scholarly journals Quinomycin A targets Notch signaling pathway in pancreatic cancer stem cells

Oncotarget ◽  
2015 ◽  
Vol 7 (3) ◽  
pp. 3217-3232 ◽  
Author(s):  
Sivapriya Ponnurangam ◽  
Prasad R. Dandawate ◽  
Animesh Dhar ◽  
Ossama W. Tawfik ◽  
Rajashri R. Parab ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Pancreatic Cancer Stem Cells

Abstract 4214: Quinomycin A affects pancreatic cancer stem cells in part through suppression of notch signaling pathway

2015 ◽  
Author(s):  
Dharmalingam Subramaniam ◽  
Sivapriya Ponnurangam ◽  
Afreen Sayed ◽  
Animesh Dhar ◽  
Dan A. Dixon ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Pancreatic Cancer Stem Cells

scholarly journals Cancer Stem Cells, Quo Vadis? The Notch Signaling Pathway in Tumor Initiation and Progression

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1879 ◽  
Author(s):  
Christian T. Meisel ◽  
Cristina Porcheri ◽  
Thimios A. Mitsiadis
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Cell Fate ◽  
Adult Life ◽  
Notch Pathway ◽  
Notch Signaling Pathway ◽  
Fine Tuning ◽  
Cell Fate Decisions

The Notch signaling pathway regulates cell proliferation, cytodifferentiation and cell fate decisions in both embryonic and adult life. Several aspects of stem cell maintenance are dependent from the functionality and fine tuning of the Notch pathway. In cancer, Notch is specifically involved in preserving self-renewal and amplification of cancer stem cells, supporting the formation, spread and recurrence of the tumor. As the function of Notch signaling is context dependent, we here provide an overview of its activity in a variety of tumors, focusing mostly on its role in the maintenance of the undifferentiated subset of cancer cells. Finally, we analyze the potential of molecules of the Notch pathway as diagnostic and therapeutic tools against the various cancers.

scholarly journals Epigenetic Regulation of SOX9 by the NF-κB Signaling Pathway in Pancreatic Cancer Stem Cells

Stem Cells ◽  
2013 ◽  
Vol 31 (8) ◽  
pp. 1454-1466 ◽  
Author(s):  
Lei Sun ◽  
Lesley A. Mathews ◽  
Stephanie M. Cabarcas ◽  
Xiaohu Zhang ◽  
Acong Yang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Signaling Pathway ◽  
Epigenetic Regulation ◽  
Pancreatic Cancer Stem Cells

732 - Novel Marmelin Analog MRL16 Targets Notch Signaling Pathway in Colon Cancer Stem Cells

2018 ◽  
Vol 154 (6) ◽  
pp. S-151
Author(s):  
Dharmalingam Subramaniam ◽  
Sivapriya Ponnurangam ◽  
Prasad Dandawate ◽  
Ossama Tawfik ◽  
Roy A. Jensen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Colon Cancer Stem Cells

scholarly journals Suppressive Effect of α-mangostin for Cancer Stem Cells in Colorectal Cancer via the Notch Pathway

2021 ◽  
Author(s):  
Min Kyoung Jo ◽  
Chang Mo Moon ◽  
Eun Ju Kim ◽  
Jee Hee Kwan ◽  
Xiang Fei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Flow Cytometry ◽  
Cancer Stem Cells ◽  
Cell Viability ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Suppressive Effect ◽  
Notch Signaling Pathway ◽  
Dependent Manner

Abstract Background: Since colon cancer stem cells (CSCs) play an important role in chemoresistance and in tumor recurrence and metastasis, targeting of CSCs has emerged as a sophisticated strategy for cancer therapy. α-mangostin (αM) has been confirmed to have antiproliferative and apoptotic effects on cancer cells. This study aimed to evaluate the selective inhibition of αM on CSCs in colorectal cancer (CRC) and the suppressive effect on 5-fluorouracil (5-FU)-induced CSCs. Methods: The cell viability assay was performed to determine the optimal concentration of αM. A sphere forming assay and flow cytometry with CSC markers were carried out to evaluate the αM-mediated inhibition of CSCs. Western blot analysis and quantitative real-time PCR were performed to investigate the effects of αM on the Notch signaling pathway and colon CSCs. The in vivo anticancer efficacy of αM in combination with 5-FU was investigated using a xenograft mouse model. Results: αM inhibited the cell viability and reduced the number of spheres in HT29 and SW620 cells. αM treatment decreased CSCs and suppressed the 5-FU-induced an increase in CSCs on flow cytometry. αM markedly suppressed Notch1, NICD1, and Hes1 in the Notch signaling pathway in a time- and dose-dependent manner. Moreover, αM attenuated CSC markers CD44 and CD133, in a manner similar to that upon DAPT treatment, in HT29 cells. In xenograft mice, the tumor and CSC makers were suppressed in the αM group and in the αM group with 5-FU treatment. Conclusion: This study shows that low-dose αM inhibits CSCs in CRC and suppresses 5-FU–induced augmentation of CSCs via the Notch signaling pathway.

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