ArticleCell death and differentiation2014
PKCλ/ι signaling promotes triple-negative breast cancer growth and metastasis.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Auranofin Suppresses Cancer Cell Invasion by Inhibiting Heparanase-1 Expression via the aPKC-NF-κB Pathway.International journal of molecular sciences · 2026Article
- Protein Kinase C Family: Structures, Biological Functions, Diseases, and Pharmaceutical Interventions.MedComm · 2025Review
- PKC-International journal of molecular sciences · 2025Article
- Review
- Proteasome Inhibitor MG-132 and PKC-ι-Specific Inhibitor ICA-1S Degrade Mutant p53 and Induce Apoptosis in Ovarian Cancer Cell Lines.International journal of molecular sciences · 2025Article
- Targeted therapy approaches for epithelial-mesenchymal transition in triple negative breast cancer.Frontiers in oncology · 2024Review
- Macrophages-aPKCJournal of experimental & clinical cancer research : CR · 2022Article
- Glyoxalase 1 and protein kinase Cλ as potential therapeutic targets for late-stage breast cancer.Oncology letters · 2021Article
- Identification of Key Phospholipids That Bind and Activate Atypical PKCs.Biomedicines · 2021Article
- Recurrent copy number gains drive PKCι expression and PKCι-dependent oncogenic signaling in human cancers.Advances in biological regulation · 2020Article
- Article
- The Dual Roles of the Atypical Protein Kinase Cs in Cancer.Cancer cell · 2019Review
- Anti-EGF Receptor Aptamer-Guided Co-Delivery of Anti-Cancer siRNAs and Quantum Dots for Theranostics of Triple-Negative Breast Cancer.Theranostics · 2019Article
- Preclinical testing of 5-amino-1-((1R,2S,3S,4R)-2,3-dihydroxy-4-methylcyclopentyl)-1H-imidazole-4-carboxamide: a potent protein kinase C-ι inhibitor as a potential prostate carcinoma therapeutic.Anti-cancer drugs · 2019Article
- Activation of atypical protein kinase C by sphingosine 1-phosphate revealed by an aPKC-specific activity reporter.Science signaling · 2019Article
- Molecular Mechanisms and Emerging Therapeutic Targets of Triple-Negative Breast Cancer Metastasis.Frontiers in oncology · 2018Review
- A 3q gene signature associated with triple negative breast cancer organ specific metastasis and response to neoadjuvant chemotherapy.Scientific reports · 2017Article
- Methylene blue photodynamic therapy induces selective and massive cell death in human breast cancer cells.BMC cancer · 2017Article
- Targeting oncogenic protein kinase Cι for treatment of mutant KRAS LADC.Small GTPases · 2017Article
- Phosphorylated Protein Kinase C (Zeta/Lambda) Expression in Colorectal Adenocarcinoma and Its Correlation with Clinicopathologic Characteristics and Prognosis.Journal of Cancer · 2017Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is a distinct breast cancer subtype defined by the absence of estrogen receptor (ER), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/neu), and the patients with TNBC are often diagnosed with higher rates of recurrence and metastasis. Because of the absence of ER, PR and HER2/neu expressions, TNBC patients are insensitive to HER2-directed and endocrine therapies available for breast cancer treatment. Here, we report that expression of atypical protein kinase C isoform, PKCλ/ι, significantly increased and activated in all invasive breast cancer (invasive ductal carcinoma or IDC) subtypes including the TNBC subtype. Because of the lack of targeted therapies for TNBC, we choose to study PKCλ/ι signaling as a potential therapeutic target for TNBC. Our observations indicated that PKCλ/ι signaling is highly active during breast cancer invasive progression, and metastatic breast cancers, the advanced stages of breast cancer disease that developed more frequently in TNBC patients, are also characterized with high levels of PKCλ/ι expression and activation. Functional analysis in experimental mouse models revealed that depletion of PKCλ/ι significantly reduces TNBC growth as well as lung metastatic colonization. Furthermore, we have identified a PKCλ/ι-regulated gene signature consisting of 110 genes, which are significantly associated with indolent to invasive progression of human breast cancer and poor prognosis. Mechanistically, cytokines such as TGFβ and IL1β could activate PKCλ/ι signaling in TNBC cells and depletion of PKCλ/ι impairs NF-κB p65 (RelA) nuclear localization. We observed that cytokine-PKCλ/ι-RelA signaling axis, at least in part, involved in modulating gene expression to regulate invasion of TNBC cells. Overall, our results indicate that induction and activation of PKCλ/ι promote TNBC growth, invasion and metastasis. Thus, targeting PKCλ/ι signaling could be a therapeutic option for breast cancer, including the TNBC subtype.
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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 OpenQuestion graph.