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Exploration of inhibitors targeting KIF18A with ploidy-specific lethality
Qingsong Chen1, Xiangyang Le1, Qianbin Li1
1Department of Medicinal Chemistry, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410013, Hunan, China; Hunan Key Laboratory of Small Molecules for Diagnosis and Treatment of Chronic Disease, Changsha 410013, Hunan, China; Hunan Key Laboratory of Organ Fibrosis, Changsha 410013, Hunan, China.
Abstract:
Currently, various antimitotic inhibitors applied in tumor therapy. However, these inhibitors exhibit targeted toxicity to some extent. As a motor protein, kinesin family member 18A (KIF18A) is crucial to spindle formation and is associated with tumors exhibiting ploidy-specific characteristics such as chromosomal aneuploidy, whole-genome doubling (WGD), and chromosomal instability (CIN). Differing from traditional antimitotic targets, KIF18A exhibits tumor-specific selectivity. The functional loss or attenuation of KIF18A results in vulnerability of tumor cells with ploidy-specific characteristics, with lesser effects on diploid cells. Research on inhibitors targeting KIF18A with ploidy-specific lethality holds significant importance. This review provides a brief overview of the regulatory mechanisms of the ploidy-specific lethality target KIF18A and the research advancements in its inhibitors, aiming to facilitate the development of KIF18A inhibitors.
Insights
Kinesin family member 18A (KIF18A) is a novel cancer target. Inhibitors targeting KIF18A show tumor-specific selectivity, offering a promising new avenue for cancer therapy development.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Antimitotic inhibitors are used in cancer therapy but have limitations in targeted toxicity.
- Kinesin family member 18A (KIF18A) is a motor protein vital for spindle formation and linked to tumor ploidy characteristics like aneuploidy, whole-genome doubling (WGD), and chromosomal instability (CIN).
- KIF18A exhibits tumor-specific selectivity, unlike traditional antimitotic targets.
Purpose of the Study:
- To review the regulatory mechanisms of KIF18A as a target for ploidy-specific lethality.
- To summarize research advancements in KIF18A inhibitors.
- To facilitate the development of novel KIF18A-targeting cancer therapies.
Main Methods:
- Literature review of KIF18A's role in cancer.
- Analysis of KIF18A's regulatory mechanisms in relation to ploidy.
- Survey of current research on KIF18A inhibitors.
Main Results:
- Functional loss or attenuation of KIF18A selectively sensitizes tumor cells with ploidy-specific characteristics to cell death.
- Diploid cells are less affected by KIF18A inhibition.
- KIF18A inhibitors demonstrate potential for tumor-specific lethality.
Conclusions:
- KIF18A represents a promising target for developing cancer therapies with improved tumor specificity.
- Targeting KIF18A exploits the vulnerabilities of cancer cells with specific ploidy states.
- Further research into KIF18A inhibitors is crucial for advancing cancer treatment strategies.
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