Figure 4 from Selective Depletion of Cancer Cells with Extrachromosomal DNA via Lentiviral Infection

figure

posted on 2025-08-28, 10:20 authored by Eunhee Yi, Amit D. Gujar, Dacheng Zhao, Kentaro Suina, Xue Jin, Katharina Pardon, Qinghao Yu, Larisa Kagermazova, Emmanuel E. Korsah, Noah A. Dusseau, Jef D. Boeke, Anton G. Henssen, Roel G.W. Verhaak

ecDNA reintegration does not cause the depletion of the ecDNA+ population. A, Relative quantification of MYC copy was tested by qPCR in parental, ecDNA+, HSR+, and lentivirally transduced PC3 cell lines (t test, **, P < 0.01; ns = 4). B, Copy-number variation (CNV) analysis results show a comparable copy-number ratio (CR) around the MYC amplification region between parental and transduced PC3 cells. C, CNV analysis results show a comparable CR around the DHFR amplification region between parental and transduced HeLa-MTX-Res cells. D, AmpliconArchitect results show a high similarity in the MYC amplicon structure between parental and transduced PC3 cells. *The closer it is to 1 in the range of 0–1, the more similar the structure is. E, AmpliconArchitect results show a high similarity in the DHFR amplicon structure between parental and transduced HeLa-MTX-Res cells. *The closer it is to 1 in the range of 0–1, the more similar the structure is.

Funding

Elsa U. Pardee Foundation (EUPF)

National Cancer Institute (NCI)

United States Department of Health and Human Services

Find out more...

Cancer Research UK (CRUK)

National Institutes of Health (NIH)

Deutsche Krebshilfe (German Cancer Aid)

European Research Council (ERC)

History

Related Materials

1.
DOI - Is supplement to Selective Depletion of Cancer Cells with Extrachromosomal DNA via Lentiviral Infection

ARTICLE ABSTRACT

Extrachromosomal DNA (ecDNA), a major focal oncogene amplification mode found across cancer, has recently regained attention as an emerging cancer hallmark, with a pervasive presence across cancers. With technical advancements such as high-coverage sequencing and live-cell genome imaging, we can now investigate the behaviors and functions of ecDNA. However, we still lack an understanding of how to eliminate ecDNA. We observed depletion of cells containing ecDNA during lentiviral but not transposon-based transduction, whereas we sought to investigate the mechanism of ecDNA behavior. This discovery may provide critical information on utilizing a lentiviral system in emerging ecDNA research. Additionally, this observation suggests specific sensitivities for cells with ecDNA. ecDNA is an essential factor in cancer progression. We found that a group of cancer cells with ecDNA is selectively depleted after lentiviral infection. This finding provides promise for ecDNA-specific targeting, suggests the need for caution in using lentivirus, and offers alternative ways to study ecDNA.