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Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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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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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
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Related Experiment Video

Updated: Apr 17, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
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PI3K/Akt signaling in osteosarcoma.

Jian Zhang1, Xiao-Hua Yu2, Yi-Guo Yan1

  • 1Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.

Clinica Chimica Acta; International Journal of Clinical Chemistry
|February 24, 2015
PubMed
Summary

Targeting the PI3K/Akt pathway offers a promising strategy for treating osteosarcoma (OS), a common childhood bone cancer. Inhibiting this pathway could lead to more effective anti-OS agents and improved patient outcomes.

Keywords:
AktOSPI3KPTENmTOR

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Osteosarcoma (OS) is the most prevalent nonhematologic bone malignancy in pediatric and adolescent populations.
  • Despite advancements in chemotherapy, patient prognosis for OS remains poor, necessitating novel therapeutic strategies.
  • The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway is frequently hyperactivated in OS and drives tumor progression.

Purpose of the Study:

  • To review the critical roles of the PI3K/Akt pathway in osteosarcoma initiation and development.
  • To highlight the therapeutic potential of targeting the PI3K/Akt pathway in osteosarcoma treatment.
  • To elucidate how targeting this pathway can advance understanding of OS pathogenesis and treatment design.

Main Methods:

  • Literature review of studies investigating the PI3K/Akt pathway in osteosarcoma.
  • Analysis of evidence linking PI3K/Akt hyperactivation to OS characteristics like proliferation, invasion, and chemoresistance.
  • Examination of small molecule inhibitors targeting the PI3K/Akt pathway for anti-OS potential.

Main Results:

  • The PI3K/Akt pathway is implicated in multiple facets of OS progression, including tumorigenesis, metastasis, and resistance to chemotherapy.
  • Inhibition of the PI3K/Akt pathway has demonstrated potential as a therapeutic approach for osteosarcoma.
  • Small molecule inhibitors targeting this pathway are under investigation for their efficacy against OS.

Conclusions:

  • The PI3K/Akt pathway is a key driver in osteosarcoma development and progression.
  • Targeting the PI3K/Akt pathway represents a promising therapeutic avenue for osteosarcoma.
  • Further research into PI3K/Akt inhibitors will refine OS treatment strategies and deepen pathogenetic understanding.