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mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Cancer-Associated STAT3 Mutations Maintain ES Cell Self-Renewal Through Phosphorylation-Independent Mechanisms.

Tadayuki Akagi1, Shota Nakamura1, Tomoya Tamaru1

  • 1Department of Life, Environment, and Applied Chemistry, Faculty of Engineering, Fukuoka Institute of Technology, Fukuoka, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|July 14, 2026
PubMed
Summary

Disease-associated mutations in Signal transducer and activator of transcription 3 (STAT3) maintain embryonic stem cell self-renewal independently of STAT3 phosphorylation. These findings offer insights into stem cell regulation in development and disease.

Keywords:
STAT3 mutationsY640Fcancer‐associated mutationsembryonic stem cellspluripotencyself‐renewal

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Published on: November 18, 2009

Area of Science:

  • Stem cell biology
  • Molecular genetics
  • Human disease mechanisms

Background:

  • Signal transducer and activator of transcription 3 (STAT3) is crucial for embryonic stem (ES) cell self-renewal.
  • Aberrant STAT3 activity and mutations are implicated in various human diseases.
  • Understanding STAT3's role in stem cells is vital for developmental and pathological insights.

Purpose of the Study:

  • To investigate the impact of specific disease-associated STAT3 mutations (Y640F and G656insF) on ES cell properties.
  • To determine the mechanism by which these STAT3 mutations affect ES cell self-renewal.
  • To explore the independence of these mutations from endogenous STAT3 signaling.

Main Methods:

  • Utilized embryonic stem (ES) cells carrying disease-associated STAT3 mutations (Y640F, G656insF).
  • Assessed ES cell self-renewal capacity in the absence of standard self-renewal factors (LIF, MEK/GSK3 inhibitors).
  • Analyzed STAT3 transcriptional activity and phosphorylation status post-LIF stimulation.
  • Employed STAT3 knockout ES cells to evaluate mutation function independently of endogenous STAT3.

Main Results:

  • STAT3 mutations Y640F and G656insF sustained ES cell self-renewal without LIF or MEK/GSK3 inhibition.
  • Mutated STAT3 exhibited enhanced transcriptional activity but unchanged phosphorylation levels after LIF stimulation.
  • The effects of these STAT3 mutations were independent of endogenous STAT3, confirmed in STAT3 knockout ES cells.

Conclusions:

  • Disease-associated STAT3 mutations can maintain stem cell self-renewal through novel, phosphorylation-independent pathways.
  • These findings elucidate how specific STAT3 mutations influence stem cell behavior in both normal development and disease states.
  • Highlights a potential mechanism for STAT3-driven pathologies originating from stem cell dysregulation.