The Role of SAP30 in High-Risk Neuroblastoma

Neuroblastoma (NB) is a pediatric malignancy arising from neural-crest derived progenitor cells, with high-risk cases exhibiting poor survival and frequent relapse (Mahapatra, 2023; Vo, 2022). Increasing evidence points to autophagy as a stress-adaptive mechanism leveraged by cancer cells to support survival, particularly in response to chemotherapy (Pathania, 2025). However, the transcriptional regulation of autophagy in NB remains poorly understood. Sin3A Associated Protein 30 (SAP30) is a chromatin-associated transcriptional regulator previously implicated in tumor aggressiveness, but its functional role in NB has not been explored (Pathania, 2025; Zhang, 1998). In this study, we investigated the effects of SAP30 regulation in the MYCN-amplified NB19 cell line using lentiviral constructs for overexpression and shRNA-mediated knockdown. Western blot analysis confirmed successful SAP30 modulation at the protein level. Phase-contrast microscopy revealed that SAP30 knockdown cells exhibited visibly reduced confluency and altered morphology relative to control cells, suggesting impaired proliferation. In contrast, SAP30 overexpression resulted in elevated protein levels, supporting the functional integrity of the construct. All NB19 cultures were confirmed to be free of mycoplasma contamination. Together, these findings suggest that SAP30 may promote NB cell growth and support a proliferative phenotype, positioning it as a candidate oncogene in high-risk NB. While further studies are necessary to assess the impact of SAP30 on autophagy and downstream networks, these initial results highlight its potential as a therapeutic target. Future investigations will focus on delineating the molecular mechanisms by which SAP30 promotes tumor progression and whether SAP30 inhibition sensitizes NB cells to chemotherapeutic stress.