively discovered that NOX4 was an essential mediator for hypoxia-induced histone methylation modification and EMT in PC cells.

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