Related Experiment Video

Updated: Oct 6, 2025

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs
10:32

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs

Published on: December 19, 2019

11.1K

Signaling by the tyrosine kinase Yes promotes liver cancer development

Jean-Philippe Guégan1, Marjorie Lapouge1,2, Laure Voisin1

  • 1Institute for Research in Immunology and Cancer, Montreal, Quebec, Canada.

Science Signaling
|January 18, 2022
PubMed

Insights

Researchers identified a new oncogenic pathway in hepatocellular carcinoma (HCC) mediated by the tyrosine kinase Yes. This pathway drives liver cancer cell growth and is linked to poor patient survival, suggesting Yes as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Signal Transduction

Background:

  • Hepatocellular carcinoma (HCC) often presents at late stages with limited treatment options due to poorly understood oncogenic mechanisms.
  • Unlike other cancers, HCC lacks a dominant, targetable oncogene, hindering effective pharmacological intervention.

Purpose of the Study:

  • To identify novel oncogenic signaling pathways in HCC.
  • To investigate the role of the tyrosine kinase Yes in HCC development and progression.
  • To explore YAP/TAZ as downstream effectors in Yes-mediated oncogenesis.

Main Methods:

  • Utilized genetic and pharmacological interventions in cellular and mouse models of HCC.
  • Assessed the necessity of Yes activity for HCC cell proliferation.
  • Investigated the sufficiency of activated Yes in inducing liver tumorigenesis.
  • Examined the phosphorylation and nuclear localization of YAP/TAZ by Yes.
  • Correlated Src family kinase activation with YAP status in human HCC samples.

Main Results:

  • Yes kinase activity is essential for HCC cell proliferation and liver tumorigenesis.
  • Yes phosphorylates and activates YAP/TAZ, promoting their nuclear accumulation and transcriptional activity.
  • YAP/TAZ function as critical effectors in Yes-driven hepatocyte transformation.
  • High Yes activity in human HCC correlates with increased tumor burden and shorter patient survival.

Conclusions:

  • The tyrosine kinase Yes mediates a novel oncogenic signaling pathway in HCC.
  • Yes and its downstream targets YAP/TAZ are key drivers of liver cancer.
  • Yes represents a promising therapeutic target for hepatocellular carcinoma.

More Related Videos

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays07:42

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays

Published on: September 19, 2018

8.1K
Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line06:24

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

586

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...
3.9K
Receptor Tyrosine Kinases01:26

Receptor Tyrosine Kinases

Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
14.9K
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...
6.6K
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...
4.1K
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.5K
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...
6.4K