STR-428
Cat.No.: CSC-C6653J
Species: Homo sapiens (Human)
Source: Ascites
Morphology: Lymphocyte-Like
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The STR-428 cell line is a human diffuse large B-cell lymphoma (DLBCL) cell line established from the ascitic tumor cells of a male patient with malignant effusion lymphoma. Unlike classical primary effusion lymphoma, STR-428 is negative for human herpesvirus-8 (HHV-8) and thus provides a novel model for study of HHV-8-independent lymphomatous effusions and aggressive B-cell malignancies. The cell line is lymphocyte-like in morphology and grows in suspension culture. It has been reported to have an approximate doubling time of 48 hours under standard culture conditions.
Immunophenotypic analysis has shown the expression of mature B-cell markers like CD19, CD20, CD22, CD10 and HLA-DR, but not of T-cell-associated markers. Cytogenetics showed complex abnormalities involving both the BCL2 and MYC oncogenes, including t(14;18)(q32;q21) translocation and additional MYC-associated rearrangements. These genetic alterations are related to aggressive behavior of lymphoma and therefore STR-428 may be a useful model to study the molecular mechanisms of B-cell lymphoma development and progression. The STR-428 has been used in studies of lymphoma biology, oncogenic signaling, regulation of apoptosis, and therapeutic response. This cell line has also been used in more recent studies to investigate the metabolic pathways involved in the survival and proliferation of lymphoma cells. As a well characterized model for B-cell lymphoma, STR-428 provides a relevant in vitro platform for research on lymphoma pathogenesis, discovery of biomarkers and evaluation of potential anti-cancer agents.
Bim Downregulation Mediates Resistance to Polatuzumab Vedotin in DLBCL Cell Models
Polatuzumab vedotin (Pola) has improved outcomes for diffuse large B-cell lymphoma (DLBCL) in both relapsed/refractory and frontline settings, yet management of post-Pola progression remains a clinical challenge. To evaluate retreatment feasibility, Kawasaki et al. developed two Pola-resistant DLBCL models-SU-DHL-4 and STR-428-via long-term exposure. STR-428-derived resistant clones (STR-428-Pola-R-5 and -9) exhibited 17.6- and 27.7-fold higher IC₅₀ values than parental cells (Fig. 1A).
Mechanistic analysis revealed that resistance was not due to loss of CD79b or upregulation of multidrug resistance protein MDR1 and was not associated with increased Bcl-xL expression (Fig. 1B). Instead, immunoblotting showed marked downregulation of the pro-apoptotic Bcl-2 family member Bim in both resistant clones, an effect also induced by short-term Pola exposure (Fig. 1B). Stable knockdown of Bim in parental STR-428 cells reduced Pola-induced caspase-3 cleavage (Fig. 1C) and significantly decreased sensitivity to Pola (Fig. 1D).
These findings identify Bim downregulation as a novel mechanism of Pola resistance in DLBCL, independent of target loss or drug efflux pumps. This suggests that strategies to restore Bim expression may overcome resistance and improve responses in patients progressing after Pola-based therapy.
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