scholarly journals Investigation of the expression of RIF1 gene on head and neck, pancreatic and brain cancer and cancer stem cells

2016 ◽  
Vol 39 (6) ◽  
pp. 43 ◽  
Author(s):  
Hacer E GursesCila ◽  
Muradiye Acar ◽  
Furkan B Barut ◽  
Mehmet Gunduz ◽  
Reidar Grenman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Head And Neck ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines

Purpose: Recent studies have shown that cancer stem cells are resistant to chemotherapy. The aim of this study was to compare RIF1 gene expression in head and neck, pancreatic cancer and glioma cell lines and the cancer stem cells isolated from these cell lines. Methods: UT-SCC-74 from Turku University and UT-SCC-74B primary tumor metastasis and neck cancer cell lines, YKG-1 glioma cancer cell line from RIKEN, pancreatic cancer cell lines and ASPC-1 cells from ATCC were grown in cell culture. To isolate cancer stem cells, ALDH-1 for UT-SCC-74 and UT-SCC-74B cell line, CD-133 for YKG-1 cell line and CD-24 for ASPC-1 cell line, were used as markers of cancer stem cells. RNA isolation was performed for both cancer lines and cancer stem cells. RNAs were converted to cDNA. RIF1 gene expression was performed by qRT-PCR analysis. RIF1 gene expression was compared with cancer cell lines and cancer stem cells isolated from these cell lines. The possible effect of RIF1 gene was evaluated. Results: In the pancreatic cells, RIF1 gene expression in the stem cell-positive cell line was 256 time that seen in the stem cell-negative cell line. Conclusion: Considering the importance of RIF1 in NHEJ and of NHEJ in pancreatic cancer, RIF1 may be one of the genes that plays an important role in the diagnoses and therapeutic treatment of pancreatic cancer. The results of head and neck and brain cancers are inconclusive and further studies are required to elucidate the connection between RIF1 gene and these other types of cancers.

scholarly journals Oral cancer stem cells drive tumourigenesis through activation of stromal fibroblasts

2019 ◽  
Author(s):  
Mohanad J.N Al-Magsoosi ◽  
Daniel W Lambert ◽  
Syed Ali Khurram ◽  
Simon A Whawell
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Oral Cancer ◽  
Cancer Stem Cells ◽  
Conditioned Medium ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumour Progression ◽  
Cancer Cell Lines ◽  
Stromal Fibroblasts

Abstract Background: Cancer stem cells (CSC) are a subpopulation of cells within a tumour that are primarily responsible for tumour progression and resistance to therapy. Fibroblasts in the stromal tissue surrounding a tumour are also involved with its progression and fibroblast ‘activation’ is an independent prognostic marker in oral cancer. We hypothesise that CSCs can be isolated from oral cancer cell lines using functional assays and that they may drive tumour progression through communication with stromal fibroblasts. Methods: CSCs were isolated from oral cancer cell lines (H357 and SCC4) by their rapid adherence to fibronectin or resistance to cisplatin. Conditioned medium from both CSC and unsorted H357 and SCC4 cell lines were applied to cultures of NOFs for 24 hours. The gene and protein expression of the activation markers alpha smooth muscle action (αSMA) and interleukin-6 was assessed using qPCR and immunofluorescence. Expression of CSC markers and αSMA were examined in OSCC tissue using immunohistochemistry. Results: Cells isolated using both methods expressed significantly increased levels of stem cell markers CD24, CD44 and CD29 compared to unsorted cells. Adherent cells exhibited lower growth rate, higher colony forming efficiency and increased cisplatin resistance compared to unsorted cells. Conversely, the cisplatin-resistant cells adhered to fibronectin in greater numbers than unsorted cells. Expression of αSMA and IL-6 was increased in NOFs following exposure to either H357 or SCC4 CSC conditioned medium. In OSCC tissue there was a positive correlation between expression of αSMA and both CD24 and CD44. Conclusions: Rapid adherence to fibronectin and chemo-resistance effectively isolates a sub-population of cells from cell lines which show stem cell-like characteristics. Our data also suggests that factors released by CSC can activate fibroblasts towards a CAF-like phenotype, which together with evidence of correlation between markers of both in vivo, provides evidence of a mechanism by which such cells can drive tumour progression.

scholarly journals The Telomerase Inhibitor Imetelstat Depletes Cancer Stem Cells in Breast and Pancreatic Cancer Cell Lines

2010 ◽  
Vol 70 (22) ◽  
pp. 9494-9504 ◽  
Author(s):  
Immanual Joseph ◽  
Robert Tressler ◽  
Ekaterina Bassett ◽  
Calvin Harley ◽  
Christen M. Buseman ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Telomerase Inhibitor

Abstract 3339: Elimination of cancer stem cells in pancreatic cancer cell lines by a combinatorial therapy

