scholarly journals Expression of Cathepsin E and Its Suppression with Intestinalization in Epithelial Cells and Tumor Cells in Rat Glandular Stomach Treated with N-methyl-N'-nitro-N-nitrosoguanidine.

2001 ◽  
Vol 14 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Hirofumi Yuasa ◽  
Satoshi Yoneyama ◽  
Masao Ichinose ◽  
Kazumasa Miki ◽  
Tetsuya Tsukamoto ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tumor Cells ◽  
Glandular Stomach ◽  
Cathepsin E

Fetal rat glandular stomach epithelial cells differentiate into surface mucous cells which express cathepsin E in the absence of mesenchymal cells in primary culture

1994 ◽  
Vol 56 (1-2) ◽  
pp. 83-89 ◽  
Author(s):  
Hiroshi Fukamachi ◽  
Masao Ichinose ◽  
Satoshi Ishihama ◽  
Shinko Tsukada ◽  
Sadao Yasugi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Culture ◽  
Mesenchymal Cells ◽  
Glandular Stomach ◽  
Mucous Cells ◽  
Cathepsin E ◽  
Fetal Rat

Cathepsin E is Expressed in Fetal Rat Glandular Stomach Epithelial Cells in Primary Culture in the Absence of Mesenchymes

1995 ◽  
pp. 357-361
Author(s):  
Hiroshi Fukamachi ◽  
Masao Ichinose ◽  
Satoshi Ishihama ◽  
Shinko Tsukada ◽  
Chie Furihata ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Culture ◽  
Glandular Stomach ◽  
Cathepsin E ◽  
Fetal Rat

Fetal rat glandular stomach epithelial cells differentiate into surface mucous cells which express cathepsin E in the absence of mesenchymal cells in primary culture

1994 ◽  
Vol 56 (1) ◽  
pp. 0083 ◽  
Author(s):  
Hiroshi Fukamachi ◽  
Masao Ichinose ◽  
Satoshi Ishihama ◽  
Shinko Tsukada ◽  
Sadao Yasugi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Culture ◽  
Mesenchymal Cells ◽  
Glandular Stomach ◽  
Mucous Cells ◽  
Cathepsin E ◽  
Fetal Rat

scholarly journals Pulmonary adenocarcinoma in cattle

2014 ◽  
pp. 4358-4363 ◽  
Author(s):  
Diogo Sousa Z ◽  
Luis Rivera C ◽  
Didier Quevedo C ◽  
Ana Claudia Gorino ◽  
Simone Biagio C ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tumor Cells ◽  
Adult Female ◽  
Histopathological Examination ◽  
Abdominal Cavity ◽  
Pulmonary Adenocarcinoma ◽  
Immunohistochemical Examination ◽  
Histopathological Findings ◽  
Hematoxylin Eosin ◽  
Neoplastic Epithelial Cells

ABSTRACTThe Macroscopic, histological and immunohistochemical aspects of lung acinar adenocarcinoma and the presence of nodules in the abdominal cavity of an adult female bovine are reported. In the necropsy analysis samples were collected from the: lung, heart, spleen, liver, pancreas, kidney, uterus, intestine, brain, and from nodules found in the lung and abdominal cavity, which were routinely processed to be stained by hematoxylin-eosin and for an immunohistochemistry exam with the antibodies: cytokeratin (dilution 1:200 μL) and vimentin (dilution 1:1000 μL). The histopathological examination revealed neoplastic epithelial cells with acini formation. The immunohistochemical examination of the tumor cells showed positive marking for cytokeratin and the absence of marking for vimentin. According to anatomical, morphological, and histopathological findings, as well as the result of the immunohistochemical examination, the tumor was characterized as lung acinar adenocarcinoma.

scholarly journals Dual targeting of folate receptor-expressing glioma tumor-associated macrophages and epithelial cells in the brain using a carbon nanosphere–cationic folate nanoconjugate

2019 ◽  
Vol 1 (9) ◽  
pp. 3555-3567 ◽  
Author(s):  
Chandra Kumar Elechalawar ◽  
Dwaipayan Bhattacharya ◽  
Mohammed Tanveer Ahmed ◽  
Halley Gora ◽  
Kathyayani Sridharan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tumor Cells ◽  
Folate Receptor ◽  
Tumor Associated Macrophages ◽  
Dual Targeting ◽  
Dual Strategy ◽  
Glioma Tumor ◽  
The Brain

