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Charting host structural variations in cervical cancer by long-read sequencing pinpoints a functional deletion in PIAS1.

Created on 31 Aug 2026

Authors

Shijia Hao, Shuaibing Yang, Qianqian Zhao, Leiming Jiang, Li Zhou, Qingsong Qin, Jianzhen Xu

Published in

Genomics. Pages 111311. Aug 30, 2026. Epub Aug 30, 2026.

Abstract

Host structural variations (SVs) are critical in cancer development but their landscape and interaction with HPV integration in cervical carcinogenesis remain unclear. In this study, we performed Nanopore long-read sequencing on five HPV-positive cervical cancer tissues and two cell lines to profile host SVs. We identified thousands of SVs and statistically demonstrated their significant enrichment in genomic windows ±25 to ±50 kb from HPV integration sites. Cross-sample analysis revealed 60 shared SVs, including a recurrent deletion within the PIAS1 gene. Multi-omics integration (Hi-C, H3K27ac ChIP-seq, and TCGA data) showed that this deletion is associated with reduced PIAS1 expression, disruption of local topologically associating domains, advanced pathological tumor stage, and poorer overall survival. Functional assays confirmed that PIAS1 deficiency inhibits cervical cancer cell proliferation and migration. Our findings identify a PIAS1 deletion as a candidate driver event, and underscore the pivotal role of host genomic instability in HPV-associated oncogenesis.

PMID:
42669360
Bibliographic data and abstract were imported from PubMed on 31 Aug 2026.

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