Related Experiment Video

Updated: Jun 27, 2025

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
12:52

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

15.8K

YANK2 activated by Fyn promotes glioma tumorigenesis via the mTOR-independent p70S6K activation pathway

Yue Shi1, Yue Cheng1,2, Wei Wang1

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.

Scientific Reports
|May 7, 2024
PubMed

Insights

Researchers discovered a new pathway, Fyn-YANK2-p70S6K, that drives glioma growth. Targeting YANK2 (yet another kinase 2) offers a potential new therapeutic strategy for this incurable brain tumor.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Glioblastomas (GBM) remain an incurable brain tumor with limited treatment options.
  • Targeted therapies against receptor tyrosine kinases (RTKs) have shown minimal benefit for GBM patients.
  • Understanding novel mechanisms of glioma growth is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of Ser/Thr protein kinase YANK2 (yet another kinase 2) in glioma progression.
  • To identify upstream regulators and downstream effectors of YANK2 in glioma.
  • To explore the Fyn-YANK2-p70S6K signaling axis as a potential therapeutic target.

Main Methods:

  • Analysis of YANK2 expression in glioma tissues.
  • In vitro and in vivo experiments to assess the impact of YANK2 on glioma growth and proliferation.
  • Investigation of the interaction between oncogene Fyn and YANK2, including phosphorylation site analysis (Y110).
  • Identification of YANK2 as an upstream kinase of p70S6K and determination of the phosphorylation site (T389).

Main Results:

  • YANK2 is upregulated in glioma tissues and promotes glioma growth and proliferation.
  • Oncogene Fyn directly phosphorylates YANK2 at Y110, enhancing its stability and promoting glioma growth.
  • YANK2 directly phosphorylates p70S6K at T389, indicating its role as a novel upstream kinase.
  • A new mTOR-independent signaling pathway, Fyn-YANK2-p70S6K, was identified that promotes glioma growth.

Conclusions:

  • YANK2 is a potential oncogene that promotes glioma growth through the Fyn-YANK2-p70S6K pathway.
  • This pathway represents a novel mechanism of p70S6K activation, independent of mTOR.
  • YANK2 is a promising novel therapeutic target for glioma treatment.
Keywords:
FynGliomaTumorigenesisYANK2p70S6K

More Related Videos

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

6.9K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:39

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

77

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

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.
The mTOR pathway or the...
3.8K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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...
3.5K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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...
6.3K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.4K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.5K