4196) and an anti-ACTB mouse monoclonal antibody (GenScript, A00702), respectively.... Reporting for specific materials, systems and methods Materials & experimental systems Methods n/a Involved in the study n/a Involved in the study Unique biological materials Antibodies Eukaryotic cell lines Palaeontology Animals and other organisms Human research participants ChIP-seq Flow cytometry MRI-based neuroimaging Antibodies Antibodies used LIN28B Antibody #4196 (Cell Signaling Technology, Cat #4196S, Lot #5) 1:1000 dilution Anti-ACTB Mouse Monoclonal Antibody (GenScript, Cat #A00702, Lot #15E000905) 1:5000 dilution of 0.
Transposable elements (TEs) are an abundant and rich genetic resource of regulatory sequences1-3. Cryptic regulatory elements within TEs can be epigenetically reactivated in cancer to influence oncogenesis in a process termed onco-exaptation4. However, the prevalence and impact of TE onco-exaptation events across cancer types are poorly characterized. Here, we analyzed 7,769 tumors and 625 normal datasets from 15 cancer types, identifying 129 TE cryptic promoter-activation events involving 106 oncogenes across 3,864 tumors. Furthermore, we interrogated the AluJb-LIN28B candidate: the genetic deletion of the TE eliminated oncogene expression, while dynamic DNA methylation modulated promoter activity, illustratin... More
Transposable elements (TEs) are an abundant and rich genetic resource of regulatory sequences1-3. Cryptic regulatory elements within TEs can be epigenetically reactivated in cancer to influence oncogenesis in a process termed onco-exaptation4. However, the prevalence and impact of TE onco-exaptation events across cancer types are poorly characterized. Here, we analyzed 7,769 tumors and 625 normal datasets from 15 cancer types, identifying 129 TE cryptic promoter-activation events involving 106 oncogenes across 3,864 tumors. Furthermore, we interrogated the AluJb-LIN28B candidate: the genetic deletion of the TE eliminated oncogene expression, while dynamic DNA methylation modulated promoter activity, illustrating the necessity and sufficiency of a TE for oncogene activation. Collectively, our results characterize the global profile of TE onco-exaptation and highlight this prevalent phenomenon as an important mechanism for promiscuous oncogene activation and ultimately tumorigenesis.