2010 ◽  
Author(s):  
Carmen Visús ◽  
Antonio Lozano-Leon ◽  
YangYang Wang ◽  
YooJung Chang ◽  
David C. Whitcomb ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Combinatorial Therapy

scholarly journals Oral cancer stem cells drive tumourigenesis through activation of stromal fibroblasts

2019 ◽  
Author(s):  
Mohanad J.N Al-Magsoosi ◽  
Daniel W Lambert ◽  
Syed Ali Khurram ◽  
Simon A Whawell
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Oral Cancer ◽  
Cancer Stem Cells ◽  
Conditioned Medium ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumour Progression ◽  
Cancer Cell Lines ◽  
Stromal Fibroblasts

Abstract Background: Cancer stem cells (CSC) are a subpopulation of cells within a tumour that are primarily responsible for tumour progression and resistance to therapy. Fibroblasts in the stromal tissue surrounding a tumour are also involved with its progression and fibroblast ‘activation’ is an independent prognostic marker in oral cancer. We hypothesise that CSCs can be isolated from oral cancer cell lines using functional assays and that they may drive tumour progression through communication with stromal fibroblasts. Methods: CSCs were isolated from oral cancer cell lines (H357 and SCC4) by their rapid adherence to fibronectin or resistance to cisplatin. Conditioned medium from both CSC and unsorted H357 and SCC4 cell lines were applied to cultures of NOFs for 24 hours. The gene and protein expression of the activation markers alpha smooth muscle action (αSMA) and interleukin-6 was assessed using qPCR and immunofluorescence. Expression of CSC markers and αSMA were examined in OSCC tissue using immunohistochemistry. Results: Cells isolated using both methods expressed significantly increased levels of stem cell markers CD24, CD44 and CD29 compared to unsorted cells. Adherent cells exhibited lower growth rate, higher colony forming efficiency and increased cisplatin resistance compared to unsorted cells. Conversely, the cisplatin-resistant cells adhered to fibronectin in greater numbers than unsorted cells. Expression of αSMA and IL-6 was increased in NOFs following exposure to either H357 or SCC4 CSC conditioned medium. In OSCC tissue there was a positive correlation between expression of αSMA and both CD24 and CD44. Conclusions: Rapid adherence to fibronectin and chemo-resistance effectively isolates a sub-population of cells from cell lines which show stem cell-like characteristics. Our data also suggests that factors released by CSC can activate fibroblasts towards a CAF-like phenotype, which together with evidence of correlation between markers of both in vivo, provides evidence of a mechanism by which such cells can drive tumour progression.

Gastrin regulates growth of human pancreatic cancer in a tonic and autocrine fashion

1996 ◽  
Vol 270 (5) ◽  
pp. R1078-R1084 ◽  
Author(s):  
J. P. Smith ◽  
A. Shih ◽  
Y. Wu ◽  
P. J. McLaughlin ◽  
I. S. Zagon
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Pancreatic Cancer ◽  
Growth Media ◽  
Human Pancreatic Cancer Cell ◽  
Cell Extracts

The gastrointestinal peptides gastrin and cholecystokinin (CCK) stimulate growth of human pancreatic cancer through a CCK-B/gastrin- like receptor. In the present study we evaluated whether growth of human pancreatic cancer is endogenously regulated by gastrin. Immunohistomical examination of BxPC-3 cells and tumor xenografts revealed specifc gastrin immunoreactivity. Gastrin was detected by radioimmunoassay in pancreatic cancer cell extracts and in pancreatic cancer cell extracts and in the growth media. With use of reverse-transcriptase polymerase chain reaction gastrin gene expression was detected in both cultured BxPC-3 cancer cells and transplanted tumors, as well as seven addition human pancreatic cancer cell lines. Growth of BxPC-3 human pancreatic cancer cell in serum-free medium was inhibited by the addition of the CCK-B/gastrin receptor antagonist L-365,260, and gastrin treatment reversed the inhibitory effect of the antagonist. A selective gastrin antibody (Ab repressed growth of BxPC-3 cells. Gastrin immunoreactivity was detected in fresh human pancreatic cancer specimens but not in normal human pancreatic tissue. These data provide the first evidence that growth of a human pancreatic cancer is tonically stimulated by the autocrine production of gastrin. Evidence for the ubiquity of this system was provided by the detection of gastrin gene expression in multiple human pancreatic cancer cell lines and detection of gastrin in cell lines and fresh pancreatic tumors.

scholarly journals Cancer stem cells and cisplatin‐resistant cells isolated from non‐small‐lung cancer cell lines constitute related cell populations

2014 ◽  
Vol 3 (5) ◽  
pp. 1099-1111 ◽  
Author(s):  
Blanca D. Lopez‐Ayllon ◽  
Veronica Moncho‐Amor ◽  
Ander Abarrategi ◽  
Inmaculada Ibañez Cáceres ◽  
Javier Castro‐Carpeño ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cell Populations ◽  
Lung Cancer Cell ◽  
Related Cell ◽  
Resistant Cells
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