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Cancer Chemoprevention

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A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (10 February 2017) | Viewed by 123472

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Prof. Dr. Santosh K. Katiyar

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Guest Editor

Departments of Dermatology and Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: causes, mechanisms and chemoprevention of cancers; immunology/photoimmunology; inflammatory mediators; oxidative stress; DNA damage and DNA repair mechanisms; epigenetic regulators; cell cycle check points; apoptosis; use of genetically modified animal models as well as tumor models

Special Issue Information

Dear Colleagues,

Cancer is a leading cause of death world-wide. Treatment of cancer is more difficult if cancer cells are metastasized to distant parts of the body. Current available treatment options are not sufficient to save lives, therefore alternative innovative strategies are required to prevent or treat the disease. Chemoprevention of cancer seems to be the best strategy or approach to protect from this disease and increase the span of healthy life in human beings. The approach may include regular intake of phytochemicals, dietary or non-dietary, which are non-toxic in nature but have potent anti-carcinogenic properties.

Prof. Dr. Santosh K. Katiyar
Guest Editor

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Keywords

cancer chemoprevention
phytochemicals or synthetic anti-cancer agents
epigenetic regulators
microRNA
DNA damage/repair
immunology
T cell subsets
cell cycle regulators
inflammatory mediators
oxidative stress
cell cycle check points
apoptosis
angiogenesis

Published Papers (13 papers)

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Research

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2211 KiB

Open AccessArticle

Docosahexaenoic Acid Induces Expression of Heme Oxygenase-1 and NAD(P)H:quinone Oxidoreductase through Activation of Nrf2 in Human Mammary Epithelial Cells

by Hye-Yoon Bang, Sin-Aye Park, Soma Saeidi, Hye-Kyung Na and Young-Joon Surh

Molecules 2017, 22(6), 969; https://doi.org/10.3390/molecules22060969 - 10 Jun 2017

Cited by 28 | Viewed by 6347

Abstract

Docosahexaenoic acid (DHA), an ω-3 fatty acid abundant in fish oils, has diverse health beneficial effects, such as anti-oxidative, anti-inflammatory, neuroprotective, and chemopreventive activities. In this study, we found that DHA induced expression of two representative antioxidant/cytoprotective enzymes, heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase (NQO1), in human mammary epithealial (MCF-10A) cells. DHA-induced upregulation of these enzymes was accompanied by enhanced translocation of the redox-sensitive transcription factor Nrf2 into the nucleus and its binding to antioxidant response element. Nrf2 gene silencing by siRNA abolished the DHA-induced expression of HO-1 and NQO1 proteins. When MCF-10A cells were transfected with mutant constructs in which the cysteine 151 or 288 residue of Keap1 was replaced by serine, DHA-induced expression of HO-1 and NQO1 was markedly reduced. Moreover, DHA activated protein kinase C (PKC)δ and induced Nrf2 phosphorylation. DHA-induced phosphorylation of Nrf2 was abrogated by the pharmacological PKCδ inhibitor rottlerin or siRNA knockdown of its gene expression. The antioxidants N-acetyl-l-cysteine and Trolox attenuated DHA-induced activation of PKCδ, phosphorylation of Nrf2, and and its target protein expression. In conclusion, DHA activates Nrf2, possibly through modification of critical Keap1 cysteine 288 residue and PKCδ-mediated phosphorylation of Nrf2, leading to upregulation of HO-1 and NQO1 expression. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessArticle

Daucosterol Inhibits the Proliferation, Migration, and Invasion of Hepatocellular Carcinoma Cells via Wnt/β-Catenin Signaling

by Junquan Zeng, Xing Liu, Xiaofei Li, Yongliang Zheng, Bin Liu and Youzhang Xiao

Molecules 2017, 22(6), 862; https://doi.org/10.3390/molecules22060862 - 02 Jun 2017

