ArticleOncotarget2016
ERN1 and ALPK1 inhibit differentiation of bi-potential tumor-initiating cells in human breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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
14 citing papers in PubMed, 21 citations in OpenAlex.
- Leukocyte-intrinsic ER stress responses contribute to chemotherapy-induced peripheral neuropathy.Science translational medicine · 2025Article
- The importance of ALPK1 kinase functionality as a potential biomarker for inflammatory diseases.Molecular biology reports · 2025Review
- The Role of Microbiota-Derived Metabolites in Colorectal Cancer.International journal of molecular sciences · 2023Review
- IRAK2 Downregulation in Triple-Negative Breast Cancer Cells Decreases Cellular Growth In Vitro and Delays Tumour Progression in Murine Models.International journal of molecular sciences · 2023Article
- Systematic Review of the Role of Alpha-Protein Kinase 1 in Cancer and Cancer-Related Inflammatory Diseases.Cancers · 2022Review
- Targeting UPR signaling pathway by dasatinib as a promising therapeutic approach in chronic myeloid leukemia.Medical oncology (Northwood, London, England) · 2022Article
- Transcriptome Analysis Reveals Key miRNA-mRNA Pathways in Ovarian Tissues of Yunshang Black Goats With Different Kidding Numbers.Frontiers in endocrinology · 2022Article
- Long noncoding RNA HAR1A regulates oral cancer progression through the alpha-kinase 1, bromodomain 7, and myosin IIA axis.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Breast cancer stem cells: A review of their characteristics and the agents that affect them.Molecular carcinogenesis · 2021Review
- ADP-heptose: a bacterial PAMP detected by the host sensor ALPK1.Cellular and molecular life sciences : CMLS · 2021Review
- ALPK1 hotspot mutation as a driver of human spiradenoma and spiradenocarcinoma.Nature communications · 2019Article
- ANLN and KDR Are Jointly Prognostic of Breast Cancer Survival and Can Be Modulated for Triple Negative Breast Cancer Control.Frontiers in genetics · 2019Article
- Prognostic values of distinct CBX family members in breast cancer.Oncotarget · 2017Article
- Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
Cancers are heterogeneous by nature. While traditional oncology screens commonly use a single endpoint of cell viability, altering the phenotype of tumor-initiating cells may reveal alternative targets that regulate cellular growth by processes other than apoptosis or cell division. We evaluated the impact of knocking down expression of 420 kinases in bi-lineage triple-negative breast cancer (TNBC) cells that express characteristics of both myoepithelial and luminal cells. Knockdown of ERN1 or ALPK1 induces bi-lineage MDA-MB-468 cells to lose the myoepithelial marker keratin 5 but not the luminal markers keratin 8 and GATA3. In addition, these cells exhibit increased β-casein production. These changes are associated with decreased proliferation and clonogenicity in spheroid cultures and anchorage-independent growth assays. Confirmation of these assays was completed in vivo, where ERN1- or ALPK1-deficient TNBC cells are less tumorigenic. Finally, treatment with K252a, a kinase inhibitor active on ERN1, similarly impairs anchorage-independent growth of multiple breast cancer cell lines. This study supports the strategy to identify new molecular targets for types of cancer driven by cells that retain some capacity for normal differentiation to a non-tumorigenic phenotype. ERN1 and ALPK1 are potential targets for therapeutic development.
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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.