Voltage-gated sodium channels (VGSCs) play pivotal roles in cancer progression and have emerged as promising therapeutic targets and biomarkers. VGSCs comprise multiple subtypes with distinct tissue distributions, influencing tumour characteristics in different ways. Among these, the tetrodotoxin-sensitive α-subunits and the β1 subunit, commonly found in breast cancer, have been implicated in metastasis and tumour aggressiveness. The NaV1.5 channel and its neonatal variant (nNaV1.5) are overexpressed in aggressive cancers such as breast, prostate, colorectal, and lung cancers, thereby enhancing their invasive capacity. nNaV1.5 is particularly significant due to its tumour-specific expression and strong association with poor prognosis, especially in breast cancer, where it regulates cell proliferation, invasion, and tumour microenvironment remodelling. This review highlights nNaV1.5 as a critical ion channel that drives metastasis through ion regulation, extracellular acidification, and cytoskeletal remodelling. We further evaluate current therapeutic strategies, including siRNA, monoclonal antibodies, and small-molecule inhibitors, while addressing translational challenges such as tumour heterogeneity, drug delivery limitations, and off-target cardiotoxicity due to its similarity with the adult isoform. In addition, we explore the potential of nNaV1.5 as a biomarker subject to epigenetic regulations by factors including RE1-silencing transcription factor (REST) and histone deacetylase 2 (HDAC2), which may facilitate patient stratification and treatment optimization. By integrating mechanistic insights, therapeutic opportunities, and translational challenges, this review goes beyond descriptive summaries to provide a framework for advancing nNaV1.5 research from preclinical studies toward clinical application in cancer therapy.

Background: There has been increasing evidence showing that stingless bee honey exhibits anti-oxidant, anti-inflammatory and anti-cancer properties. Pharmacologically-active components in honey such as flavonoids and phenolic constituents are known to contribute to its medicinal benefits. To the best of our knowledge, this is the first study on evaluating anticancer effects of locally-produced Malaysian stingless bee honey from Heterotrigona itama sp. on malignant glioma cells. Methods: Proliferation and apoptosis studies of U-87 MG cells following stingless bee honey treatment were carried out using MTS assay and acridine orange/propidium iodide dual staining, respectively. Results: Results demonstrated time and dose-dependent cytotoxicity using 0.625%, 1.25% and 10% stingless bee honey (P < 0.05). IC50 values were calculated using cells treated with 10% stingless bee honey. It was also observed that 10% stingless bee honey induced nuclear shrinkage, chromatin condensation and nucleus fragmentation, indicating that cellular changes were consistent with the apoptotic characteristics of the cells. Conclusion: These data provide a good basis for further evaluation of the medicinal properties of stingless bee honey from Heterotrigona itama sp. This source of honey may serve as a potential therapy for malignant glioma.

We described an intracranial immature teratoma in a 13 year old Malay boy who presented with history of chronic headache and blurring of vision. Physical findings revealed bilateral papilloedema but no other localizing sign. A Magnetic Resonance Imaging of the brain revealed a suprasellar well defined lobulated midline heterogenous mass which was intraoperatively described as mainly solid tumour with multiple small cystic component filled with yellowish jelly like material. Histopathological finding confirmed the case as immature teratoma. Molecular genetic analysis of p53 and p27 genes revealed substitution of nucleotide G to C at location nucleotide 12139, exon 4 of gene p53. No alteration was detected at exon 5-6 and 8 of p53 gene and exon 1 and 2 of p27 gene. This is the first case report of an intracranial immature teratoma with genetic mutation occuring in a Malay boy.