Cited by 33 | Viewed by 5980

Abstract

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. The purpose of this study was to determine the effects of daucosterol on HCC by investigating Wnt/β-catenin signaling. In this study, HepG2 and SMMC-7721 cells were treated with varying concentrations of daucosterol, and the corresponding inhibitory effects on HCC cells were examined via CCK-8 assays. Cell migration and invasion abilities were detected via transwell assays. β-Catenin and phospho (p)-β-catenin levels were analyzed via western blotting. Our results showed that daucosterol reduced the proliferation, migration, and invasion capacities of HCC cells in a concentration-dependent manner. In addition, daucosterol reduced the levels of β-catenin and p-β-catenin in HepG2 and SMMC-7721 cells. Furthermore, the Wnt signaling pathway inhibitor SB-216763 was used to treat HepG2 and SMMC-7721 cells with daucosterol. Our results showed that co-treatment with daucosterol and SB-216763 abolished the effects of daucosterol on cell inhibition ratios, cell migration, and cell invasion. These findings indicated that daucosterol inhibited cell migration and invasion in HCC cells via the Wnt/β-catenin signaling pathway. Therefore, our study highlights the use of daucosterol as a promising therapeutic strategy for HCC treatment. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessArticle

Absorption, Metabolic Stability, and Pharmacokinetics of Ginger Phytochemicals

by Rao Mukkavilli, Chunhua Yang, Reenu Singh Tanwar, Ahmed Ghareeb, Latika Luthra and Ritu Aneja

Molecules 2017, 22(4), 553; https://doi.org/10.3390/molecules22040553 - 30 Mar 2017

Cited by 43 | Viewed by 8962

Abstract

We have previously demonstrated promising anticancer efficacy of orally-fed whole ginger extract (GE) in preclinical prostate models emphasizing the importance of preservation of the natural “milieu”. Essentially, GE primarily includes active ginger phenolics viz., 6-gingerol (6G), 8-gingerol (8G), 10-gingerol (10G), and 6-shogaol (6S). However, the druglikeness properties of active GE phenolics like solubility, stability, and metabolic characteristics are poorly understood. Herein, we determined the physicochemical and biochemical properties of GE phenolics by conducting in vitro assays and mouse pharmacokinetic studies with and without co-administration of ketoconazole (KTZ). GE phenolics showed low to moderate solubility in various pH buffers but were stable in simulated gastric and intestinal fluids, indicating their suitability for oral administration. All GE phenolics were metabolically unstable and showed high intrinsic clearance in mouse, rat, dog, and human liver microsomes. Upon oral administration of 250 mg/kg GE, sub-therapeutic concentrations of GE phenolics were observed. Treatment of plasma samples with β-glucuronidase (βgd) increased the exposure of all GE phenolics by 10 to 700-fold. Co-administration of KTZ with GE increased the exposure of free GE phenolics by 3 to 60-fold. Interestingly, when the same samples were treated with βgd, the exposure of GE phenolics increased by 11 to 60-fold, suggesting inhibition of phase I metabolism by KTZ but little effect on glucuronide conjugation. Correlating the in vitro and in vivo results, it is reasonable to conclude that phase II metabolism seems to be the predominant clearance pathway for GE phenolics. We present evidence that the first-pass metabolism, particularly glucuronide conjugation of GE phenolics, underlies low systemic exposure. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessArticle

Induction of G2M Arrest by Flavokawain A, a Kava Chalcone, Increases the Responsiveness of HER2-Overexpressing Breast Cancer Cells to Herceptin

by Danielle D. Jandial, Lauren S. Krill, Lixia Chen, Chunli Wu, Yu Ke, Jun Xie, Bang H. Hoang and Xiaolin Zi

Molecules 2017, 22(3), 462; https://doi.org/10.3390/molecules22030462 - 14 Mar 2017

Cited by 44 | Viewed by 6825

Abstract

HER2/neu positive breast tumors predict a high mortality and comprise 25%–30% of breast cancer. We have shown that Flavokawain A (FKA) preferentially reduces the viabilities of HER2-overexpressing breast cancer cell lines (i.e., SKBR3 and MCF7/HER2) versus those with less HER2 expression (i.e., MCF7 and MDA-MB-468). FKA at cytotoxic concentrations to breast cancer cell lines also has a minimal effect on the growth of non-malignant breast epithelial MCF10A cells. FKA induces G2M arrest in cell cycle progression of HER2-overexpressing breast cancer cell lines through inhibition of Cdc2 and Cdc25C phosphorylation and downregulation of expression of Myt1 and Wee1 leading to increased Cdc2 kinase activities. In addition, FKA induces apoptosis in SKBR3 cells by increasing the protein expression of Bim and BAX and decreasing expression of Bcl₂, Bcl_X/L, XIAP, and survivin. FKA also downregulates the protein expression of HER-2 and inhibits AKT phosphorylation. Herceptin plus FKA treatment leads to an enhanced growth inhibitory effect on HER-2 overexpressing breast cancer cell lines through downregulation of Myt1, Wee1, Skp2, survivin, and XIAP. Our results suggest FKA as a promising and novel apoptosis inducer and G2 blocking agent that, in combination with Herceptin, enhances for the treatment of HER2-overexpressing breast cancer. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessArticle

