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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.6
- 수록면
- 293 - 298 (6page)
- DOI
- https://doi.org/10.5483/BMBRep.2023-0230
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초록· 키워드
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Microtubule acetylation has been shown to regulate actin filamentdynamics by modulating signaling pathways that controlactin organization, although the precise mechanisms remainunknown. In this study, we found that the downregulation ofmicrotubule acetylation via the disruption ATAT1 (which encodesα-tubulin N-acetyltransferase 1) inhibited the expressionof RhoA, a small GTPase involved in regulating the organizationof actin filaments and the formation of stress fibers. Analysisof RHOA promoter and chromatin immunoprecipitationassays revealed that C/EBPβ is a major regulator of RHOA expression.
Interestingly, the majority of C/EBPβ in ATAT1 knockout(KO) cells was found in the nucleus as a 27-kDa fragment(referred to as C/EBPβp27) lacking the N-terminus of C/EBPβ.
Overexpression of a gene encoding a C/EBPβp27-mimicking proteinvia an N-terminal deletion in C/EBPβ led to competitivebinding with wild-type C/EBPβ at the C/EBPβ binding site inthe RHOA promoter, resulting in a significant decrease of RHOAexpression. We also found that cathepsin L (CTSL), which isoverexpressed in ATAT1 KO cells, is responsible for C/EBPβp27formation in the nucleus. Treatment with a CTSL inhibitor ledto the restoration of RHOA expression by downregulation ofC/EBPβp27 and the invasive ability of ATAT1 KO MDA-MB-231breast cancer cells. Collectively, our findings suggest that thedownregulation of microtubule acetylation associated with ATAT1deficiency suppresses RHOA expression by forming C/EBPβp27in the nucleus through CTSL. We propose that CTSL and C/EBPβp27may represent a novel therapeutic target for breast cancertreatment.
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