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Record W1581566476 · doi:10.1158/1538-7445.am2014-4053

Abstract 4053: Formin-binding protein-17 (FBP17) is a target of p53 and promotes invadopodia formation in breast cancer cells

2014· article· en· W1581566476 on OpenAlexaff
Harish Chander, K. Christopher Watts, Justin Pogmore, Peter Truesdell, Colin D. Brien, Andrew W. Craig

Bibliographic record

VenueCancer Research · 2014
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCellular Mechanics and Interactions
Canadian institutionsDalhousie UniversityQueen's University
Fundersnot available
KeywordsInvadopodiaCortactinCancer researchDownregulation and upregulationGene silencingCDC42CancerBiologyCell biologyCancer cellChemistryCellActinCytoskeleton

Abstract

fetched live from OpenAlex

Abstract Invadopodia are extracellular matrix (ECM)-degrading structures that promote tissue invasion and metastasis of tumor cells. A family of adaptor proteins with F-BAR and SH3 domains, including FBP17 and Toca-1, have been identified as key scaffolds for recruiting actin regulatory proteins (eg. Cdc42, formins, N-WASP, dynamin) to promote formation of invadopodia in bladder and breast cancers, respectively. In this study, we investigated the potential role of FBP17 in breast cancer models. We observed FBP17 expression in normal breast epithelial cells (MCF10A), and at higher levels in basal breast cancer cell lines (MDA-MB-231) compared to luminal cell lines. Since basal breast cancers frequently harbor mutations in tumor suppressor p53, we tested whether wild-type (WT) p53 regulates expression of FBP17, which may explain higher expression in basal breast cancers. Camptothecin (CPT) treatment of WT p53-expressing breast cancer cells (MCF-7, DU4475) led to a dose dependent reduction in FBP17 mRNA and protein levels, and this was inversely correlated with p53 levels or its target p21WAF1. The downregulation of FBP17 was also observed using Nutlin-3, an Mdm2 inhibitor, indicating that WT p53 activation by multiple methods causes a rapid downregulation of FBP17. Currently we are testing whether this is a direct or indirect effect of p53 on FBP17 gene expression. As expected, FBP17 formed complexes with actin regulatory proteins (dynamin, cortactin, Arp2/3) that accumulate and promote invadopodia formation in MDA-MB-231 cells. Stable silencing of FBP17 in these cells led to a significant reduction in ECM degradation. This is consistent with FBP17 promoting invadopodia formation. Tumor xenograft models are in progress to determine whether FBP17 also promotes tumor metastasis. FBP17 expression levels in human breast tumors are currently being tested to determine whether altered expression occurs in molecular subtypes with frequent mutations in p53 (HER2, basal) and in their metastases. Overall, these results are consistent with FBP17 participating in cancer cell invasion, and supports further studies of its role in cancer metastasis. Citation Format: Harish Chander, Kathleen Watts, Justin Pogmore, Peter Truesdell, Colin Brien, Andrew W B Craig. Formin-binding protein-17 (FBP17) is a target of p53 and promotes invadopodia formation in breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4053. doi:10.1158/1538-7445.AM2014-4053

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.011

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0030.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.030
GPT teacher head0.333
Teacher spread0.304 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations4
Published2014
Admission routes1
Has abstractyes

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