The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression.
In: ELife, Jg. 11 (2022-11-16)
Online
academicJournal
Zugriff:
Human prostate cancer can result from chromosomal rearrangements that lead to aberrant ETS gene expression. The mechanisms that lead to fusion-independent ETS factor upregulation and prostate oncogenesis remain relatively unknown. Here, we show that two neighboring transcription factors, Capicua ( CIC ) and ETS2 repressor factor ( ERF ), which are co-deleted in human prostate tumors can drive prostate oncogenesis. Concurrent CIC and ERF loss commonly occur through focal genomic deletions at chromosome 19q13.2. Mechanistically, CIC and ERF co-bind the proximal regulatory element and mutually repress the ETS transcription factor, ETV1 . Targeting ETV1 in CIC and ERF -deficient prostate cancer limits tumor growth. Thus, we have uncovered a fusion-independent mode of ETS transcriptional activation defined by concurrent loss of CIC and ERF .
Competing Interests: NG, HS, WW, RP, YL, JK, ES, FF, FH, RO No competing interests declared
(© 2022, Gupta et al.)
| Titel: |
The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression.
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| Autor/in / Beteiligte Person: | Gupta, N ; Song, H ; Wu, W ; Ponce, RK ; Lin, YK ; Kim, JW ; Small, EJ ; Feng, FY ; Huang, FW ; Okimoto, RA |
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| Zeitschrift: | ELife, Jg. 11 (2022-11-16) |
| Veröffentlichung: | Cambridge, UK : eLife Sciences Publications, Ltd., 2012-, 2022 |
| Medientyp: | academicJournal |
| ISSN: | 2050-084X (electronic) |
| DOI: | 10.7554/eLife.77072 |
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