Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

LC3C-Mediated Autophagy Selectively Regulates the Met RTK and HGF-Stimulated Migration and Invasion

1 Dec 2019

Abstract excerpt

The Met/hepatocyte growth factor (HGF) receptor tyrosine kinase (RTK) is deregulated in many cancers and is a recognized target for cancer therapies. Following HGF stimulation, the signaling output of Met is tightly controlled by receptor internalization and sorting for degradation or recycling. Here, we uncover a role for autophagy in selective degradation of Met and regulation of Met-dependent cell migration...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Endoplasmic Reticulum Stress and Disease
Share to Pancreatic function and diabetes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31851933
DOI: 10.1016/j.celrep.2019.11.063

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

LC3C-Mediated Autophagy Selectively Regulates the Met RTK and HGF-Stimulated Migration and InvasionPMID 31851933Read ↗

LC3C mediates selective autophagy of the MET RTK, inhibiting cancer cell invasionSemantic proximity Read ↗

Met endosomal signalling: in the right place, at the right time.Semantic proximity Read ↗

Targeting the c-Met Signaling Pathway in CancerSemantic proximity Read ↗

Met/Hepatocyte growth factor receptor ubiquitination suppresses transformation and is required for Hrs phosphorylation.Semantic proximity Read ↗

Met–HER3 crosstalk supports proliferation via MPZL3 in MET-amplified cancer cellsSemantic proximity Read ↗

Targeting mesenchymal-epithelial transition factor signaling in cancer: from genetic alterations to clinical advances and future prospects.Semantic proximity Read ↗

The HGF-MET axis coordinates liver cancer metabolism and autophagy for chemotherapeutic resistanceSemantic proximity Read ↗

Met-HER3 crosstalk supports proliferation via MPZL3 in <i>MET</i> -amplified cancer cellsSemantic proximity Read ↗

The MET Oncogene Network of Interacting Cell Surface ProteinsSemantic proximity Read ↗

Extracellular matrix guidance of autophagy: a mechanism regulating cancer growthSemantic proximity Read ↗

Targeting the hepatocyte growth factor/Met pathway in cancer.Semantic proximity Read ↗

Novel AKT1-GLI3-VMP1 Pathway Mediates KRAS Oncogene-induced Autophagy in Cancer CellsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.