[Invadopodia regulation: a new function for p27 in cellular invasion].

Med Sci (Paris)

Centre de recherches en cancérologie de Toulouse (CRCT), Inserm UMR1037, université Toulouse III Paul Sabatier, CNRS ERL5294, 31000 Toulouse, France.

Published: December 2017

Download full-text PDF

Source
http://dx.doi.org/10.1051/medsci/20173312002DOI Listing

Publication Analysis

Top Keywords

[invadopodia regulation
4
regulation function
4
function p27
4
p27 cellular
4
cellular invasion]
4
[invadopodia
1
function
1
p27
1
cellular
1
invasion]
1

Similar Publications

Nuclear podosomes regulates cellular migration in Tau and Alzheimer's disease.

Adv Protein Chem Struct Biol

January 2025

Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences Hospital (NIMHANS), Institute of National Importance, Bangalore, Karnataka, India. Electronic address:

The neuronal cytoskeleton has remained a less explored area of research in establishing neuroprotection. HDAC6 has been studied with respect to many neurodegenerative diseases, especially AD. It exhibits the ability to interact with various cytoskeletal proteins and to promote migration in cells.

View Article and Find Full Text PDF

NOX proteins and ROS generation: role in invadopodia formation and cancer cell invasion.

Biol Res

December 2024

Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, 5090000, Valdivia, Chile.

NADPH oxidases (NOX) are membrane-bound proteins involved in the localized generation of reactive oxygen species (ROS) at the cellular surface. In cancer, these highly reactive molecules primarily originate in mitochondria and via NOX, playing a crucial role in regulating fundamental cellular processes such as cell survival, angiogenesis, migration, invasion, and metastasis. The NOX protein family comprises seven members (NOX1-5 and DUOX1-2), each sharing a catalytic domain and an intracellular dehydrogenase site.

View Article and Find Full Text PDF

Autophagy Regulator Rufy 4 Promotes Osteoclastic Bone Resorption by Orchestrating Cytoskeletal Organization via Its RUN Domain.

Cells

October 2024

Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan.

Rufy4, a protein belonging to the RUN and FYVE domain-containing protein family, participates in various cellular processes such as autophagy and intracellular trafficking. However, its role in osteoclast-mediated bone resorption remains uncertain. In this study, we investigated the expression and role of the gene in osteoclasts using small interfering RNA (siRNA) transfection and gene overexpression systems.

View Article and Find Full Text PDF

YAP signaling orchestrates the endothelin-1-guided invadopodia formation in high-grade serous ovarian cancer.

Biosci Rep

December 2024

Preclinical Models and New Therapeutic Agents Unit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Regina Elena National Cancer Institute, Rome, Italy.

The high-grade serous ovarian cancer (HG-SOC) is a notoriously challenging disease, characterized by a rapid peritoneal dissemination. HG-SOC cells leverage actin-rich membrane protrusions, known as invadopodia, to degrade the surrounding extracellular matrix (ECM) and invade, initiating the metastatic cascade. In HG-SOC, the endothelin-1 (ET-1)/endothelin A receptor (ETAR)-driven signaling coordinates invadopodia activity, however how this axis integrates pro-oncogenic signaling routes, as YAP-driven one, impacting on the invadopodia-mediated ECM degradation and metastatic progression, deserves a deeper investigation.

View Article and Find Full Text PDF

BLNK negatively regulates innate antifungal immunity through inhibiting c-Cbl-mediated macrophage migration.

Proc Natl Acad Sci U S A

October 2024

Department of Infection and Immunity, Clinical Medicine Scientific and Technical Innovation Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.

Article Synopsis
  • B cell linker protein (BLNK) is essential for signaling in B cells, but its role in macrophages during C-type lectin receptor (CLR) signaling is not well understood.
  • The study reveals that CLRs activate BLNK, which hinders macrophage migration by disrupting podosome ring formation in response to fungal components.
  • BLNK deficiency leads to increased macrophage migration and enhanced resistance to fungal infections by promoting the recruitment of specific macrophages to affected tissues.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!