ArticleScientific reports2018
E-cadherin loss induces targetable autocrine activation of growth factor signalling in lobular breast cancer.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 75 citations in OpenAlex.
- Toward targeted therapeutics for lobular breast cancer.The Journal of clinical investigation · 2026Review
- Invasive lobular breast cancer in young patients without adjuvant systemic treatment: 15-year survival outcomes.Breast cancer research and treatment · 2026Article
- Transcriptomic Insights into Lobular Breast Cancer Biology and Patient Outcomes: Analysis of the MINDACT Clinical Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Breast cancer ovarian metastases show increased activity of GPCR pathways.bioRxiv : the preprint server for biology · 2026Article
- High Expression of PAPP-A Predicts Poor Outcomes in Oestrogen Receptor-Positive Breast Cancer Patients.Cancer medicine · 2026Article
- Cancer-associated fibroblast driven paracrine IL-6/STAT3 signaling promotes migration and dissemination in invasive lobular carcinoma.Breast cancer research : BCR · 2025Article
- Molecular targets and therapies associated with poor prognosis of triple‑negative breast cancer (Review).International journal of oncology · 2025Review
- Afadin loss induces breast cancer metastasis through destabilisation of E-cadherin to F-actin linkage.The Journal of pathology · 2025Article
- Unraveling complexity and leveraging opportunities in uncommon breast cancer subtypes.NPJ breast cancer · 2025Review
- E-Cadherin-Mediated Cell-Cell Adhesion and Invasive Lobular Breast Cancer.Advances in experimental medicine and biology · 2025Review
- A Phase I Trial of Alpelisib Combined With Capecitabine in Patients With HER2-Negative Metastatic Breast Cancer.Clinical breast cancer · 2024Article
- International survey on invasive lobular breast cancer identifies priority research questions.NPJ breast cancer · 2024Article
- Case report: Cutaneous metastases as a first manifestation from breast cancer with concurrent gastric metastases.Frontiers in pharmacology · 2024Article
- GRHL2 Regulation of Growth/Motility Balance in Luminal versus Basal Breast Cancer.International journal of molecular sciences · 2023Article
- Loss of E-cadherin Induces IGF1R Activation and Reveals a Targetable Pathway in Invasive Lobular Breast Carcinoma.Molecular cancer research : MCR · 2022Article
- The Chaperone System in Breast Cancer: Roles and Therapeutic Prospects of the Molecular Chaperones Hsp27, Hsp60, Hsp70, and Hsp90.International journal of molecular sciences · 2022Review
- Multi-omics analyses provide novel biological insights to distinguish lobular ductal types of invasive breast cancers.Breast cancer research and treatment · 2022Article
- "The emerging role of capivasertib in breast cancer".Breast (Edinburgh, Scotland) · 2022Review
- Inter-observer agreement for the histological diagnosis of invasive lobular breast carcinoma.The journal of pathology. Clinical research · 2022Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Despite the fact that loss of E-cadherin is causal to the development and progression of invasive lobular carcinoma (ILC), options to treat this major breast cancer subtype are limited if tumours develop resistance to anti-oestrogen treatment regimens. This study aimed to identify clinically targetable pathways that are aberrantly active downstream of E-cadherin loss in ILC. Using a combination of reverse-phase protein array (RPPA) analyses, mRNA sequencing, conditioned medium growth assays and CRISPR/Cas9-based knock-out experiments, we demonstrate that E-cadherin loss causes increased responsiveness to autocrine growth factor receptor (GFR)-dependent activation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt signalling. Autocrine activation of GFR signalling and its downstream PI3K/Akt hub was independent of oncogenic mutations in PIK3CA, AKT1 or PTEN. Analyses of human ILC samples confirmed growth factor production and pathway activity. Pharmacological inhibition of Akt using AZD5363 or MK2206 resulted in robust inhibition of cell growth and survival of ILC cells, and impeded tumour growth in a mouse ILC model. Because E-cadherin loss evokes hypersensitisation of PI3K/Akt activation independent of oncogenic mutations in this pathway, we propose clinical intervention of PI3K/Akt in ILC based on functional E-cadherin inactivation, irrespective of activating pathway mutations.
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