Abstract
Cancer is a condition characterized by remarkably enhanced rates of cell proliferation paired with evasion of cell death. These deregulated cellular processes take place following genetic mutations leading to the activation of oncogenes, the loss of tumor suppressor genes, and the disruption of key signaling pathways that control and promote homeostasis. Plant extracts and plant-derived compounds have historically been utilized as medicinal remedies in different cultures due to their anti-inflammatory, antioxidant, and antimicrobial properties. Many chemotherapeutic agents used in the treatment of cancer are derived from plants, and the scientific interest in discovering plant-derived chemicals with anticancer potential continues today. Curcumin, a turmeric-derived polyphenol, has been reported to possess antiproliferative and proapoptotic properties. In the present review, we summarize all the in vitro and in vivo studies examining the effects of curcumin in prostate cancer.
Highlights
Prostate CancerCancer is a disease caused by genetic and environmental factors. It is characterized by the accumulation of DNA mutations that activate genes coding for proteins driving proliferation (proto-oncogenes) or inhibit genes that induce apoptosis and tumor suppression (tumor suppressor genes) [1]
The available in vitro studies have shown that curcumin is able to inhibit viability, proliferation, survival, migration/invasion, and adhesion of various human prostate cancer cells
The antiproliferative, antisurvival, and antimigratory effects of curcumin in prostate cancer cells may be due to the inhibition of the Akt/mechanistic target of rapamycin (mTOR), Ras/mitogen-activated protein kinase (MAPK) signaling pathways, decreased NF-κB activation, enhanced proapoptoptic caspase and PARP cleavage, and the inhibition of members of the antiapoptotic B-cell lymphoma-2 (Bcl-2) family of proteins (Figure 3)
Summary
Cancer is a disease caused by genetic and environmental factors. It is characterized by the accumulation of DNA mutations that activate genes coding for proteins driving proliferation (proto-oncogenes) or inhibit genes that induce apoptosis and tumor suppression (tumor suppressor genes) [1]. Alterations in cellular signaling mechanisms lead to the development of hallmark capabilities of cancer cells such as genome instability/mutation, enabling replicative immortality, dysregulating cellular energetics, uncontrolled proliferation, evasion of growth suppressors, resisting apoptosis, tumor-promoting inflammation, inducing angiogenesis, metastasis to different body tissues away from the tumor’s original location, and avoiding the immune system [2,3]. Surgery and radiation therapy are inefficient against metastasized tumors, hormone deprivation therapy is ineffective against androgen-insensitive/castrate-resistant cancers, and chemotherapy’s adverse effects may heavily impair a patient’s quality of life. Use of novel compounds that target the specific signaling cascades associated with enhanced survival and metastatic potential of prostate cancer will increase patient survival rate, while avoiding the detrimental effects associated with chemotherapy
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