Functional analysis indicates it may regulate key cancer pathways. Importantly, in vitro experiments confirm its tumor-promoting effects in breast cancer, providing a foundation for further study of BEND3's mechanisms and therapeutic implications.
BEND3 is highly expressed in HCC and strongly correlates with poor clinical outcomes. Functional and mechanistic analyses indicate that BEND3 enhances HCC progression by promoting proliferation, migration and invasion via EMT induction and PI3K/AKT/mTOR pathway activation.
Our results demonstrated that inhibiting the UPS using a selective UBA1 inhibitor, TAK-243, is an effective anti-cancer strategy for SCLC. We determined a distinct transcriptomic-stratified (YAP1low and BEND3high) population of SCLC that is sensitive to UBA1-inhibition therapy with TAK-243 as a single agent and a radiosensitizer.
Our results demonstrated that inhibiting the UPS using a selective UBA1 inhibitor, TAK-243, is an effective anti-cancer strategy for SCLC. We determined a distinct transcriptomic-stratified (YAP1 and BEND3) population of SCLC that is sensitive to UBA1-inhibition therapy with TAK-243 as a single agent and a radiosensitizer.