Abstract

Cancer is a devastating disease condition and is the second most common etiology of death globally. After decades of research in the field of hematological malignancies and cellular therapeutics, we are still looking for therapeutic agents with the most efficacies and least toxicities. Curcumin is one of the cancer therapeutic agents that is derived from the Curcuma longa (turmeric) plant, and still in vitro and in vivo research is going on to find its beneficial effects on various cancers. Due to its potency to affect multiple targets of different cellular pathways, it is considered a promising agent to tackle various cancers alone or in combination with the existing chemotherapies. This review covers basic properties, mechanism of action, potential targets (molecules and cell-signaling pathways) of curcumin, as well as its effect on various solid and hematological malignancies.

Highlights

  • BackgroundCancer is a life-threatening disease and is one of the leading causes of death in developed countries

  • This review focuses on the clinical effects of curcumin and its role as a drug for breast cancer, lung cancer, prostate cancer, and hematological and other malignancies

  • They found that pre-treatment with LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, enhanced curcumin-induced autophagy and apoptosis by modifying B-cell lymphoma-2 (Bcl-2) expression and subsequent autophagosome formation in MCF-7 breast cancer cells [36]

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Summary

Introduction

Cancer is a life-threatening disease and is one of the leading causes of death in developed countries. The overexpression of Bcl-2 blocks curcumininduced autophagy through its inhibitory interaction with Beclin-1 in MCF-7 cells, which is a core component of the Beclin-1/PI3KC3 (phosphatidylinositol 3-kinase catalytic subunit type 3) complex involved in autophagosome nucleation They found that pre-treatment with LY294002, a PI3K inhibitor, enhanced curcumin-induced autophagy and apoptosis by modifying Bcl-2 expression and subsequent autophagosome formation in MCF-7 breast cancer cells [36]. Guo-Hua Zhu et al reported that curcumin significantly induces apoptosis and partially suppresses invasion in SHI-1 cells (acute monocytic leukemia cell line) in vitro Their results from polymerase chain reaction (PCR) and western blotting showed that curcumin increased the FasL mRNA level; inhibited Bcl-2, NF-κB, and ERK expression; and activated p38 MAPKs, JNKs, and caspase-3. Curcumin affects multiple other proteins and pathways, such as c-Jun/activator protein 1 (AP-1), cyclin D1, CDK-4, phosphatidylinositol 3-kinase (PI3K)/mechanistic target of rapamycin (mTOR)/E-twenty six proto-oncogene 2 (ETS2) pathway to reduce proliferation, cell growth in androgen-sensitive prostate cancer cell lines [7779].

Conclusions
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40. Khuder SA
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