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Identification of the KIF18A alpha-4 helix as a therapeutic target for chromosomally unstable tumor cells
Katherine Schutt1, Katelyn A Queen1, Kira Fisher1
1Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT.
Abstract:
The mitotic kinesin, KIF18A, is required for proliferation of cancer cells that exhibit chromosome instability (CIN), implicating it as a promising target for treatment of a subset of aggressive tumor types. Determining regions of the KIF18A protein to target for inhibition will be important for the design and optimization of effective small molecule inhibitors. In this study, we investigated the effects of mutating S284 within the alpha-4 helix of KIF18A, which was previously identified as a phosphorylated residue. Mutations in S284 cause relocalization of KIF18A from the plus-ends of spindle microtubules to the spindle poles. Furthermore, KIF18A S284 mutants display loss of KIF18A function and fail to support proliferation in CIN tumor cells. Interestingly, similar effects on KIF18A localization and function were seen after treatment of CIN cells with KIF18A inhibitory compounds that are predicted to interact with residues within the alpha-4 helix. These data implicate the KIF18A alpha-4 helix as an effective target for inhibition and demonstrate that small molecules targeting KIF18A selectively limit CIN tumor cell proliferation and result in phenotypically similar effects on mitosis at the single cell level compared to genetic perturbations.
Insights
The mitotic kinesin KIF18A is crucial for cancer cell proliferation. Targeting its alpha-4 helix with small molecules effectively inhibits chromosome instability (CIN) tumor growth.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- KIF18A is a mitotic kinesin essential for chromosome instability (CIN) cancer cell proliferation.
- Targeting KIF18A is a promising strategy for aggressive tumor types.
- Identifying specific KIF18A regions for inhibition is key for drug development.
Approach:
- Investigated the role of serine 284 (S284) mutation in the KIF18A alpha-4 helix.
- Observed KIF18A relocalization and loss of function in S284 mutants.
- Compared effects of genetic mutation with KIF18A inhibitory compounds.
Key Points:
- Mutating S284 in KIF18A's alpha-4 helix disrupts its microtubule localization and function.
- KIF18A S284 mutants impair proliferation in CIN tumor cells.
- Small molecules targeting the KIF18A alpha-4 helix mimic genetic perturbation effects.
Conclusions:
- The KIF18A alpha-4 helix is a viable target for therapeutic inhibition.
- Small molecule inhibitors targeting KIF18A selectively reduce CIN tumor cell proliferation.
- Inhibition of KIF18A leads to mitosis defects similar to genetic mutations.
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