ArticleThe Journal of biological chemistry2016
Identification of NEK3 Kinase Threonine 165 as a Novel Regulatory Phosphorylation Site That Modulates Focal Adhesion Remodeling Necessary for Breast Cancer Cell Migration.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- PCID2 is essential for spermatogonial differentiation by regulating alternative splicing.Cellular and molecular life sciences : CMLS · 2026Article
- Depression and breast cancer: research progress and prospects from an interdisciplinary perspective.Frontiers in immunology · 2026Review
- NEK kinases in cell cycle regulation, DNA damage response, and cancer progression.Tissue & cell · 2025Review
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- The NIMA-related kinase family and cancer.Frontiers in oncology · 2025Review
- Deregulated kinase action in prostate cancer: molecular basis and therapeutic implications.Endocrine-related cancer · 2023Review
- Breast Cancer and Prolactin - New Mechanisms and Models.Endocrinology · 2022Review
- In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022Review
- Analysis of the effect of NEKs on the prognosis of patients with non-small-cell lung carcinoma based on bioinformatics.Scientific reports · 2022Article
- Prolactin receptor gene transcriptional control, regulatory modalities relevant to breast cancer resistance and invasiveness.Frontiers in endocrinology · 2022Review
- The Relevant Participation of Prolactin in the Genesis and Progression of Gynecological Cancers.Frontiers in endocrinology · 2021Review
- Biallelic loss of function NEK3 mutations deacetylate α-tubulin and downregulate NUP205 that predispose individuals to cilia-related abnormal cardiac left-right patterning.Cell death & disease · 2020Article
- Comprehensive substrate specificity profiling of the human Nek kinome reveals unexpected signaling outputs.eLife · 2019Article
- Progesterone receptors (PR) mediate STAT actions: PR and prolactin receptor signaling crosstalk in breast cancer models.The Journal of steroid biochemistry and molecular biology · 2018Review
- In depth analysis of kinase cross screening data to identify chemical starting points for inhibition of the Nek family of kinases.MedChemComm · 2018Review
- Overexpression of NEK3 is associated with poor prognosis in patients with gastric cancer.Medicine · 2018Article
- The landscape of DNA methylation-mediated regulation of long non-coding RNAs in breast cancer.Oncotarget · 2017Article
- Cell matrix adhesions in cancer: The proteins that form the glue.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulating evidence supports a role for prolactin (PRL) in the development and progression of human breast cancer. Although PRL is an established chemoattractant for breast cancer cells, the precise molecular mechanisms of how PRL regulates breast cancer cell motility and invasion are not fully understood. PRL activates the serine/threonine kinase NEK3, which was reported to enhance breast cancer cell migration, invasion, and the actin cytoskeletal reorganization necessary for these processes. However, the specific mechanisms of NEK3 activation in response to PRL signaling have not been defined. In this report, a novel PRL-inducible regulatory phosphorylation site within the activation segment of NEK3, threonine 165 (Thr-165), was identified. Phosphorylation at NEK3 Thr-165 was found to be dependent on activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway using both pharmacological inhibition and siRNA-mediated knockdown approaches. Strikingly, inhibition of phosphorylation at NEK3 Thr-165 by expression of a phospho-deficient mutant (NEK3-T165V) resulted in increased focal adhesion size, formation of zyxin-positive focal adhesions, and reorganization of the actin cytoskeleton into stress fibers. Concordantly, NEK3-T165V cells exhibited migratory defects. Together, these data support a modulatory role for phosphorylation at NEK3 Thr-165 in focal adhesion maturation and/or turnover to promote breast cancer cell migration.
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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.