ArticleNature communications2016
TOM1L1 drives membrane delivery of MT1-MMP to promote ERBB2-induced breast cancer cell invasion.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- TOM1 family proteins: from cargo sorting to immune dysregulation and cancer.Cell communication and signaling : CCS · 2026Review
- Genetic determinants of drug-induced gingival overgrowth.Scientific reports · 2026Article
- Tethered Exosomes Containing the Matrix Metalloproteinase MT1-MMP Contribute to Extracellular Matrix Degradation.Journal of extracellular vesicles · 2025Article
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- TOM1L1 mediated the sort of tumor suppressive miR-378a-3p into exosomes and the excretion out of cells to promote ESCC progression.Cancer gene therapy · 2025Article
- Unveiling the Role of Protein Posttranslational Modifications in Glioma Prognosis.CNS neuroscience & therapeutics · 2025Article
- Integrative analysis of m6A-SNPs and single-cell RNA sequencing reveals key drivers of endocrine combined with CDK4/6 inhibitor therapy resistance in ER+ breast cancer.Frontiers in pharmacology · 2025Article
- Exploring the correlation between Tom1L1 and the efficacy of neoadjuvant chemotherapy for locally progressive mid-low rectal cancer.BMC cancer · 2024Article
- Cytoplasmic Tail of MT1-MMP: A Hub of MT1-MMP Regulation and Function.International journal of molecular sciences · 2023Review
- Article
- Identification of a pyroptosis-related prognosis gene signature and its relationship with an immune microenvironment in gliomas.Medicine · 2022Article
- Mechanisms underlying melanoma invasion as a consequence of MLK3 loss.Experimental cell research · 2022Article
- Integrative genomic analysis of N6-methyladenosine-single nucleotide polymorphisms (mBioengineered · 2021Article
- Membrane-type I matrix metalloproteinase (MT1-MMP), lipid metabolism, and therapeutic implications.Journal of molecular cell biology · 2021Review
- Protein Trafficking or Cell Signaling: A Dilemma for the Adaptor Protein TOM1.Frontiers in cell and developmental biology · 2021Review
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Identification of Pan-Cancer Biomarkers Based on the Gene Expression Profiles of Cancer Cell Lines.Frontiers in cell and developmental biology · 2021Article
- Profiles of alternative splicing landscape in breast cancer and their clinical significance: an integrative analysis based on large-sequencing data.Annals of translational medicine · 2021Article
- Identification of Core Genes Involved in the Progression of Cervical Cancer Using an Integrative mRNA Analysis.International journal of molecular sciences · 2020Article
- Protrudin-mediated ER-endosome contact sites promote MT1-MMP exocytosis and cell invasion.The Journal of cell biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ERBB2 overexpression in human breast cancer leads to invasive carcinoma but the mechanism is not clearly understood. Here we report that TOM1L1 is co-amplified with ERBB2 and defines a subgroup of HER2(+)/ER(+) tumours with early metastatic relapse. TOM1L1 encodes a GAT domain-containing trafficking protein and is a SRC substrate that negatively regulates tyrosine kinase signalling. We demonstrate that TOM1L1 upregulation enhances the invasiveness of ERBB2-transformed cells. This pro-tumoural function does not involve SRC, but implicates membrane-bound membrane-type 1 MMP (MT1-MMP)-dependent activation of invadopodia, membrane protrusions specialized in extracellular matrix degradation. Mechanistically, ERBB2 elicits the indirect phosphorylation of TOM1L1 on Ser321. The phosphorylation event promotes GAT-dependent association of TOM1L1 with the sorting protein TOLLIP and trafficking of the metalloprotease MT1-MMP from endocytic compartments to invadopodia for tumour cell invasion. Collectively, these results show that TOM1L1 is an important element of an ERBB2-driven proteolytic invasive programme and that TOM1L1 amplification potentially enhances the metastatic progression of ERBB2-positive breast cancers.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.