DUT (Deoxyuridine Triphosphatase)

Thus, CDADC1 underpins a previously unrecognized mechanism of intrinsic chemoresistance in cancer cells and has a nonredundant role in protecting from gemcitabine toxicity. CDADC1 reveals a clinically relevant metabolic pathway that might be exploited to enhance the efficacy of deoxycytidine analogs but calls for assessing CDADC1 status to avoid lethal toxicities.

These findings highlight the potential of using Ellen-ΔORF8-tet-off-scIL12 as a novel VZV-based oncolytic virotherapy.

Taken together, our data suggest that dUTPase could be a good target to eradicate liver CSCs resistant to 5-fluorouracil. β-HIVS is a small molecule that could decrease dUTPase expression and target EpCAM+ liver CSCs.

Acquired chemoresistance to proteasome inhibitors (PIs), such as bortezomib (BTZ), becomes an intractable obstacle in management of multiple myeloma (MM) in the clinic, but the underlying mechanisms are still not well elucidated...DUT inhibition partially attenuated mitochondrial modulation, instead favored an early impairment of mitochondrial integrity upon BTZ exposure so as to restrict MM progression and overcome drug resistance to BTZ treatment both in vitro and in vivo. In conclusion, we unveiled previously unrecognized effects of DUT on acquired drug resistance of MM, thus manipulating DUT may be efficacious for sensitizing MM cells to PIs.

The knockdown of PSMB6 and HSPA9 by siRNA significantly downregulated the proliferation of A549 and H358 cells. The proposed score model may function as a promising risk prediction tool for patients with lung adenocarcinoma and provide insights into the molecular regulation mechanism of lung adenocarcinoma.