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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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mTOR Signaling and Cancer Progression03:03

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Related Experiment Video

Updated: Jun 17, 2026

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
06:29

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells

Published on: July 30, 2020

Physiological and oncogenic Aurora-A pathway.

Toshiaki Saeki1, Mutsuko Ouchi, Toru Ouchi

  • 1Department of Breast Oncology, Saitama Medical School, Japan.

International Journal of Biological Sciences
|December 17, 2009
PubMed
Summary
This summary is machine-generated.

Aurora-A kinase, a key factor in cell division, drives human cancer by causing genome instability. Understanding its role in cell signaling is crucial for developing new cancer therapies.

Keywords:
Aurora-ACell CycleCheckpointGenome InstabilityPhosphorylationPlk1mTOR

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Aurora kinases are vital for mitosis and cytokinesis.
  • Aurora-A is frequently overexpressed in various human cancers.
  • Aurora-A overexpression is linked to genome instability and tumorigenesis.

Purpose of the Study:

  • To review recent advancements in understanding Aurora-A's role in human carcinogenesis.
  • To highlight the significance of Aurora-A in cancer development and progression.

Main Methods:

  • Literature review of in vitro and in vivo studies.
  • Analysis of cell signaling pathways involving Aurora-A.
  • Summary of research on Aurora-A's oncogenic mechanisms.

Main Results:

  • Aurora-A overexpression induces tumorigenesis via genome instability.
  • Cell signaling crosstalk involving Aurora-A is essential for transformed phenotypes.
  • Recent studies provide insights into Aurora-A's multifaceted role in cancer.

Conclusions:

  • Aurora-A is a critical driver of human carcinogenesis.
  • Targeting Aurora-A may offer therapeutic strategies for cancer treatment.
  • Further research into Aurora-A signaling pathways is warranted.