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FX11 inhibits aerobic glycolysis and growth of neuroblastoma cells
Eric J Rellinger1, Brian T Craig1, Alexandra L Alvarez1
1Department of Pediatric Surgery, Vanderbilt University Medical Center, Nashville, TN.
Background:
The MYC family of proteins promotes neuroblastoma tumorigenesis at least in part through the induction of aerobic glycolysis by promoting the transcription of key glycolytic enzymes, such as LDHA. FX11 is a selective inhibitor of LDHA that has demonstrated preclinical efficacy in adult cancers. Herein, we hypothesized that FX11 would inhibit aerobic glycolysis and block growth of neuroblastoma cells.
Methods:
We surveyed 3 MYCN-single copy and 5 MYCN-amplified neuroblastoma cell lines to correlate C-MYC/N-MYC protein levels with LDHA expression. Cell viability was measured with FX11 using a tetrazolium-based assay. Cell cycle analysis using propidium iodide with flow cytometry was performed to evaluate for growth arrest. Immunoblotting demonstrated PARP and Caspase 3 cleavage as evidence of apoptosis.
Results:
LDHA is frequently expressed in both MYCN--amplified and MYCN-single copy cell lines. N-MYC and C-MYC protein levels did not correlate with LDHA protein expression. FX11 inhibits aerobic glycolysis and growth in three MYCN-amplified and one MYCN-single copy neuroblastoma cell lines. FX11 induces modest G1 cell cycle arrest with selective induction of apoptosis.
Conclusion:
Small molecule LDHA inhibition is capable of blocking aerobic glycolysis and growth of neuroblastoma cell lines in vitro and merits further in vivo evaluation of its preclinical efficacy in neuroblastomas.
Insights
FX11, an LDHA inhibitor, effectively reduces neuroblastoma cell growth and induces apoptosis. This study suggests FX11 warrants further investigation for neuroblastoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MYC proteins drive neuroblastoma by increasing aerobic glycolysis via enzymes like LDHA.
- FX11 is a known LDHA inhibitor with preclinical success in adult cancers.
Purpose of the Study:
- To investigate if FX11 inhibits aerobic glycolysis and neuroblastoma cell growth.
- To evaluate the correlation between MYC protein levels and LDHA expression in neuroblastoma cell lines.
Main Methods:
- Assessed LDHA expression in MYCN-amplified and single-copy neuroblastoma cell lines.
- Measured cell viability, cell cycle arrest, and apoptosis induction following FX11 treatment.
- Utilized tetrazolium-based assays, flow cytometry, and immunoblotting.
Main Results:
- LDHA was commonly expressed across neuroblastoma cell lines, independent of MYCN amplification status.
- FX11 demonstrated efficacy in inhibiting growth and aerobic glycolysis in multiple neuroblastoma cell lines.
- FX11 treatment led to G1 cell cycle arrest and induced apoptosis.
Conclusions:
- Targeting LDHA with small molecules like FX11 can inhibit neuroblastoma cell growth and aerobic glycolysis.
- FX11 shows preclinical promise for neuroblastoma treatment and warrants further in vivo studies.
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