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Targeting the fatty acid binding proteins disrupts multiple myeloma cell cycle progression and MYC signaling
Mariah Farrell1,2,3, Heather Fairfield1,2,3, Michelle Karam1
1Center for Molecular Medicine, Maine Health Institute for Research, Scarborough, United States.
Abstract:
Multiple myeloma is an incurable plasma cell malignancy with only a 53% 5-year survival rate. There is a critical need to find new multiple myeloma vulnerabilities and therapeutic avenues. Herein, we identified and explored a novel multiple myeloma target: the fatty acid binding protein (FABP) family. In our work, myeloma cells were treated with FABP inhibitors (BMS3094013 and SBFI-26) and examined in vivo and in vitro for cell cycle state, proliferation, apoptosis, mitochondrial membrane potential, cellular metabolism (oxygen consumption rates and fatty acid oxidation), and DNA methylation properties. Myeloma cell responses to BMS309403, SBFI-26, or both, were also assessed with RNA sequencing (RNA-Seq) and proteomic analysis, and confirmed with western blotting and qRT-PCR. Myeloma cell dependency on FABPs was assessed using the Cancer Dependency Map (DepMap). Finally, MM patient datasets (CoMMpass and GEO) were mined for FABP expression correlations with clinical outcomes. We found that myeloma cells treated with FABPi or with FABP5 knockout (generated via CRISPR/Cas9 editing) exhibited diminished proliferation, increased apoptosis, and metabolic changes in vitro. FABPi had mixed results in vivo, in two pre-clinical MM mouse models, suggesting optimization of in vivo delivery, dosing, or type of FABP inhibitors will be needed before clinical applicability. FABPi negatively impacted mitochondrial respiration and reduced expression of MYC and other key signaling pathways in MM cells in vitro. Clinical data demonstrated worse overall and progression-free survival in patients with high FABP5 expression in tumor cells. Overall, this study establishes the FABP family as a potentially new target in multiple myeloma. In MM cells, FABPs have a multitude of actions and cellular roles that result in the support of myeloma progression. Further research into the FABP family in MM is warrented, especially into the effective translation of targeting these in vivo.
Insights
Fatty acid binding proteins (FABPs) are identified as a novel target for multiple myeloma (MM). Inhibiting FABPs reduces MM cell proliferation and survival, suggesting FABP-targeted therapies could offer new avenues for treating this incurable cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Multiple myeloma (MM) is an aggressive plasma cell cancer with poor prognosis.
- Current treatments face limitations, necessitating novel therapeutic targets.
- The fatty acid binding protein (FABP) family represents an unexplored area in MM biology.
Purpose of the Study:
- To investigate the FABP family as a potential therapeutic target in multiple myeloma.
- To evaluate the effects of FABP inhibition on MM cell behavior and metabolism.
- To correlate FABP expression with clinical outcomes in MM patients.
Main Methods:
- In vitro and in vivo studies using MM cell lines and pre-clinical mouse models.
- Treatment with FABP inhibitors (BMS3094013, SBFI-26) and CRISPR/Cas9 gene editing.
- Assessment of cell cycle, apoptosis, mitochondrial function, and cellular metabolism.
- RNA sequencing, proteomic analysis, western blotting, and qRT-PCR.
- Analysis of MM patient datasets (CoMMpass, GEO) for FABP expression and survival correlation.
Main Results:
- FABP inhibition and FABP5 knockout reduced MM cell proliferation and induced apoptosis in vitro.
- FABP inhibition altered cellular metabolism and mitochondrial respiration, downregulating MYC.
- In vivo studies showed mixed results, indicating a need for optimized delivery and dosing.
- High FABP5 expression in patient tumors correlated with worse overall and progression-free survival.
Conclusions:
- The FABP family plays a significant role in supporting multiple myeloma progression.
- Targeting FABPs presents a promising novel therapeutic strategy for MM.
- Further research is warranted to translate FABP inhibition into effective in vivo treatments for MM.
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