Betulinic Acid-Mediated Apoptosis in Human Prostate Cancer Cells Involves p53 and Nuclear Factor-Kappa B (NF-κB) Pathways

by Eswar Shankar, Ailin Zhang, Daniel Franco and Sanjay Gupta

Molecules 2017, 22(2), 264; https://doi.org/10.3390/molecules22020264 - 10 Feb 2017

Cited by 54 | Viewed by 6675

Abstract

Defects in p53 and nuclear factor-kappa B (NF-κB) signaling pathways are frequently observed in the initiation and development of various human malignancies, including prostate cancer. Clinical studies demonstrate higher expression of NF-κB/p65/RelA, NF-κB/p50/RelB, and cRel as well as downregulation of the p53 network in primary prostate cancer specimens and in metastatic tumors. Betulinic acid (BA), is a triterpenoid that has been reported to be an effective inducer of apoptosis through modification of several signaling pathways. Our objective was to investigate the pathways involved in BA-induced apoptosis in human prostate cancer cells. We employed the androgen-responsive LNCaP cells harboring wild-type p53, and androgen-refractory DU145 cells possessing mutated p53 with high constitutive NF-κB activity. Inhibition of cell survival by BA at 10 and 20 µM concentrations occurred as a result of alteration in Bax/Bcl-2 ratio in both cell lines that led to an increased cytochrome C release, caspase activation and poly(ADP)ribose polymerase (PARP) cleavage, leading to apoptosis. BA treatment resulted in stabilization of p53 through increase in phosphorylation at Ser15 in LNCaP cells, but not in DU145 cells, and induction of cyclin kinase inhibitor p21/Waf1 in both cell types. Furthermore, treatment of both prostate cancer cells with BA decreased the phosphorylation of IκB kinase (IKK)α and I-kappa-B-alpha (IκBα) inhibiting the nuclear location of NF-κB/p65 causing cytosolic accumulation and resulting in its decreased nuclear binding. We demonstrate that BA may induce apoptosis by stabilizing p53 and downregulating NF-κB pathway in human prostate cancer cells, irrespective of the androgen association, and therefore can potentially be developed as a molecule of interest in cancer chemoprevention. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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1438 KiB

Open AccessArticle

Arsenic Induces p62 Expression to Form a Positive Feedback Loop with Nrf2 in Human Epidermal Keratinocytes: Implications for Preventing Arsenic-Induced Skin Cancer

by Palak Shah, Elaine Trinh, Lei Qiang, Lishi Xie, Wen-Yang Hu, Gail S. Prins, Jingbo Pi and Yu-Ying He

Molecules 2017, 22(2), 194; https://doi.org/10.3390/molecules22020194 - 24 Jan 2017

Cited by 34 | Viewed by 7310

Abstract

Exposure to inorganic arsenic in contaminated drinking water poses an environmental public health threat for hundreds of millions of people in the US and around the world. Arsenic is a known carcinogen for skin cancer. However, the mechanism by which arsenic induces skin cancer remains poorly understood. Here, we have shown that arsenic induces p62 expression in an autophagy-independent manner in human HaCaT keratinocytes. In mouse skin, chronic arsenic exposure through drinking water increases p62 protein levels in the epidermis. Nrf2 is required for basal and arsenic-induced p62 up-regulation. p62 knockdown reduces arsenic-induced Nrf2 activity, and induces sustained p21 up-regulation. p62 induction is associated with increased proliferation in mouse epidermis. p62 knockdown had little effect on arsenic-induced apoptosis, while it decreased cell proliferation following arsenic treatment. Our findings indicate that arsenic induces p62 expression to regulate the Nrf2 pathway in human keratinocytes and suggest that targeting p62 may help prevent arsenic-induced skin cancer. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessArticle

Design, Synthesis and Evaluation of Indene Derivatives as Retinoic Acid Receptor α Agonists

by Xianghong Guan, Peihua Luo, Qiaojun He, Yongzhou Hu and Huazhou Ying

Molecules 2017, 22(1), 32; https://doi.org/10.3390/molecules22010032 - 27 Dec 2016

Cited by 6 | Viewed by 7321

Abstract

A series of novel indene-derived retinoic acid receptor α (RARα) agonists have been designed and synthesized. The use of receptor binding, cell proliferation and cell differentiation assays demonstrated that most of these compounds exhibited moderate RARα binding activity and potent antiproliferative activity. In particular, 4-((3-isopropoxy-2,3-dihydro-1H-inden-5-yl)-carbamoyl)benzoic acid (36d), which showed a moderate binding affinity, exhibited a great potential to induce the differentiation of NB4 cells (68.88% at 5 μM). Importantly, our work established indene as a promising skeleton for the development of novel RARα agonists. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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5641 KiB

Open AccessArticle

Cryptolepine, a Plant Alkaloid, Inhibits the Growth of Non-Melanoma Skin Cancer Cells through Inhibition of Topoisomerase and Induction of DNA Damage

by Harish C. Pal and Santosh K. Katiyar

Molecules 2016, 21(12), 1758; https://doi.org/10.3390/molecules21121758 - 21 Dec 2016

Cited by 42 | Viewed by 6688

Abstract

Topoisomerases have been shown to have roles in cancer progression. Here, we have examined the effect of cryptolepine, a plant alkaloid, on the growth of human non-melanoma skin cancer cells (NMSCC) and underlying mechanism of action. For this purpose SCC-13 and A431 cell lines were used as an in vitro model. Our study reveals that SCC-13 and A431 cells express higher levels as well as activity of topoisomerase (Topo I and Topo II) compared with normal human epidermal keratinocytes. Treatment of NMSCC with cryptolepine (2.5, 5.0 and 7.5 µM) for 24 h resulted in marked decrease in topoisomerase activity, which was associated with substantial DNA damage as detected by the comet assay. Cryptolepine induced DNA damage resulted in: (i) an increase in the phosphorylation of ATM/ATR, BRCA1, Chk1/Chk2 and γH2AX; (ii) activation of p53 signaling cascade, including enhanced protein expressions of p16 and p21; (iii) downregulation of cyclin-dependent kinases, cyclin D1, cyclin A, cyclin E and proteins involved in cell division (e.g., Cdc25a and Cdc25b) leading to cell cycle arrest at S-phase; and (iv) mitochondrial membrane potential was disrupted and cytochrome c released. These changes in NMSCC by cryptolepine resulted in significant reduction in cell viability, colony formation and increase in apoptotic cell death. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Review

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1107 KiB

Open AccessReview

Oleuropein and Cancer Chemoprevention: The Link is Hot

by Ammad Ahmad Farooqi, Sundas Fayyaz, Ana Sanches Silva, Antoni Sureda, Seyed Fazel Nabavi, Andrei Mocan, Seyed Mohammad Nabavi and Anupam Bishayee

Molecules 2017, 22(5), 705; https://doi.org/10.3390/molecules22050705 - 29 Apr 2017

Cited by 48 | Viewed by 7768

Abstract

Cancer comprises a collection of related diseases characterized by the existence of altered cellular pathways resulting in an abnormal tendency for uncontrolled growth. A broad spectrum, coordinated, and personalized approach focused on targeting diverse oncogenic pathways with low toxicity and economic natural compounds can provide a real benefit as a chemopreventive and/or treatment of this complex disease. Oleuropein, a bioactive phenolic compound mainly present in olive oil and other natural sources, has been reported to modulate several oncogenic signalling pathways. This review presents and critically discusses the available literature about the anticancer and onco-suppressive activity of oleuropein and the underlying molecular mechanisms implicated in the anticarcinogenic and therapeutic effects. The existence of limitations and the promising perspectives of research on this phenolic compound are also critically analyzed and discussed. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessReview

Cancer Chemoprevention by Phytochemicals: Nature’s Healing Touch

by Haseeb Zubair, Shafquat Azim, Aamir Ahmad, Mohammad Aslam Khan, Girijesh Kumar Patel, Seema Singh and Ajay Pratap Singh

