Related Experiment Video
Updated: Sep 20, 2025
10:21
Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
Published on: September 20, 2024
545
PI3Kγ in Tumour Inflammation: Bridging Immune Response and Cancer Progression-A Mini-Review.
Anghesom Ghebremedhin1,2, Judith A Varner1,2
1Moores Cancer Center, University of California, San Diego, California, USA.
Immunology
|May 28, 2025
Summary
Phosphatidylinositol 3-kinase gamma (PI3Kγ) drives tumour inflammation and progression by affecting immune cells. Targeting PI3Kγ offers a promising strategy to inhibit cancer growth and reduce inflammation.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Phosphatidylinositol 3-kinase gamma (PI3Kγ) is a key regulator of inflammatory and immune responses.
- PI3Kγ influences myeloid cell activity, contributing to tumour progression and metastasis.
- The tumour microenvironment is significantly shaped by PI3Kγ-mediated inflammatory processes.
Purpose of the Study:
- To review the diverse roles of PI3Kγ in tumour-associated inflammation.
- To highlight PI3Kγ's involvement in immune cell polarization and cytokine production.
- To explore the therapeutic potential of targeting PI3Kγ in cancer treatment.
Main Methods:
- Literature review of studies investigating PI3Kγ in cancer.
- Analysis of PI3Kγ's role in immune cell trafficking and function.
- Examination of PI3Kγ's impact on tumour cell-stromal interactions.
Main Results:
- PI3Kγ promotes myeloid cell recruitment and activation within the tumour microenvironment.
- PI3Kγ influences cytokine profiles, exacerbating tumour-associated inflammation.
- PI3Kγ activity is linked to tumour cell proliferation, survival, and metastasis.
Conclusions:
- PI3Kγ is a critical mediator of inflammation in cancer.
- Targeting PI3Kγ presents a viable therapeutic strategy for inhibiting tumour growth.
- Modulating PI3Kγ could reduce inflammation-driven tumorigenesis and improve cancer therapy outcomes.
Related Concept Videos
01:22PI3K/mTOR/AKT Signaling Pathway
4.0K
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...
4.0K
01:19Interactions Between Signaling Pathways
6.6K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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...
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...
6.6K
03:03mTOR Signaling and Cancer Progression
3.9K
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.
The mTOR pathway or the...
The mTOR pathway or the...
3.9K
01:15Activation of Integrins
3.6K
Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...
3.6K
02:17The Tumor Microenvironment
6.8K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.8K
01:20The JAK-STAT Signaling Pathway
9.3K
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...
9.3K