KIF18A
Kinesin Family Member 18A: A Mitotic Kinesin Involved in Chromosome Congression and Cancer
Gene Information Card
| Symbol | KIF18A |
|---|---|
| Full Name | kinesin family member 18A |
| Gene Type | protein-coding |
| Chromosomal Location | 11p14.1 |
| NCBI Gene ID | 81930 ncbi.nlm.nih.gov/gene/81930 |
| Ensembl ID | ENSG00000121621 |
| UniProt ID | Q8NI77 |
| OMIM ID | 611271 |
| HGNC ID | 29441 |
| Aliases | MS-KIF18A, KNSL8, kinesin-like protein 8 |
Description
KIF18A encodes a member of the kinesin-8 family of microtubule-based motor proteins. This protein plays a critical role in mitosis by regulating microtubule dynamics and chromosome congression. It localizes to the plus ends of kinetochore microtubules and suppresses microtubule growth, ensuring proper chromosome alignment and segregation. KIF18A is overexpressed in various cancers and is associated with poor prognosis, making it a potential therapeutic target.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Breast cancer | Overexpression of KIF18A promotes cell proliferation and migration; knockdown reduces tumor growth in xenograft models. | PMID: 29367642 |
| Colorectal cancer | High KIF18A expression correlates with advanced stage and poor survival; silencing induces mitotic arrest and apoptosis. | PMID: 31065047 |
| Lung adenocarcinoma | KIF18A upregulation drives chromosomal instability and aneuploidy; associated with aggressive tumor behavior. | PMID: 32015549 |
| Hepatocellular carcinoma | KIF18A overexpression enhances cell cycle progression and invasion; potential biomarker for prognosis. | PMID: 30523342 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Testis | 15.2 | Medium |
| Bone marrow | 10.8 | Medium |
| Lymph node | 8.5 | Medium |
| Brain | 3.1 | Low |
| Liver | 1.2 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HeLa | 18.5 | Cervical cancer cell line; high expression |
| MCF7 | 12.3 | Breast cancer cell line; moderate expression |
| A549 | 9.8 | Lung cancer cell line; moderate expression |
| HEK293 | 4.2 | Embryonic kidney; low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1672C>T (p.Arg558Cys) | Missense | <0.01% (COSMIC) | Unknown functional impact; reported in colorectal cancer |
| c.2144A>G (p.Asn715Ser) | Missense | <0.01% (COSMIC) | Unknown functional impact; reported in lung cancer |
| c.1237G>A (p.Glu413Lys) | Missense | <0.01% (COSMIC) | Unknown functional impact; reported in breast cancer |
Mutation functional classification
Loss of Function (LOF)
No confirmed loss-of-function mutations reported in KIF18A in human cancers; experimental knockdown in cell lines leads to mitotic defects.
Gain of Function (GOF)
Overexpression of wild-type KIF18A is observed in multiple cancers, suggesting a gain-of-function through increased protein levels rather than activating mutations.
Dominant Negative (DN)
No dominant-negative mutations have been characterized for KIF18A.
View complete mutation data：
Gene Ontology (GO)
| • microtubule motor activity | • ATP binding |
| • microtubule binding | • plus-end-directed microtubule motor activity |
| • mitotic cell cycle | • chromosome congression |
| • kinetochore localization | • cell division |
Pathways
• Mitotic Prometaphase (Reactome: R-HSA-68877)
• Resolution of Sister Chromatid Cohesion (Reactome: R-HSA-2500257)
• Kinesins (Reactome: R-HSA-983189)
Protein Summary
KIF18A is a 898-amino acid protein (UniProt Q8NI77) belonging to the kinesin-8 family. It contains an N-terminal motor domain with ATPase activity, a central coiled-coil stalk, and a C-terminal tail domain. The motor domain binds microtubules and uses ATP hydrolysis to generate plus-end-directed motility. KIF18A accumulates at the plus ends of kinetochore microtubules, where it suppresses microtubule polymerization, thereby controlling chromosome oscillations and alignment during metaphase. Its dysregulation contributes to chromosomal instability and tumorigenesis.
Related Services
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