Knockout of SIN3B modulates transcriptional programs and cell survival in cutaneous melanoma.

Knockout of SIN3B modulates transcriptional programs and cell survival in cutaneous melanoma.

Publication date: May 18, 2025

SIN3 is a critical component of the histone deacetylase complex. Utilizing whole transcriptome data from melanoma patient samples we reveal that elevated levels of SIN3B are associated with poor survival outcomes with in vitro studies showing increased SIN3B expression in BRAF-mutant metastatic melanoma cell lines. The generation of isogenic SIN3B knockout cell lines indicated that SIN3B disruption led to a decrease in pathways associated with tumor invasion, migration, and cell-cell interactions. Moreover, pooled genome-wide CRISPR/Cas9 screens highlighted POLE4 and STK11 as crucial for the fitness and survival of SIN3B-knockout melanoma cells suggesting a role for these genes in epistasis with SIN3B. In summary, our findings suggest that SIN3B plays a pivotal role in modulating the behavior of melanoma cells, with implications for tumor growth and response to therapy.

Concepts Keywords
Genome CRISPR-Cas9
Pharmacol melanoma
Stk11 POLE4
Survival SIN3B
Tumor STK11

Semantics

Type Source Name
disease MESH melanoma
pathway KEGG Melanoma
disease MESH tumor

Original Article

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