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Updated: Sep 26, 2025

Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line
Published on: February 17, 2016
AC-265347 Inhibits Neuroblastoma Tumor Growth by Induction of Differentiation without Causing Hypocalcemia
Eliana Gonçalves-Alves1, Marta Garcia1,2, Carlos J Rodríguez-Hernández1,2
1Developmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Hospital Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.
Abstract:
Neuroblastoma is the most common extracranial solid tumor of childhood, with heterogeneous clinical manifestations ranging from spontaneous regression to aggressive metastatic disease. The calcium-sensing receptor (CaSR) is a G protein-coupled receptor (GPCR) that senses plasmatic fluctuation in the extracellular concentration of calcium and plays a key role in maintaining calcium homeostasis. We have previously reported that this receptor exhibits tumor suppressor properties in neuroblastoma. The activation of CaSR with cinacalcet, a positive allosteric modulator of CaSR, reduces neuroblastoma tumor growth by promoting differentiation, endoplasmic reticulum (ER) stress and apoptosis. However, cinacalcet treatment results in unmanageable hypocalcemia in patients. Based on the bias signaling shown by calcimimetics, we aimed to identify a new drug that might exert tumor-growth inhibition similar to cinacalcet, without affecting plasma calcium levels. We identified a structurally different calcimimetic, AC-265347, as a promising therapeutic agent for neuroblastoma, since it reduced tumor growth by induction of differentiation, without affecting plasma calcium levels. Microarray analysis suggested biased allosteric modulation of the CaSR signaling by AC-265347 and cinacalcet towards distinct intracellular pathways. No upregulation of genes involved in calcium signaling and ER stress were observed in patient-derived xenografts (PDX) models exposed to AC-265347. Moreover, the most significant upregulated biological pathways promoted by AC-265347 were linked to RHO GTPases signaling. AC-265347 upregulated cancer testis antigens (CTAs), providing new opportunities for CTA-based immunotherapies. Taken together, this study highlights the importance of the biased allosteric modulation when targeting GPCRs in cancer. More importantly, the capacity of AC-265347 to promote differentiation of malignant neuroblastoma cells provides new opportunities, alone or in combination with other drugs, to treat high-risk neuroblastoma patients.
Insights
A new drug, AC-265347, shows promise for treating neuroblastoma by promoting cancer cell differentiation without causing harmful hypocalcemia. This discovery offers new therapeutic avenues for high-risk neuroblastoma patients.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Neuroblastoma is a common childhood cancer with varied outcomes.
- The calcium-sensing receptor (CaSR) has shown tumor suppressor properties in neuroblastoma.
- Existing CaSR activator cinacalcet inhibits tumor growth but causes hypocalcemia.
Purpose of the Study:
- To identify a novel calcimimetic that inhibits neuroblastoma growth without causing hypocalcemia.
- To investigate the biased signaling of calcimimetics targeting the CaSR.
- To explore new therapeutic strategies for high-risk neuroblastoma.
Main Methods:
- Screening of structurally different calcimimetics.
- In vitro and in vivo testing of AC-265347 in neuroblastoma models.
- Microarray analysis to study CaSR signaling pathways and gene expression.
- Assessment of plasma calcium levels.
Main Results:
- AC-265347 demonstrated tumor growth inhibition by inducing differentiation, without affecting plasma calcium levels.
- AC-265347 and cinacalcet exhibited biased allosteric modulation of CaSR signaling.
- AC-265347 upregulated RHO GTPases signaling and cancer testis antigens (CTAs).
- No significant upregulation of calcium signaling or ER stress genes was observed with AC-265347.
Conclusions:
- AC-265347 is a promising therapeutic agent for neuroblastoma, inducing differentiation without hypocalcemia.
- Biased allosteric modulation of GPCRs is a viable strategy in cancer therapy.
- AC-265347 offers potential for novel immunotherapies targeting CTAs and combination treatments for high-risk neuroblastoma.
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