KIF18A as a potential biomarker to distinguish different breast cancer subtypes based on receptor status
Abstract The inhibition of KIF18A selectively reduces the viability of chromosomally unstable cancers due to increased mitotic vulnerability. KIF18A expression was also reported to be upregulated and associated with tumor aggressiveness in certain cancer types including breast cancer. Here, I first showed that KIF18A mRNA expression is higher in triple-negative breast cancer (TNBC) than in non-TNBC. I also found that ER (estrogen receptor)-negative and PR (progesterone receptor)-negative breast cancer cells have higher KIF18A mRNA expression compared to ER-positive and PR-positive breast cancer cells, respectively. In contrast, HER2-positive breast tumors have higher KIF18A expression compared to HER2-negative breast tumors. In terms of PAM50 breast cancer subtypes, KIF18A transcript levels were found to be the highest in basal-like breast cancer, followed by HER2-enriched, luminal B, normal-like and luminal A. Besides, in non-TNBC, cells with high AR (androgen receptor) mRNA expression have higher KIF18A mRNA expression than cells with low AR mRNA expression. Both non-TNBC and TNBC cells with high BRCA1 and BRCA2 mRNA expression levels were observed to have higher KIF18A mRNA expression than those with low BRCA1 and BRCA2 mRNA expression levels, respectively. Combined, this study demonstrates that breast tumors with low and high expression of ER, PR, HER2, AR and BRCA1/2 have differential transcript levels of KIF18A, pointing that KIF18A might contribute to the molecular differences between different breast cancer subtypes..
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:5 |
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Enthalten in: |
Genome instability & disease - 5(2024), 2 vom: 15. März, Seite 89-96 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Berkel, Caglar [VerfasserIn] |
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Links: |
Volltext [lizenzpflichtig] |
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Themen: |
Androgen receptor |
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Anmerkungen: |
© Shenzhen University School of Medicine; Fondazione Istituto FIRC di Oncologia Molecolare 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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doi: |
10.1007/s42764-024-00126-8 |
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funding: |
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PPN (Katalog-ID): |
SPR055423760 |
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520 | |a Abstract The inhibition of KIF18A selectively reduces the viability of chromosomally unstable cancers due to increased mitotic vulnerability. KIF18A expression was also reported to be upregulated and associated with tumor aggressiveness in certain cancer types including breast cancer. Here, I first showed that KIF18A mRNA expression is higher in triple-negative breast cancer (TNBC) than in non-TNBC. I also found that ER (estrogen receptor)-negative and PR (progesterone receptor)-negative breast cancer cells have higher KIF18A mRNA expression compared to ER-positive and PR-positive breast cancer cells, respectively. In contrast, HER2-positive breast tumors have higher KIF18A expression compared to HER2-negative breast tumors. In terms of PAM50 breast cancer subtypes, KIF18A transcript levels were found to be the highest in basal-like breast cancer, followed by HER2-enriched, luminal B, normal-like and luminal A. Besides, in non-TNBC, cells with high AR (androgen receptor) mRNA expression have higher KIF18A mRNA expression than cells with low AR mRNA expression. Both non-TNBC and TNBC cells with high BRCA1 and BRCA2 mRNA expression levels were observed to have higher KIF18A mRNA expression than those with low BRCA1 and BRCA2 mRNA expression levels, respectively. Combined, this study demonstrates that breast tumors with low and high expression of ER, PR, HER2, AR and BRCA1/2 have differential transcript levels of KIF18A, pointing that KIF18A might contribute to the molecular differences between different breast cancer subtypes. | ||
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