Structural variation drives enhancer hijacking via 3D genome disruption in ccRCC

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Authors: Yu Dong, Wenjiao Xia, Zitong Yang, Liangliang Ren, Hongru Wang, Yiyang Zhou, Qinchen Li, Zhi Chen, Zhinan Xia, Yue Zheng, Feifan Wang, Ning He
+13 more Bing Cheng, Dongmei Ma, Wei Shao, Wei Guo, Shuwen Wang, Ziqiao Liu, Junxiao Shen, Yiming Qi, Xuke Gong, Juan Jin, Bo Xie, Guixin Zhu, Cheng Zhang
Cited by: 1
References: 87

Abstract

Clear cell renal cell carcinoma (ccRCC) is an aggressive malignancy associated with single-nucleotide variants in VHL, PBRM1, and SETD2. However, the role of structural variation (SV)-which have broader genomic impacts-and 3D genome architecture in ccRCC remains inadequately understood. Here, we reported a comprehensive molecular characterization. Through multi-omics analysis, we identify novel SV-associated oncogenic targets and reveal multidimensional 3D genome reorganization during ccRCC progression. We elucidate the dynamic interplay between SV and 3D chromatin architecture, demonstrating how structural rearrangements drive oncogenic dysregulation through 3D genome reorganization. Notably, an unrecognized pathogenic enhancer hijacking event is discovered and experimentally validated, leading to constitutive activation of the proto-oncogene SEMA5B. Furthermore, we developed a machine learning-based prognostic framework using enhancer hijacking signatures. Collectively, this work establishes a valuable resource for ccRCC research by elucidating how SVs and 3D genome reorganization collectively drive oncogenesis, and translates these findings into a clinically applicable prognostic tool.

Fields of Study & Subjects

Renal cell carcinoma treatment Microtubule and mitosis dynamics Cancer Genomics and Diagnostics

Publication details

Journal / source
npj Digital Medicine
Publisher
Springer Science and Business Media LLC
Volume
9
Issue
1
Pages
85–85
Publication date
6 January 2026
Language
EN