{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sakamoto T"],"funding":["the Japan Society for the Promotion of Science"],"pagination":["71"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9862866"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["Chronic infection with Kaposi's sarcoma-associated herpes virus (KSHV) in B lymphocytes causes primary effusion lymphoma (PEL), the most aggressive form of KSHV-related cancer, which is resistant to conventional chemotherapy. In this study, we report that the BCBL-1 KSHV<sup>+</sup> PEL cell line does not harbor oncogenic mutations responsible for its aggressive malignancy. Assuming that KSHV viral oncogenes play crucial roles in PEL proliferation, we examined the effect of cyclin-dependent kinase 9 (CDK9) inhibitor FIT-039 on KSHV viral gene expression and KSHV<sup>+</sup> PEL proliferation. We found that FIT-039 treatment impaired the proliferation of KSHV<sup>+</sup> PEL cells and the expression of KSHV viral genes in vitro. The effects of FIT-039 treatment on PEL cells were further evaluated in the PEL xenograft model that retains a more physiological environment for the growth of PEL growth and KSHV propagation, and we confirmed that FIT-039 administration drastically inhibited PEL growth in vivo. Our current study indicates that FIT-039 is a potential new anticancer drug targeting KSHV for PEL patients."],"journal":["BMC cancer"],"pubmed_title":["Application of the CDK9 inhibitor FIT-039 for the treatment of KSHV-associated malignancy."],"pmcid":["PMC9862866"],"funding_grant_id":["15H05721"],"pubmed_authors":["Ueda K","Ajiro M","Hagiwara M","Watanabe A","Matsushima S","Sakamoto T"],"additional_accession":[]},"is_claimable":false,"name":"Application of the CDK9 inhibitor FIT-039 for the treatment of KSHV-associated malignancy.","description":"Chronic infection with Kaposi's sarcoma-associated herpes virus (KSHV) in B lymphocytes causes primary effusion lymphoma (PEL), the most aggressive form of KSHV-related cancer, which is resistant to conventional chemotherapy. In this study, we report that the BCBL-1 KSHV<sup>+</sup> PEL cell line does not harbor oncogenic mutations responsible for its aggressive malignancy. Assuming that KSHV viral oncogenes play crucial roles in PEL proliferation, we examined the effect of cyclin-dependent kinase 9 (CDK9) inhibitor FIT-039 on KSHV viral gene expression and KSHV<sup>+</sup> PEL proliferation. We found that FIT-039 treatment impaired the proliferation of KSHV<sup>+</sup> PEL cells and the expression of KSHV viral genes in vitro. The effects of FIT-039 treatment on PEL cells were further evaluated in the PEL xenograft model that retains a more physiological environment for the growth of PEL growth and KSHV propagation, and we confirmed that FIT-039 administration drastically inhibited PEL growth in vivo. Our current study indicates that FIT-039 is a potential new anticancer drug targeting KSHV for PEL patients.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-22T08:49:19.197Z","creation":"2024-11-19T19:09:17.735Z"},"accession":"S-EPMC9862866","cross_references":{"pubmed":["36670405"],"doi":["10.1186/s12885-023-10540-y"]}}