Related Experiment Video
Updated: May 4, 2026

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts
Published on: October 9, 2016
The STAT3-Ser/Hes3 signaling axis in cancer
Steven W Poser1, Deric M Park2, Andreas Androutsellis-Theotokis3
1Innate Repair Laboratory, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität, Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.
Abstract:
Disrupting the regenerative capacity of tumorigenic cells is a major focus in medicine. These regenerative properties are carried by a subpopulation of cells within the tumor, termed cancer stem cells. Current therapies don't effectively tackle the disease suggesting these cells employ yet unidentified molecular mechanisms allowing them to evade targeting. Recent observations in neural stem cells reveal an extraordinary plasticity in the signaling pathways they utilize to grow. These findings are being extended to the cancer stem cell field, illuminating conceptually novel treatment strategies. Tumorigenic cells can make use of distinct, even opposing pathways, including JAK/STAT and the non-canonical STAT3-Ser/Hes3 signaling axis. This plasticity may not be confined to the cancer stem cell population, but may be shared by various cell types within the tumor, blurring the line distinguishing cancer stem cells from other tumor cell types. The implications to anti-cancer medicine are highly significant, since these findings demonstrate that inhibiting one cell growth pathway may actually enhance the activity of alternative ones. Drug discovery programs will also benefit from these concepts.
Insights
Cancer stem cells possess unique plasticity, utilizing diverse signaling pathways like JAK/STAT for regeneration. Understanding this adaptability is key to developing novel cancer therapies that overcome treatment resistance.
Area of Science:
- Oncology
- Stem Cell Biology
- Molecular Medicine
Background:
- Cancer stem cells (CSCs) are crucial for tumor regeneration and treatment resistance.
- Current therapies often fail to eradicate CSCs due to unidentified molecular mechanisms.
- Recent research highlights the plasticity of neural stem cells' signaling pathways.
Purpose of the Study:
- To explore the signaling pathway plasticity in cancer stem cells.
- To identify novel molecular mechanisms underlying CSC regenerative capacity.
- To inform the development of more effective anti-cancer treatment strategies.
Main Methods:
- Investigating the JAK/STAT signaling pathway in CSCs.
- Analyzing the non-canonical STAT3-Ser/Hes3 signaling axis.
- Comparing signaling pathway utilization across different tumor cell types.
Main Results:
- CSCs exhibit remarkable plasticity, employing distinct and opposing signaling pathways for growth.
- The JAK/STAT and non-canonical STAT3-Ser/Hes3 pathways are utilized by tumorigenic cells.
- This plasticity may extend beyond CSCs, blurring cell type distinctions within tumors.
Conclusions:
- Inhibiting one signaling pathway in cancer may inadvertently activate alternative pro-growth pathways.
- Targeting CSC plasticity offers a conceptually novel approach to anti-cancer drug discovery.
- Understanding pathway redundancy is critical for overcoming therapeutic resistance in cancer.
Related Concept Videos
The JAK-STAT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
PI3K/mTOR/AKT Signaling Pathway
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Abnormal Proliferation

