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BIRC5基因敲低通过调节PPARγ途径和铜死亡改善肝细胞癌进展。

BIRC5 knockdown ameliorates hepatocellular carcinoma progression via regulating PPARγ pathway and cuproptosis.

作者信息

Mai Yanxing, Ji Zhuocheng, Tan Yujing, Feng Lei, Qin Jiasheng

机构信息

Department of Geriatrics, Guangdong, Zhujiang Hospital of Southern Medical University, No. 253 Gongye Avenue, Guangzhou, 510282, China.

Second Department of Hepatobiliary Surgery, Guangdong, Zhujiang Hospital of Southern Medical University, No. 253 Gongye Avenue, Haizhu District, Guangzhou, 510282, China.

出版信息

Discov Oncol. 2024 Nov 25;15(1):706. doi: 10.1007/s12672-024-01592-y.

DOI:10.1007/s12672-024-01592-y
PMID:39585552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11589110/
Abstract

BACKGROUND

Hepatocellular carcinoma (HCC) with complex molecular carcinogenesis represents a kind of prevalent neoplasm occurring in the liver. The objective of this study is to illustrate the function of baculoviral inhibitor of apoptosis repeat containing 5 (BIRC5) and underlying action mechanisms in HCC progression.

METHODS

Comprehensive bioinformatics methods were conducted to screen differentially expressed genes (DEGs), cuproptosis-associated DEGs, and hub genes. The correlation between BIRC5 and immune cell infiltration, prognosis value was evaluated. The specific effects of BIRC5 silencing on HCC cells was validated by functional assays, and the impact on tumorigenicity and cuproptosis was also elucidated in vivo. Additionally, the effects of BIRC5 deficiency on PPAR pathway were determined using Oroxin A in vitro.

RESULTS

A total of 45 cuproptosis-associated DEGs and 9 hub genes were discovered through bioinformatics. Then 6 core genes were confirmed in Hep-3B and SK-Hep-1 cells with 4 genes upregulated and 2 genes downregulated. Therein, BIRC5 was positively correlated with the infiltration of CD8 T cells, macrophages, and highly expressed BIRC5 exhibited poor prognosis of overall survival in HCC. Furthermore, BIRC5 deletion inhibited the PPARγ pathway, thereby restraining the malignant phenotypes of HCC cells and tumorigenesis in vivo. Additionally, silencing of BIRC5 contributed to the initiation of cuproptosis in HCC.

CONCLUSIONS

BIRC5 silencing attenuated HCC through blocking PPARγ pathway and regulating cuproptosis, which may offer therapeutic implications against HCC.

摘要

背景

具有复杂分子致癌机制的肝细胞癌（HCC）是一种常见的肝脏肿瘤。本研究的目的是阐明含杆状病毒凋亡抑制重复序列5（BIRC5）在HCC进展中的作用及其潜在作用机制。

方法

采用综合生物信息学方法筛选差异表达基因（DEGs）、铜死亡相关DEGs和枢纽基因。评估BIRC5与免疫细胞浸润、预后价值之间的相关性。通过功能实验验证BIRC5沉默对HCC细胞的具体影响，并在体内阐明其对肿瘤发生和铜死亡的影响。此外，在体外使用奥洛辛A确定BIRC5缺乏对PPAR通路的影响。

结果

通过生物信息学共发现45个铜死亡相关DEGs和9个枢纽基因。然后在Hep-3B和SK-Hep-1细胞中确认了6个核心基因，其中4个基因上调，2个基因下调。其中，BIRC5与CD8 T细胞、巨噬细胞的浸润呈正相关，高表达的BIRC5在HCC患者的总生存预后较差。此外，BIRC5缺失抑制了PPARγ通路，从而抑制了HCC细胞的恶性表型和体内肿瘤发生。此外，BIRC5沉默促进了HCC中铜死亡的启动。

结论

BIRC5沉默通过阻断PPARγ通路和调节铜死亡来减轻HCC，这可能为HCC的治疗提供启示。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/4d4fd3ea460c/12672_2024_1592_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/0cdd0c6174e1/12672_2024_1592_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/e28912cfcbc0/12672_2024_1592_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/9241ee6c0960/12672_2024_1592_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/d2bad58d6aa0/12672_2024_1592_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/5a35b41a1567/12672_2024_1592_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/766739197893/12672_2024_1592_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/5f1c8a075b65/12672_2024_1592_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/4d4fd3ea460c/12672_2024_1592_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/0cdd0c6174e1/12672_2024_1592_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/e28912cfcbc0/12672_2024_1592_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/9241ee6c0960/12672_2024_1592_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/d2bad58d6aa0/12672_2024_1592_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/5a35b41a1567/12672_2024_1592_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/766739197893/12672_2024_1592_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/5f1c8a075b65/12672_2024_1592_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e85/11589110/4d4fd3ea460c/12672_2024_1592_Fig8_HTML.jpg

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