HKBMM
Cat.No.: CSC-C6466J
Species: Homo sapiens (Human)
Source: Brain
Morphology: other
Culture Properties: Adherent cells
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Store in liquid nitrogen.
HKBMM is a human malignant meningioma cell line established from a high-grade meningioma, a tumor originating in the meninges, the protective membranes surrounding the brain and spinal cord. This cell line provides a valuable in vitro model to study the biology of aggressive meningiomas, which are characterized by rapid growth, invasiveness, and potential for recurrence.
HKBMM cells exhibit adherent growth with polygonal to spindle-shaped morphology typical of meningeal tumor cells. They express markers consistent with meningioma identity, including vimentin and EMA (epithelial membrane antigen), and retain key molecular features of high-grade meningiomas, making them suitable for mechanistic studies of tumor progression, cell proliferation, and migration.
This cell line is widely used in neuro-oncology research to investigate tumor biology, including signaling pathways, tumor-microenvironment interactions, and resistance mechanisms. HKBMM is also applied in preclinical studies for evaluating therapeutic strategies, such as chemotherapeutic agents, targeted treatments, and novel anti-tumor compounds. Its human origin and malignant phenotype make HKBMM a highly relevant tool for advancing our understanding of meningioma pathogenesis and supporting the development of improved therapies.
Dose-Dependent and ROS Mediated Anti-cancer Effects of Avenaciolide
Anti-cancer effects of avenaciolide, a water-insoluble natural product of Aspergillus avenaceus, was examined using human malignant meningioma cells (HKBMM) and normal dermal fibroblasts (HDFn). Avenaciolide had dose-dependent anti-cancer effects on HKBMM cells, showing significant effects at 160 µM or higher concentrations (Fig. 1). The cell death-inducing concentration of avenaciolide on HDFn cells was 200 µM or higher. Higher concentrations of avenaciolide caused less cell death in HDFn cells than in HKBMM cells, suggesting the possibility that avenaciolide might be a targeted anti-cancer drug.
Katsuzawa et al. then examined the mechanism of avenaciolide-induced cell death. Pretreatment with 5 mM NAC significantly reduced avenaciolide-induced cell death in HKBMM cells (Fig. 2). ROS production by avenaciolide was visualized using CellROX green, showing strong fluorescence after 1-1.5 hours of exposure to 200 µM avenaciolide (Fig. 3). NAC pretreatment significantly suppressed ROS production. These findings suggest that avenaciolide induces ROS production and subsequent cell death in HKBMM cells.
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