Control of stem cells and cancer stem cells by Hedgehog signaling: Pharmacologic clues from pathway dissection

2013 ◽  
Vol 85 (5) ◽  
pp. 623-628 ◽  
Author(s):  
Sonia Coni ◽  
Paola Infante ◽  
Alberto Gulino
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Hedgehog Signaling

scholarly journals Non-Canonical Hedgehog Signaling Is a Positive Regulator of the WNT Pathway and Is Required for the Survival of Colon Cancer Stem Cells

Cell Reports ◽  
2017 ◽  
Vol 21 (10) ◽  
pp. 2813-2828 ◽  
Author(s):  
Joseph L. Regan ◽  
Dirk Schumacher ◽  
Stephanie Staudte ◽  
Andreas Steffen ◽  
Johannes Haybaeck ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Hedgehog Signaling ◽  
Wnt Pathway ◽  
Positive Regulator ◽  
Colon Cancer Stem Cells

scholarly journals The FDA-Approved Anti-Asthma Medicine Ciclesonide Inhibits Lung Cancer Stem Cells through Hedgehog Signaling-Mediated SOX2 Regulation

2020 ◽  
Vol 21 (3) ◽  
pp. 1014 ◽  
Author(s):  
Hack Sun Choi ◽  
Su-Lim Kim ◽  
Ji-Hyang Kim ◽  
Dong-Sun Lee
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Small Interfering Rna ◽  
Hedgehog Signaling ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Protein Levels ◽  
Lung Cancer Stem Cells ◽  
Interfering Rna

Ciclesonide is an FDA-approved glucocorticoid (GC) used to treat asthma and allergic rhinitis. However, its effects on cancer and cancer stem cells (CSCs) are unknown. Our study focuses on investigating the inhibitory effect of ciclesonide on lung cancer and CSCs and its underlying mechanism. In this study, we showed that ciclesonide inhibits the proliferation of lung cancer cells and the growth of CSCs. Similar glucocorticoids, such as dexamethasone and prednisone, do not inhibit CSC formation. We show that ciclesonide is important for CSC formation through the Hedgehog signaling pathway. Ciclesonide reduces the protein levels of GL1, GL2, and Smoothened (SMO), and a small interfering RNA (siRNA) targeting SMO inhibits tumorsphere formation. Additionally, ciclesonide reduces the transcript and protein levels of SOX2, and an siRNA targeting SOX2 inhibits tumorsphere formation. To regulate breast CSC formation, ciclesonide regulates GL1, GL2, SMO, and SOX2. Our results unveil a novel mechanism involving Hedgehog signaling and SOX2 regulated by ciclesonide in lung CSCs, and also open up the possibility of targeting Hedgehog signaling and SOX2 to prevent lung CSC formation.

Cancer Stem Cells Equipped with Powerful Hedgehog Signaling and Better Epigenetic Memory: Avenues to Look for Cancer Therapeutics

2019 ◽  
Vol 19 (11) ◽  
pp. 877-884 ◽  
Author(s):  
Ishita Tandon ◽  
Asawari Waghmode ◽  
Nilesh Kumar Sharma
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Cancer Therapeutics ◽  
Complex Nature ◽  
Epigenetic Memory ◽  
Therapeutic Approaches ◽  
Shh Signaling ◽  
Memory Power

Complex nature of the tumor is depicted at the cellular landscape by showing heterogeneity in the presence of cancer cells, cancer-associated stromal cells, mesenchymal stem cells and cancer stem cells (CSCs). One of the plausible views in cancer formation is suggested as the theory of cancer CSCs that is known as a source of initiation of tumorigenesis. In essence, these powerful CSCs are equipped with high Sonic Hedgehog (SHH) signaling and epigenetic memory power that support various tumor hallmarks. Truly, nature justifies its intent by limiting these stem cells with a potential to turn into CSCs and in turn suppressing the high risk of humans and other organisms. In short, this mini-review addresses the contribution of SHH signaling to allow reprogramming of epigenetic memory within CSCs that support tumor hallmarks. Besides, this paper explores therapeutic approaches to mitigate SHH signaling that may lead to a blockade of the pro-tumor potential of CSCs.

scholarly journals LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway

Stem Cells ◽  
2015 ◽  
Vol 34 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Mingli Zhou ◽  
Yixuan Hou ◽  
Guanglun Yang ◽  
Hailong Zhang ◽  
Gang Tu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Signaling Pathway ◽  
Hedgehog Signaling ◽  
Hedgehog Signaling Pathway ◽  
Positive Breast Cancer

scholarly journals Inhibition of hedgehog signaling depresses self-renewal of pancreatic cancer stem cells and reverses chemoresistance

2012 ◽  
Vol 41 (5) ◽  
pp. 1707-1714 ◽  
Author(s):  
FENG-TING HUANG ◽  
YONG-XUN ZHUAN-SUN ◽  
YAN-YAN ZHUANG ◽  
SHU-LI WEI ◽  
JIAN TANG ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Hedgehog Signaling ◽  
Self Renewal ◽  
Pancreatic Cancer Stem Cells

scholarly journals Sulforaphane inhibits self-renewal of lung cancer stem cells through the modulation of sonic Hedgehog signaling pathway and polyhomeotic homolog 3

AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Fanping Wang ◽  
Yanwei Sun ◽  
Xiaoyu Huang ◽  
Caijuan Qiao ◽  
Wenrui Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Lung Cancer Cells ◽  
Sonic Hedgehog Signaling ◽  
Self Renewal ◽  
Lung Cancer Stem Cells

AbstractSulforaphane (SFN), an active compound in cruciferous vegetables, has been characterized by its antiproliferative capacity. We investigated the role and molecular mechanism through which SFN regulates proliferation and self-renewal of lung cancer stem cells. CD133+ cells were isolated with MACs from lung cancer A549 and H460 cells. In this study, we found that SFN inhibited the proliferation of lung cancer cells and self-renewal of lung cancer stem cells simultaneously. Meanwhile, the mRNA and protein expressions of Shh, Smo, Gli1 and PHC3 were highly activated in CD133+ lung cancer cells. Compared with siRNA-control group, Knock-down of Shh inhibited proliferation of CD133+ lung cancer cells, and decreased the protein expression of PHC3 in CD133+ lung cancer cells. Knock-down of PHC3 also affected the proliferation and decreased the Shh expression level in CD133+ lung cancer cells. In addition, SFN inhibited the activities of Shh, Smo, Gli1 and PHC3 in CD133+ lung cancer cells. Furthermore, the inhibitory effect of SFN on the proliferation of siRNA-Shh and siRNA-PHC3 cells was weaker than that on the proliferation of siRNA-control cells. Sonic Hedgehog signaling pathway might undergo a cross-talk with PHC3 in self-renewal of lung cancer stem cells. SFN might be an effective new drug which could inhibit self-renewal of lung cancer stem cells through the modulation of Sonic Hedgehog signaling pathways and PHC3. This study could provide a novel way to improve therapeutic efficacy for lung cancer stem cells.

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