Targeting the ERK1/2 and p38 MAPK pathways attenuates Golgi tethering factor golgin-97 depletion-induced cancer progression in breast cancer.

ABSTRACT:

Background

The Golgi apparatus is widely considered a secretory center and a hub for different signaling pathways. Abnormalities in Golgi dynamics can perturb the tumor microenvironment and influence cell migration. Therefore, unraveling the regulatory network of the Golgi and searching for pharmacological targets would facilitate the development of novel anticancer therapies. Previously, we reported an unconventional role for the Golgi tethering factor golgin-97 in inhibiting breast cell motility, and its downregulation was associated with poor patient prognosis. However, the specific role and regulatory mechanism of golgin-97 in cancer progression in vivo remain unclear.

Methods

We integrated genetic knockout (KO) of golgin-97, animal models (zebrafish and xenograft mice),

SUBMITTER: Liu YC 

PROVIDER: S-EPMC11727508 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature