Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Mar 16;13(3):950.
doi: 10.3390/nu13030950.

Anticancer Mechanism of Curcumin on Human Glioblastoma

Affiliations
Review

Anticancer Mechanism of Curcumin on Human Glioblastoma

Shu Chyi Wong et al. Nutrients. .

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.

Keywords: anticancer; curcumin; glioblastoma; molecular signaling mechanism.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mode of curcumin actions as anti-cancer agent on the key molecular targets in GBM. Curcumin possesses anti-cancer properties by inhibiting signaling pathways and their downstream molecular targets; (a) retinoblastoma (RB) pathway; (b) p53 pathway; (c) JAK1,2/STAT3 pathway; (d) MAP kinase pathway; (e) P13K/Akt pathway; (f) Shh pathway; (g) NF-κB pathway. Molecular targets and signaling pathways that are upregulated and downregulated by curcumin are noted by using → and ┤, respectively.

Similar articles

Cited by

References

    1. Hanif F., Muzaffar K., Perveen K., Malhi S.M., Simjee S.U. Glioblastoma Multiforme: A Review of its Epidemiology and Pathogenesis through Clinical Presentation and Treatment. Asian Pac. J. Cancer Prev. 2017;18:3–9. - PMC - PubMed
    1. Ostrom Q.T., Cioffi G., Gittleman H., Patil N., Waite K., Kruchko C. CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2012–2016. Neuro Oncol. 2019;21:v1–v100. doi: 10.1093/neuonc/noz150. - DOI - PMC - PubMed
    1. Louis D.N., Perry A., Reifenberger G., Von Deimling A., Figarella-Branger D., Cavenee W.K. The 2016 World Health Organization Classification of Tumors of the Central Nervous System: A summary. Acta Neuropathol. 2016;131:803–820. doi: 10.1007/s00401-016-1545-1. - DOI - PubMed
    1. Fernandes C., Costa A., Osório L. Current Standards of Care in Glioblastoma Therapy. In: De Vleeschouwer S., editor. Glioblastoma [Internet] Codon Publications; Brisbane, AU, USA: Sep 27, 2017. [(accessed on 10 February 2021)]. Chapter 11. Available online: https://www.ncbi.nlm.nih.gov/books/NBK469987/ - DOI - PubMed
    1. Roy S., Lahiri D., Maji T., Biswas J. Recurrent Glioblastoma: Where we stand. South Asian J. Cancer. 2015;4:163–173. doi: 10.4103/2278-330X.175953. - DOI - PMC - PubMed

MeSH terms