Expression of Oct4, a Stem Cell Marker, in the Hamster Pancreatic Cancer Model

Pancreatology ◽  
2006 ◽  
Vol 6 (4) ◽  
pp. 406-413 ◽  
Author(s):  
Katsumichi Iki ◽  
Parviz M. Pour
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Cancer Model

scholarly journals Neoadjuvant chemotherapy with gemcitabine for pancreatic cancer increases in situ expression of the apoptosis marker M30 and stem cell marker CD44

2012 ◽  
Vol 3 (6) ◽  
pp. 1186-1190 ◽  
Author(s):  
HIDEHIRO TAJIMA ◽  
TETSUO OHTA ◽  
HIROHISA KITAGAWA ◽  
KOICHI OKAMOTO ◽  
SEISHO SAKAI ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Neoadjuvant Chemotherapy ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Apoptosis Marker

658 CD44, Pancreatic Cancer Stem Cell Marker, Positive Cells Are Responsible for the Acquiring Gemcitabine Induced Chemoresistance In Vitro

2008 ◽  
Vol 134 (4) ◽  
pp. A-96
Author(s):  
Sung Pil Hong ◽  
Jeong Youp Park ◽  
Jing Wen ◽  
Jin Wook Yoon ◽  
Kyung Hwa Park ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Stem Cell Marker ◽  
Cancer Stem Cell Marker ◽  
Cell Marker

scholarly journals Cancer Stem Cell Marker Phenotypes Are Reversible and Functionally Homogeneous in a Preclinical Model of Pancreatic Cancer

2015 ◽  
Vol 75 (21) ◽  
pp. 4582-4592 ◽  
Author(s):  
Joseph S. Dosch ◽  
Elizabeth K. Ziemke ◽  
Amrith Shettigar ◽  
Alnawaz Rehemtulla ◽  
Judith S. Sebolt-Leopold
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Stem Cell Marker ◽  
Preclinical Model ◽  
Cancer Stem Cell Marker ◽  
Cell Marker

scholarly journals Identification of a novel putative pancreatic stem/progenitor cell marker DCAMKL-1 in normal mouse pancreas

2010 ◽  
Vol 299 (2) ◽  
pp. G303-G310 ◽  
Author(s):  
Randal May ◽  
Sripathi M. Sureban ◽  
Stan A. Lightfoot ◽  
Aimee B. Hoskins ◽  
Daniel J. Brackett ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Suspension Culture ◽  
Progenitor Cell ◽  
Expression Patterns ◽  
Stem Cell Marker ◽  
Nodule Formation ◽  
Cell Marker ◽  
Pancreatic Development ◽  
Cytokeratin 14

Stem cells are critical in maintaining adult homeostasis and have been proposed to be the origin of many solid tumors, including pancreatic cancer. Here we demonstrate the expression patterns of the putative intestinal stem cell marker DCAMKL-1 in the pancreas of uninjured C57BL/6 mice compared with other pancreatic stem/progenitor cell markers. We then determined the viability of isolated pancreatic stem/progenitor cells in isotransplantation assays following DCAMKL-1 antibody-based cell sorting. Sorted cells were grown in suspension culture and injected into the flanks of athymic nude mice. Here we report that DCAMKL-1 is expressed in the main pancreatic duct epithelia and islets, but not within acinar cells. Coexpression was observed with somatostatin, NGN3, and nestin, but not glucagon or insulin. Isolated DCAMKL-1+ cells formed spheroids in suspension culture and induced nodule formation in isotransplantation assays. Analysis of nodules demonstrated markers of early pancreatic development (PDX-1), glandular epithelium (cytokeratin-14 and Ep-CAM), and isletlike structures (somatostatin and secretin). These data taken together suggest that DCAMKL-1 is a novel putative stem/progenitor marker, can be used to isolate normal pancreatic stem/progenitors, and potentially regenerates pancreatic tissues. This may represent a novel tool for regenerative medicine and a target for anti-stem cell-based therapeutics in pancreatic cancer.

411 Role of Intestinal Stem Cell Marker DCAMKL-1 in Pancreatic Cancer

2010 ◽  
Vol 138 (5) ◽  
pp. S-61
Author(s):  
Sripathi M. Sureban ◽  
Randal May ◽  
James H. Wyche ◽  
Shrikant Anant ◽  
Courtney W. Houchen
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Stem Cell Marker ◽  
Intestinal Stem Cell ◽  
Cell Marker

Abstract 408: Stem cell marker Nestin regulated the migration and invasion of pancreatic cancer cells

2010 ◽  
Author(s):  
Yoko Matsuda ◽  
Toshiyuki Ishiwata ◽  
Masao Kawamoto ◽  
Tetsushi Yamomoto ◽  
Kiyoko Kawahara ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Cancer Cells ◽  
Stem Cell Marker ◽  
Migration And Invasion ◽  
Cell Marker ◽  
Pancreatic Cancer Cells

scholarly journals Honokiol Affects Stem Cell Viability by Suppressing Oncogenic YAP1 Function to Inhibit Colon Tumorigenesis

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1607
Author(s):  
Dharmalingam Subramaniam ◽  
Sivapriya Ponnurangam ◽  
Satish Ramalingam ◽  
Deep Kwatra ◽  
Prasad Dandawate ◽  
...  
Keyword(s):  
Stem Cell ◽  
Intestinal Stem Cells ◽  
Stem Cell Marker ◽  
Hippo Signaling ◽  
Cell Marker ◽  
Cancer Model ◽  
Colon Tumorigenesis ◽  
Marker Proteins

Honokiol (HNK) is a biphenolic compound that has been used in traditional medicine for treating various ailments, including cancers. In this study, we determined the effect of HNK on colon cancer cells in culture and in a colitis-associated cancer model. HNK treatment inhibited proliferation and colony formation while inducing apoptosis. In addition, HNK suppressed colonosphere formation. Molecular docking suggests that HNK interacts with reserve stem cell marker protein DCLK1, with a binding energy of −7.0 Kcal/mol. In vitro kinase assays demonstrated that HNK suppressed the DCLK1 kinase activity. HNK also suppressed the expression of additional cancer stem cell marker proteins LGR5 and CD44. The Hippo signaling pathway is active in intestinal stem cells. In the canonical pathway, YAP1 is phosphorylated at Ser127 by upstream Mst1/2 and Lats1/2. This results in the sequestration of YAP1 in the cytoplasm, thereby not allowing YAP1 to translocate to the nucleus and interact with TEAD1-4 transcription factors to induce gene expression. However, HNK suppressed Ser127 phosphorylation in YAP1, but the protein remains sequestered in the cytoplasm. We further determined that this occurs by YAP1 interacting with PUMA. To determine if this also occurs in vivo, we performed studies in an AOM/DSS induced colitis-associated cancer model. HNK administered by oral gavage at a dose of 5mg/kg bw for 24 weeks demonstrated a significant reduction in the expression of YAP1 and TEAD1 and in the stem marker proteins. Together, these data suggest that HNK prevents colon tumorigenesis in part by inducing PUMA-YAP1 interaction and cytoplasmic sequestration, thereby suppressing the oncogenic YAP1 activity.

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