Invasion Suppressor Role of E-Cadherin in Epithelial Cancer Cell Lines

1997 ◽  
Vol 9 (4) ◽  
pp. 263
Author(s):  
Joo Young Roh ◽  
Chong Ju Lee
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Epithelial Cancer ◽  
E Cadherin

scholarly journals Chrysin enhances doxorubicin-induced cytotoxicity in human lung epithelial cancer cell lines: The role of glutathione

2012 ◽  
Vol 258 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Heather M. Brechbuhl ◽  
Remy Kachadourian ◽  
Elysia Min ◽  
Daniel Chan ◽  
Brian J. Day
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Human Lung ◽  
Cancer Cell Lines ◽  
Epithelial Cancer ◽  
Lung Epithelial

Activity of different anthracycline formulations in hormone-refractory prostate cancer cell lines: Role of golgi apparatus

2011 ◽  
Vol 226 (11) ◽  
pp. 3035-3042 ◽  
Author(s):  
Francesco Fabbri ◽  
Wainer Zoli ◽  
Silvia Carloni ◽  
Paola Ulivi ◽  
Chiara Arienti ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Golgi Apparatus ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Hormone Refractory Prostate Cancer ◽  
Prostate Cancer Cell Lines ◽  
Hormone Refractory

Preferential Energy- and Potential-Dependent Accumulation of Cisplatin–Gutathione Complexes in Human Cancer Cell Lines (GLC4 and K562): A Likely Role of Mitochondria

2006 ◽  
Vol 38 (1) ◽  
pp. 11-21 ◽  
Author(s):  
Simplice Dzamitika ◽  
Milena Salerno ◽  
Elene Pereira-Maia ◽  
Laurence Le Moyec ◽  
Arlette Garnier-Suillerot
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Human Cancer Cell ◽  
Human Cancer Cell Lines

Characterization of FOXF1 as a novel regulator of nodal metastasis in bladder cancer.

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 480-480
Author(s):  
Anirban P Mitra ◽  
Andrea Kokorovic ◽  
Tanner Miest ◽  
Vikram M Narayan ◽  
Debasish Sundi ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Differentially Expressed Gene ◽  
Cancer Cell Lines ◽  
Differentially Expressed ◽  
Bladder Cancer Cell ◽  
Primary Tumors ◽  
Orthotopic Xenografts

480 Background: Members of the forkhead transcription factor (FOX) family are important mediators of embryonic development and are known to be altered in a variety of cancers. The functional role of FOXF1 in bladder tumorigenesis and progression has not been clearly characterized thus far. This study investigated the clinical implications of differential FOXF1 expression in bladder cancer, and potential mechanisms by which its alteration can lead to tumor metastasis. Methods: Whole genome expression profiling was performed on paired primary tumors and nodal metastases from a radical cystectomy discovery cohort using Illumina HT12 v3-4 BeadChip arrays to identify FOXF1 as a top differentially expressed gene. Prognostic role of differential FOXF1 expression was validated on two independent cystectomy cohorts. Differential FOXF1 expression was also evaluated in murine orthotopic xenografts. Small interfering RNA was used to knock down FOXF1 in RT112 and UC6 bladder cancer cell lines to develop an in vitro model for assessment of metastatic potential. Next-generation sequencing and hierarchical clustering analysis were used to identify differentially altered genes secondary to FOXF1 knockdown. 186 biologically curated pathways were interrogated with internal validation to elucidate the downstream biologic mechanisms of metastasis. Results: In the discovery cohort, FOXF1 was a top differentially expressed gene with 3.6-fold lower expression in nodal metastases than paired primary tumors (n = 33, p < 0.001). Multivariable analyses in two validation cohorts (total n = 128) indicated that FOXF1 underexpression was associated with worse cancer-specific (p = 0.046) and overall survival (p = 0.006). Murine orthotopic xenografts (n = 13) established from human bladder cancer cell lines (UC3, UC6, UC14) showed FOXF1 underexpression in metastatic deposits compared with primary tumors (p = 0.004). Hierarchical clustering identified 40 differentially expressed genes between FOXF1-knockdown bladder cancer cell lines and their corresponding controls. Biological pathway interrogation showed differential enrichment for genes associated with mitogen-activated protein kinase signaling, focal adhesion and other carcinogenic pathways in FOXF1-knockdown cells compared with controls (normalized enrichment score ≥ 1.3). Conclusions: We identify and characterize FOXF1 as a novel regulatory molecule that potentially drives bladder cancer metastasis. This may be modulated through alterations in intracellular signaling and cellular adhesion. FOXF1 may serve as a prognostic biomarker that can identify patients at impending risk for metastasis who may benefit from more aggressive management.

