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RUNX3 调控的 GALNT6 通过调控 MUC1 的 O-糖基化促进肝癌细胞的迁移和侵袭。

RUNX3-Regulated GALNT6 Promotes the Migration and Invasion of Hepatocellular Carcinoma Cells by Mediating O-Glycosylation of MUC1.

机构信息

Department of Biliary-Pancreatic Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, China.

出版信息

Dis Markers. 2022 Jul 21;2022:2959846. doi: 10.1155/2022/2959846. eCollection 2022.

DOI:10.1155/2022/2959846
PMID:35909886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9334053/
Abstract

BACKGROUND

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Dysregulation of messenger RNAs (mRNA) has been recognized to be associated with HCC carcinogenesis and development. Polypeptide GalNAc Transferase 6 (GALNT6), an O-type glycosyltransferase, has been confirmed as tumor promoter in different cancers. However, the function of GALNT6 in HCC remains to be studied.

METHODS

RT-qPCR and western blot experiments were, respectively, performed for evaluating RNA expressions and protein levels. Supported by bioinformatics analysis, mechanism assays were conducted for validating the potential relation between different genes. Functional assays were implemented to analyze HCC cell migration and invasion after different transfections.

RESULTS

GALNT6 was aberrantly upregulated in HCC cells. Knockdown of GALNT6 could repress HCC cell migration and invasion. RUNX3 was verified to bind to GALNT6 promoter and activate GALNT6 transcription. GALNT6 depletion led to inhibited O-glycosylation and aggravated degradation of MUC1. MUC1 overexpression could rescue the impeded HCC cell migration and invasion induced by GALNT6 knockdown.

CONCLUSION

To sum up, GALNT6 transcriptionally activated by RUNX3 mediated the O-glycosylation of MUC1, thus exerting promoting influence on HCC cell migration and invasion.

摘要

背景

肝细胞癌（HCC）是全球癌症相关死亡的主要原因。信使 RNA（mRNA）的失调已被认为与 HCC 的发生和发展有关。多肽 N-乙酰氨基半乳糖转移酶 6（GALNT6），一种 O 型糖基转移酶，已被证实是不同癌症的肿瘤促进剂。然而，GALNT6 在 HCC 中的功能仍有待研究。

方法

分别通过 RT-qPCR 和 Western blot 实验评估 RNA 表达和蛋白水平。通过生物信息学分析支持，进行机制分析以验证不同基因之间的潜在关系。进行功能分析以分析不同转染后 HCC 细胞的迁移和侵袭。

结果

GALNT6 在 HCC 细胞中异常上调。GALNT6 的敲低可抑制 HCC 细胞的迁移和侵袭。RUNX3 被证实与 GALNT6 启动子结合并激活 GALNT6 转录。GALNT6 耗竭导致 O-糖基化抑制和 MUC1 降解加剧。MUC1 的过表达可以挽救 GALNT6 敲低引起的 HCC 细胞迁移和侵袭受阻。

结论

综上所述，RUNX3 转录激活的 GALNT6 介导了 MUC1 的 O-糖基化，从而对 HCC 细胞的迁移和侵袭发挥促进作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/355c98b6609b/DM2022-2959846.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/6d5036811275/DM2022-2959846.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/02da7a57db9c/DM2022-2959846.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/2280c65a419e/DM2022-2959846.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/355c98b6609b/DM2022-2959846.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/6d5036811275/DM2022-2959846.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/02da7a57db9c/DM2022-2959846.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/2280c65a419e/DM2022-2959846.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a8/9334053/355c98b6609b/DM2022-2959846.004.jpg

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