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Updated: May 2, 2026
A Screening Method for Identification of Heterochromatin-Promoting Drugs Using Drosophila
Published on: March 12, 2020
Systematic screen of chemotherapeutics in Drosophila stem cell tumors
Michele Markstein1, Samantha Dettorre, Julio Cho
1Department of Biology, University of Massachusetts, Amherst, MA 01003.
Abstract:
Here we report the development of an in vivo system to study the interaction of stem cells with drugs using a tumor model in the adult Drosophila intestine. Strikingly, we find that some Food and Drug Administration-approved chemotherapeutics that can inhibit the growth of Drosophila tumor stem cells can paradoxically promote the hyperproliferation of their wild-type counterparts. These results reveal an unanticipated side effect on stem cells that may contribute to tumor recurrence. We propose that the same side effect may occur in humans based on our finding that it is driven in Drosophila by the evolutionarily conserved Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway. An immediate implication of our findings is that supplementing traditional chemotherapeutics with anti-inflammatories may reduce tumor recurrence.
Insights
Some FDA-approved chemotherapeutics can paradoxically boost normal stem cell growth, potentially causing tumor recurrence. This side effect, driven by the Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway, may occur in humans.
Area of Science:
- Stem cell biology
- Cancer research
- Pharmacology
Background:
- Stem cells are crucial for tissue maintenance and repair.
- Cancer stem cells drive tumor growth and recurrence.
- Drug interactions with stem cells are not fully understood.
Purpose of the Study:
- To develop an in vivo system for studying drug-stem cell interactions.
- To investigate the effects of chemotherapeutics on normal and tumor stem cells.
- To identify mechanisms underlying unexpected drug side effects.
Main Methods:
- Utilized an adult Drosophila intestine tumor model.
- Administered Food and Drug Administration-approved chemotherapeutics.
- Analyzed stem cell proliferation and the Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway.
Main Results:
- Some chemotherapeutics inhibited tumor stem cell growth but promoted normal stem cell hyperproliferation.
- This paradoxical effect was driven by the evolutionarily conserved JAK-STAT pathway.
- Identified a potential mechanism for tumor recurrence.
Conclusions:
- Chemotherapeutics can have unintended consequences on normal stem cells.
- The JAK-STAT pathway mediates this side effect, suggesting conserved mechanisms in humans.
- Supplementing chemotherapy with anti-inflammatories may reduce tumor recurrence.
