Abstract
Glioblastoma (GBM) is the most malignant brain tumor and accounts for most adult brain tumors. Current available treatment options for GBM are multimodal, which include surgical resection, radiation, and chemotherapy. Despite the significant advances in diagnostic and therapeutic approaches, GBM remains largely resistant to treatment, with a poor median survival rate between 12 and 18 months. With increasing drug resistance, the introduction of phytochemicals into current GBM treatment has become a potential strategy to combat GBM. Phytochemicals possess multifarious bioactivities with multitarget sites and comparatively marginal toxicity. Among them, curcumin is the most studied compound described as a potential anticancer agent due to its multi-targeted signaling/molecular pathways properties. Curcumin possesses the ability to modulate the core pathways involved in GBM cell proliferation, apoptosis, cell cycle arrest, autophagy, paraptosis, oxidative stress, and tumor cell motility. This review discusses curcumin’s anticancer mechanism through modulation of Rb, p53, MAPK, P13K/Akt, JAK/STAT, Shh, and NF-κB pathways, which are commonly involved and dysregulated in preclinical and clinical GBM models. In addition, limitation issues such as bioavailability, pharmacokinetics perspectives strategies, and clinical trials were discussed.
Highlights
Brain tumors can be classified into grade I and II, grade III such as anaplastic astrocytoma, and grade IV such as glioblastoma (GBM) [1]
This study further reported that curcumin induces RANK expression through STAT3 suppression
This study revealed that inhibiting the expression of GLI1 proteins can elevate the nuclear p53 level in U87MG cells
Summary
Brain tumors can be classified into grade I and II (benign, low-grade), grade III (malignant, high-grade) such as anaplastic astrocytoma, and grade IV (highly aggressive and malignant) such as glioblastoma (GBM) [1]. In TMZ-resistant GBM tumors, numerous molecular pathways such as nuclear factor kappa light chain enhancer of activated B cells (NF-κB), p53, and JAK-STAT are found to be commonly dysregulated [8]. Curcumin can modulate multiple cellular signaling pathways and molecular targets involved in GBM tumor growth, migration, invasion, cell death, and proliferation [24,25,26,27]. A greater focus on curcumin’s anticancer potential in molecular signaling pathways that are commonly dysregulated in GBM is needed to provide a more comprehensive understanding of its therapeutic effects. This review includes the initial until recent pre-clinical and clinical studies of curcumin’s mechanisms of action in modulating several molecular pathways such as Rb, p53, MAPK, P13K/Akt, JAK/STAT, Shh, and NF-κB pathways. This review paper discusses curcumin’s related issues such as low bioavailability, pharmacokinetics, and the perspective strategies to overcome these issues
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