Comparison of Fixation Methods for the Detection of Claudin 1 and E-Cadherin in Breast Cancer Cell Lines by Immunofluorescence

2021 ◽  
pp. 002215542110552
Author(s):  
Chidalu A. Edechi ◽  
Maryam Amini ◽  
Mohammad K. Hamedani ◽  
Lucas E.L. Terceiro ◽  
Barbara E. Nickel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cellular Localization ◽  
Cancer Cell Lines ◽  
Fixation Method ◽  
Breast Cancer Cell Lines ◽  
Junction Protein ◽  
E Cadherin

The tight junction membrane protein claudin 1 and the adherens junction protein E-cadherin play critical roles in cell–cell communication and in cell signaling. As a result, their protein levels and distribution in cancer have been a focus of cancer researchers in recent years. The loss of sensitivity to contact inhibition and the establishment of invasive properties in cancer are thought to be a result of the mislocalization of these membrane proteins to the cytoplasm. However, reports on their distribution and levels have been inconsistent. It is therefore critical that the techniques used to determine the cellular localization of these proteins be both consistent and reliable. This study was undertaken to determine the optimal fixation method, methanol or formalin, for the detection of claudin 1 and E-cadherin by immunofluorescence in five different human breast cancer cell lines. Both methods exhibited staining of the cell membrane and cytoplasm, but the strongest and most distinct signals were obtained using methanol fixation. Interestingly, cell-specific differences were also observed that appeared to be associated with levels of claudin 1 and E-cadherin as seen by Western blotting. Therefore, when evaluating cellular localization of the junction proteins claudin 1 and E-cadherin, expression level and cell type differences must be considered:

scholarly journals Transcriptional hallmarks of cancer cell lines reveal an emerging role of branched chain amino acid catabolism

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ieva Antanavičiūtė ◽  
Valeryia Mikalayeva ◽  
Ieva Ceslevičienė ◽  
Gintarė Milašiūtė ◽  
Vytenis Arvydas Skeberdis ◽  
...  
Keyword(s):  
Amino Acid ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Amino Acid Catabolism ◽  
Hallmarks Of Cancer ◽  
Branched Chain Amino Acid ◽  
Branched Chain

scholarly journals Chemoresistance in H-Ferritin Silenced Cells: The Role of NF-κB

2018 ◽  
Vol 19 (10) ◽  
pp. 2969 ◽  
Author(s):  
Ilenia Aversa ◽  
Roberta Chirillo ◽  
Emanuela Chiarella ◽  
Fabiana Zolea ◽  
Maddalena Di Sanzo ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Nuclear Factor Κb ◽  
Cancer Cell Lines ◽  
Nuclear Accumulation ◽  
Therapeutic Implications ◽  
Ferritin Heavy Chain ◽  
Additional Layer ◽  
Ros Scavenger

Nuclear Factor-κB (NF-κB) is frequently activated in tumor cells contributing to aggressive tumor growth and resistance to chemotherapy. Here we demonstrate that Ferritin Heavy Chain (FHC) protein expression inversely correlates with NF-κB activation in cancer cell lines. In fact, FHC silencing in K562 and SKOV3 cancer cell lines induced p65 nuclear accumulation, whereas FHC overexpression correlated with p65 nuclear depletion in the same cell lines. In FHC-silenced cells, the p65 nuclear accumulation was reverted by treatment with the reactive oxygen species (ROS) scavenger, indicating that NF-κB activation was an indirect effect of FHC on redox metabolism. Finally, FHC knock-down in K562 and SKOV3 cancer cell lines resulted in an improved cell viability following doxorubicin or cisplatin treatment, being counteracted by the transient expression of inhibitory of NF-κB, IκBα. Our results provide an additional layer of information on the complex interplay of FHC with cellular metabolism, and highlight a novel scenario of NF-κB-mediated chemoresistance triggered by the downregulation of FHC with potential therapeutic implications.

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