BACKGROUND: Myeloid cell leukemia-1 (MCL-1)-an anti-apoptotic protein of the B-cell lymphoma 2 family-is commonly overexpressed in human cancers, promoting tumorigenesis and chemoresistance. Upregulated MCL-1 in human hepatocellular carcinoma (HCC) has been demonstrated in numerous studies, and therapeutic agents targeting this protein have been assessed. However, its prognostic significance in canine HCC remains unclear. The objective of this study was to detect MCL-1 protein in canine normal liver tissue and compare its expression level with that in HCC tissue using western blotting. Immunohistochemistry (IHC) was used to quantify MCL-1 intensity levels in normal, non-neoplastic hepatic diseases, and HCC tissues, and the differences were assessed. Additionally, the relevance of MCL-1 immunostaining to various clinical and pathological parameters was evaluated. RESULTS: MCL-1 expression was markedly elevated in HCC tissues relative to normal liver tissues (Pâ=â0.029). Additionally, all 10 normal liver tissues exhibited low IHC expression, which significantly increased as the malignancy progressed (Pâ<â0.001). In the HCC samples, high MCL-1 immunostaining was substantially correlated with metastatic status (Pâ=â0.034) and tumor size (Pâ=â0.046). Moreover, survival curve analysis revealed a significant relationship between upregulated MCL-1 and lower disease-free survival and overall survival rate (Pâ=â0.006 and Pâ=â0.031, respectively). CONCLUSION: MCL-1 expression is increased in canine HCC, and its overexpression significantly correlates to worse clinical outcomes. Therefore, MCL-1 is considered to be a promising prognostic marker.
Overexpression of MCL-1 in canine hepatocellular carcinoma and its efficacy as a prognostic marker.
犬肝细胞癌中 MCL-1 的过度表达及其作为预后标志物的有效性
阅读:10
作者:Baek Jehun, Cho Jaeho, Shin Hun-Kyeong, Kim Wan Hee
| 期刊: | BMC Veterinary Research | 影响因子: | 2.600 |
| 时间: | 2025 | 起止号: | 2025 May 16; 21(1):349 |
| doi: | 10.1186/s12917-025-04798-6 | 种属: | Canine |
| 研究方向: | 细胞生物学 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
