What question did this study set out to answer?

This research aims to determine the role of NEK9 in regulating motility in triple negative breast cancer (TNBC).

May 9, 2026Journal of Clinical and Translational Science0 citationsOpen Access

394 NEK9 modulates triple negative breast cancer cell biology.

JBJulia Boehling BABrian Anderson EMElizabeth Martin

Key Points

This research aims to determine the role of NEK9 in regulating motility in triple negative breast cancer (TNBC).
Evaluated NEK9 expression across five breast cancer and three non-breast cancer cell lines by immunoblot.
Tested the effects of NEK9 pharmacological inhibitor BA 03-53-11 on various TNBC cell lines.
Performed functional assays including scratch assay for motility and crystal violet for viability.
NEK9 expression was higher in TNBC cell lines than in other breast cancer subtypes and non-cancerous cells.
Pharmacological inhibition of NEK9 did not significantly impact cell viability or proliferation but reduced cell motility in TNBC cells.
Ongoing studies aim to further validate NEK9's role in TNBC progression.

Abstract

Objectives/Goals: The Never-in-mitosis A-related (NEK) kinases are a family of 11 poorly explored kinases that play varying roles in cellular processes. Aberrant NEK activity is implicated in various human diseases, including cancer. We hypothesize that NEK9 drives triple-negative breast cancer (TNBC) motility. Methods/Study Population: Baseline NEK9 expression was determined across five breast cancer and three non-breast cancer cell lines by immunoblot. We expanded the analysis to six additional TNBC cell lines. To determine the impact of NEK9 on TNBC biology, we evaluated the effects of NEK9 pharmacological inhibition with novel inhibitor BA 03-53-11 (BA) at 0µM, 0.5µM, 1µM, and 2µM. We treated TNBC cell lines MDA-MB-231, BT-549, HS578T, and TNBC patient-derived cell line TUBcX-4IC and performed functional assays to assess impacts on cell motility (scratch assay), viability (crystal violet staining), and proliferation (Ki-67 staining). Results/Anticipated Results: NEK9 levels were elevated in the TNBC cell line compared to other breast cancer subtypes, osteosarcoma, and non-cancerous cells. Additionally, NEK9 protein expression was variable across TNBC cell lines. While pharmacological NEK9 inhibition did not significantly alter TNBC cell viability or proliferation, we observed that NEK9 inhibition suppressed cell motility in TNBC cells compared to vehicle control. Taken together, these preliminary results support a role for NEK9 in regulating TNBC progression. Our ongoing studies aim to test NEK9-mediated motility and proliferation in additional TNBC cell lines and evaluate NEK9 as a therapeutic target for this aggressive breast cancer subtype. Discussion/Significance of Impact: TNBC is an aggressive form of breast cancer that lacks targeted therapies. Because aberrant kinase activity underpins oncogenic transformation, kinase inhibitors have emerged as ideal therapeutic agents. Elucidation of NEK9 function in TNBC is essential for the development of novel therapeutics.

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