A carbon nanosphere-based dual strategy to target tumor-associated macrophages and tumor cells in glioma lesions within the brain.

scholarly journals RHBDL2 Is a Critical Membrane Protease for Anoikis Resistance in Human Malignant Epithelial Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Tsung-Lin Cheng ◽  
Chao-Han Lai ◽  
Shinn-Jong Jiang ◽  
Jui-Hsiang Hung ◽  
Shi-Kai Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tumor Cells ◽  
Cancer Metastasis ◽  
Caspase 3 ◽  
Growth Factor Receptor ◽  
Metastatic Tumor ◽  
Anoikis Resistance ◽  
Rhomboid Protease ◽  
Egfr Activation ◽  
Kinase Phosphorylation

Anoikis resistance allows metastatic tumor cells to survive in a homeless environment. Activation of epithelial growth factor receptor (EGFR) signaling is one of the key mechanisms for metastatic tumor cells to resist anoikis, yet the regulation mechanisms of homeless-triggered EGFR activation in metastatic tumor cells remain unclear. Rhomboid-like-2 (RHBDL2), an evolutionally conserved intramembrane serine protease, can cleave the EGF ligand and thus trigger EGFR activation. Herein, we demonstrated that RHBDL2 overexpression in human epithelial cells resulted in promotion of cell proliferation, reduction of cell adhesion, and suppression of anoikis. During long-term suspension cultures, increased RHBDL2 was only detected in aggressive tumor cell lines. Treatment with the rhomboid protease inhibitor or RHBDL2 shRNA increased cleaved caspase 3, a marker of apoptosis. Finally, inhibition of EGFR activation increased the cleaved caspase 3 and attenuated the detachment-induced focal adhesion kinase phosphorylation. Taken together, these findings provide evidence for the first time that RHBDL2 is a critical molecule in anoikis resistance of malignant epithelial cells, possibly through the EGFR-mediated signaling. Our study demonstrates RHBDL2 as a new therapeutic target for cancer metastasis.

Immunohistochemical Study of the BCAR1/p130Cas Protein in Non-Malignant and Malignant Human Breast Tissue

2001 ◽  
Vol 16 (3) ◽  
pp. 172-178 ◽  
Author(s):  
S. van der Flier ◽  
T.H. van der Kwast ◽  
C.J.C. Claassen ◽  
M. Timmermans ◽  
A. Brinkman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Tumor Cells ◽  
Intracellular Signaling ◽  
Immunohistochemical Study ◽  
Tamoxifen Treatment ◽  
Breast Carcinomas ◽  
Epithelial Tumor ◽  
Variable Expression ◽  
Malignant Breast

BCAR1/p130Cas is a docking protein involved in intracellular signaling pathways and in vitro resistance of estrogen-dependent breast cancer cells to antiestrogens. The BCAR1/p130Cas protein level in primary breast cancer cytosols was found to correlate with rapid recurrence of disease. A high BCAR1/p130Cas level was also associated with a higher likelihood of resistance to first-line tamoxifen treatment in patients with advanced breast cancer. Using antibodies raised against the rat p130Cas protein, we determined by immunohistochemical methods the BCAR1/p130Cas localization in primary breast carcinomas, in tumors of stromal origin, and in non-neoplastic breast tissues. The BCAR1/p130Cas protein was detected in the cytoplasm of non-malignant and neoplastic epithelial cells and in the vascular compartment of all tissue sections analyzed. Immunohistochemistry demonstrated variable intensity of BCAR1/p130Cas staining and variation in the proportion of BCAR1/p130Cas-positive epithelial tumor cells for the different breast carcinomas. Double immunohistochemical staining for BCAR1/p130Cas and estrogen receptor confirmed coexpression in non-malignant luminal epithelial cells and malignant breast tumor cells. The stromal cells in non-malignant tissues and tumor tissues as well as breast tumors of mesodermal origin did not stain for BCAR1/p130Cas. This immunohistochemical study demonstrates a variable expression of BCAR1/p130Cas in malignant and non-malignant breast epithelial cells, which may be of benefit for diagnostic purposes.

