mProX™ Human BCL2 Stable Cell Line

Product Information

Target Family

Immune Checkpoint

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;H1975

Target Classification

Immune Checkpoint Cell Lines

Target Research Area

Cancer Research

Related Diseases

Follicular Lymphoma; High-Grade B-Cell Lymphoma Double-Hit/Triple-Hit

Gene ID

Human:596

UniProt ID

Human:P10415

Product Properties

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.

Protocols

Please visit our protocols page.

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FAQ

chat Skyler Garcia (Verified Customer)

How does BCL2 influence cancer cell survival? Aug 25 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

BCL2 is known for its role in regulating cell death by inhibiting apoptosis, thus contributing to cancer cell survival and resistance to therapy. Aug 25 2022

chat Peyton Davis (Verified Customer)

What is the role of BCL2 in mitochondrial function? May 10 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

BCL2 plays a crucial role in maintaining mitochondrial integrity and preventing the release of apoptotic factors, thus regulating the intrinsic pathway of apoptosis. May 10 2021

Published Data

Fig.1 Cell proliferation inhibition and sensitization of the H1975 cell line to g*fitin*b are achieved through the application of Bcl-2 siRNA.

In the upper panel, incubation with 50 nM of Bcl-2 siRNA, negative siRNA, or transfect reagent was carried out for 48 hours, and the cell proliferation inhibition rate was determined using the MTT assay. Significant differences were observed (*p<0.05) when compared to the negative siRNA group, and (#p<0.05) when compared to the mock group. In the lower panel, incubation with various doses of g*fitin*b for 24 hours followed transfection with Bcl-2 siRNA or not. Significant differences (*p<0.05) were noted when compared to the negative siRNA with gefitinib group, and (#p<0.05) when compared to the g*fitin*b only group.

Ref: Zou, Man, et al. "Knockdown of the Bcl-2 gene increases sensitivity to EGFR tyrosine kinase inhibitors in the H1975 lung cancer cell line harboring T790M mutation." International journal of oncology 42.6 (2013): 2094-2102.

Pubmed: 23588221

DOI: 10.3892/ijo.2013.1895

Research Highlights

T Hill, Brian. et al. "Response-Adapted, Time-Limited Venetoclax, Umbralisib and Ublituximab for Relapsed/Refractory Chronic Lymphocytic Leukemia." Blood advances, 2023.
The study aimed to explore response-adapted, time-limited therapy for patients with chronic lymphocytic leukemia (CLL) and treatment resistance to Bruton's tyrosine kinase (BTK) inhibitors. This phase 1/2 clinical trial assessed the safety and efficacy of the combination of venetoclax, umbralisib, and ublituximab (U2-VeN) in 46 patients with relapsed/refractory CLL and 5 patients with Richter's transformation (RT). Patients who achieved undetectable minimal residual disease (uMRD) after 12 cycles of treatment had it stopped. Adverse events included diarrhea and elevated liver enzymes, but no cases of tumor lysis syndrome were reported. The overall response rate for CLL was 98%, with 38% of patients achieving complete responses. 77% of patients achieved uMRD at 10-4 in bone marrow, even among those who were refractory to prior BTK inhibitors. This study demonstrates that time-limited venetoclax and U2 is a safe and highly effective combination therapy for relapsed/refractory CLL, including those previously treated with BTK inhibitors.
T Hill, Brian. et al. "Response-Adapted, Time-Limited Venetoclax, Umbralisib and Ublituximab for Relapsed/Refractory Chronic Lymphocytic Leukemia." Blood advances, 2023.
Pubmed: 37871300 DOI: 10.1182/bloodadvances.2023010693

Chen, Lizhi. et al. "Anti-cancer targets and molecular mechanisms of formononetin in treating osteosarcoma based on network pharmacology." Aging, 2023.
Osteosarcoma (OS) is a prevalent form of bone cancer that mainly affects children and adolescents. Formononetin is a compound with various pharmacological effects, including anti-tumor, anti-obesity, anti-inflammatory, and neuroprotective properties. Despite limited research, the use of formononetin in OS treatment has shown promising results, yet its mechanism of action remains unclear. To shed light on this, the current study used network pharmacology to investigate the potential mechanism of formononetin in OS treatment. Human OS cell line MG63 was treated with varying concentrations of formononetin and subsequent experiments showed significant inhibition of cell proliferation and migration. Western blotting revealed increased expression of pro-apoptotic proteins, caspase-3, p53, and p21, and decreased anti-apoptotic protein, bcl-2, in a concentration-dependent manner. Furthermore, formononetin was found to suppress the expression of SATB2, suggesting its potential role as a biomarker for OS and a therapeutic target for formononetin. These findings suggest that formononetin may be a potential candidate for OS treatment.
Chen, Lizhi. et al. "Anti-cancer targets and molecular mechanisms of formononetin in treating osteosarcoma based on network pharmacology." Aging, 2023.
Pubmed: 37870753 DOI: 10.18632/aging.205139