mProX™ Human BCL2 Stable Cell Line

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

The BCL2 protein has been studied in various medical contexts. In acute myeloid leukemia (AML), the introduction of BCL2 inhibitor venetoclax, as well as other inhibitors such as midostaurin, gilteritinib, ivosidenib, and enasidenib, has improved therapeutic options. Ivosidenib, a selective IDH1R132 inhibitor, has shown effectiveness in inducing differentiation of AML blasts and has a favorable safety profile. It can be used as a standalone therapy or in combination with chemotherapy or other biological treatments. In mantle cell lymphoma (MCL), BCL2 is overexpressed due to t(11;14)(q13; q23) translocation, leading to cell proliferation. Diagnosis of MCL without cyclin D1 or CD5 expression can be challenging, but additional studies such as SOX11 and fluorescence in situ hybridization (FISH) can support the diagnosis. Tyrosine kinase inhibitors (TKIs) like dasatinib, sorafenib, and nilotinib, used in the treatment of leukemia and hepatocellular carcinoma, have been found to inhibit vascular smooth muscle cell (VSMC) proliferation and migration. These TKIs activate inflammatory and apoptotic pathways, as evidenced by up-regulation of inflammatory biomarkers and apoptotic markers, and down-regulation of the anti-apoptotic biomarker BCL-2. Human umbilical cord mesenchymal stem cell-derived microvesicles (hUCMSC-MVs) have shown potential in inducing apoptosis and autophagy in AML cells, suggesting their use as a novel cell-to-cell communication strategy for cancer therapy. Finally, in a study on dermal fibroblasts, a hypoxic microenvironment was found to promote fibroblast migration and proliferation through a BNIP3-autophagy pathway. Hypoxia-induced autophagy was shown to induce fibroblast migration and proliferation, which could be reversed by knocking down the autophagy-related gene ATG5. Overall, BCL2 has been implicated in various diseases and therapeutic strategies, including AML, MCL, VSMC proliferation, AML cell death pathways, and fibroblast migration and proliferation in a hypoxic microenvironment.