Kinome-Wide RNAi Studies in Human Multiple Myeloma Identify a Lymphoid Restricted Kinase GRK6 as a Selectively Vulnerable Target That Regulates STAT3/MCL1.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 601-601
Author(s):  
Rodger E. Tiedemann ◽  
Yuan Xiao Zhu ◽  
Jessica Schmidt ◽  
Hongwei Yin ◽  
Quick Que ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Epithelial Cells ◽  
Tumor Cells ◽  
Research Funding ◽  
Kinase Inhibitors ◽  
Lymphoid Tissues ◽  
Myeloma Cells ◽  
Stat3 Phosphorylation ◽  
Human Multiple Myeloma

Abstract Abstract 601 A paucity of validated kinase targets in human multiple myeloma (MM) has delayed clinical deployment of kinase inhibitors in treatment strategies. We therefore conducted a kinome-wide small interfering RNA (siRNA) lethality study in MM tumor lines bearing common t(4;14), t(14;16) and t(11;14) translocations to identify critically vulnerable kinases in MM tumor cells without regard to preconceived mechanistic notions. Primary screening was performed in duplicate using an 1800-oligo siRNA library in a single-siRNA-per-well format. siRNA were transfected at low concentration (13nM) to minimize off-target effects using conditions that resulted in transfection of >95% cells and <5% background cytotoxicity. After 96 hours, viability was measured by ATP-dependent luminescence. Fifteen kinases were consistently vulnerable in MM cells, including AKT1, AK3L1, AURKA, AURKB, CDC2L1, CDK5R2, FES, FLT4, GAK, GRK6, HK1, PKN1, PLK1, SMG1, and TNK2. While several kinases (PLK1, HK1) were equally vulnerable in epithelial cells, others and particularly the G-protein coupled receptor kinase, GRK6, appeared selectively vulnerable in MM. GRK6 inhibition is selectively lethal to KMS11, OPM1, H929, KMS18 and OCI-MY5 myeloma cells and has minimal effect on 293, MCF7, SF767, A375 or A549 epithelial cells. Persistent expression of FLAG-GRK6 via cDNA rescued KMS11 cells from the lethal effect of a 3'UTR-targeted GRK6 siRNA, but not from control siRNA, validating identification of GRK6 as an essential myeloma survival kinase. Furthermore, concordant results were obtained using four different exon-based GRK6 siRNA, all of which induced GRK6 silencing and similar inhibition of KMS11 proliferation and viability. Significantly, GRK6 is ubiquitously expressed in lymphoid tissues and myeloma, but by comparison appears absent or only weakly expressed in most primary human somatic tissues. From co-immunoprecipitation experiments we demonstrate that GRK6 is highly expressed in myeloma cells via direct association with the HSP90 chaperone. Inhibition of HSP90 with geldanamycin blocks GRK6 protein expression. Importantly, direct GRK6 silencing causes rapid and selective suppression of STAT3 phosphorylation that is associated with sustained reductions in total MCL1 protein levels and MCL1 phosphorylation (within 24 hours), providing a potent mechanism for the cytotoxicity of GRK6 inhibition in MM tumor cells. GF109203X is an inhibitor of both protein kinase C and of GRK6 that causes near total inhibition of these kinases in vitro at distinct concentrations of 0.1μM and 1-10μM respectively. Notably, GF109203X was substantially cytotoxic to 10/14 myeloma tumor lines at concentrations most consistent with GRK6 inhibition (5-20μM), and was selectively more cytotoxic to myeloma tumor cells than to non-myeloma cell lines (P=0.01), highlighting the potential of GRK6 as a pharmaceutical target for selective therapeutic intervention in myeloma. As mice that lack GRK6 are healthy, inhibition of GRK6 represents a uniquely targeted novel therapeutic strategy in human multiple myeloma. Disclosures: Perkins: MMRC: Employment. Reeder:Celgene: Research Funding; Millennium: Research Funding. Fonseca:Otsuka: Consultancy; BMS: Consultancy; Amgen: Consultancy; Medtronic: Consultancy; Genzyme: Consultancy.

IL-1Ra selectively protects intestinal crypt epithelial cells, but not tumor cells, from chemotoxicity via p53-mediated upregulation of p21WAF1 and p27KIP1

2014 ◽  
Vol 82 ◽  
pp. 21-33 ◽  
Author(s):  
Xia Wang ◽  
Shunying Zhu ◽  
Lan Qian ◽  
Jing Gao ◽  
Mingyuan Wu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tumor Cells ◽  
Intestinal Crypt
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