Molecules 2017, 22(3), 395; https://doi.org/10.3390/molecules22030395 - 03 Mar 2017

Cited by 95 | Viewed by 14824

Abstract

Phytochemicals are an important part of traditional medicine and have been investigated in detail for possible inclusion in modern medicine as well. These compounds often serve as the backbone for the synthesis of novel therapeutic agents. For many years, phytochemicals have demonstrated encouraging activity against various human cancer models in pre-clinical assays. Here, we discuss select phytochemicals—curcumin, epigallocatechin-3-gallate (EGCG), resveratrol, plumbagin and honokiol—in the context of their reported effects on the processes of inflammation and oxidative stress, which play a key role in tumorigenesis. We also discuss the emerging evidence on modulation of tumor microenvironment by these phytochemicals which can possibly define their cancer-specific action. Finally, we provide recent updates on how low bioavailability, a major concern with phytochemicals, is being circumvented and the general efficacy being improved, by synthesis of novel chemical analogs and nanoformulations. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessReview

Impact of Age and Insulin-Like Growth Factor-1 on DNA Damage Responses in UV-Irradiated Human Skin

by Michael G. Kemp, Dan F Spandau and Jeffrey B. Travers

Molecules 2017, 22(3), 356; https://doi.org/10.3390/molecules22030356 - 26 Feb 2017

Cited by 42 | Viewed by 8389

Abstract

The growing incidence of non-melanoma skin cancer (NMSC) necessitates a thorough understanding of its primary risk factors, which include exposure to ultraviolet (UV) wavelengths of sunlight and age. Whereas UV radiation (UVR) has long been known to generate photoproducts in genomic DNA that promote genetic mutations that drive skin carcinogenesis, the mechanism by which age contributes to disease pathogenesis is less understood and has not been sufficiently studied. In this review, we highlight studies that have considered age as a variable in examining DNA damage responses in UV-irradiated skin and then discuss emerging evidence that the reduced production of insulin-like growth factor-1 (IGF-1) by senescent fibroblasts in the dermis of geriatric skin creates an environment that negatively impacts how epidermal keratinocytes respond to UVR-induced DNA damage. In particular, recent data suggest that two principle components of the cellular response to DNA damage, including nucleotide excision repair and DNA damage checkpoint signaling, are both partially defective in keratinocytes with inactive IGF-1 receptors. Overcoming these tumor-promoting conditions in aged skin may therefore provide a way to lower aging-associated skin cancer risk, and thus we will consider how dermal wounding and related clinical interventions may work to rejuvenate the skin, re-activate IGF-1 signaling, and prevent the initiation of NMSC. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessReview

Pomegranate for Prevention and Treatment of Cancer: An Update

by Pooja Sharma, Sarah F. McClees and Farrukh Afaq

Molecules 2017, 22(1), 177; https://doi.org/10.3390/molecules22010177 - 24 Jan 2017

Cited by 165 | Viewed by 28864

Abstract

Cancer is the second leading cause of death in the United States, and those who survive cancer may experience lasting difficulties, including treatment side effects, as well as physical, cognitive, and psychosocial struggles. Naturally-occurring agents from dietary fruits and vegetables have received considerable attention for the prevention and treatment of cancers. These natural agents are safe and cost efficient in contrast to expensive chemotherapeutic agents, which may induce significant side effects. The pomegranate (Punica granatum L.) fruit has been used for the prevention and treatment of a multitude of diseases and ailments for centuries in ancient cultures. Pomegranate exhibits strong antioxidant activity and is a rich source of anthocyanins, ellagitannins, and hydrolysable tannins. Studies have shown that the pomegranate fruit as well as its juice, extract, and oil exert anti-inflammatory, anti-proliferative, and anti-tumorigenic properties by modulating multiple signaling pathways, which suggest its use as a promising chemopreventive/chemotherapeutic agent. This review summarizes preclinical and clinical studies highlighting the role of pomegranate in prevention and treatment of skin, breast, prostate, lung, and colon cancers. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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Open AccessReview

Emerging Phytochemicals for the Prevention and Treatment of Head and Neck Cancer

by Santosh K. Katiyar

Molecules 2016, 21(12), 1610; https://doi.org/10.3390/molecules21121610 - 24 Nov 2016

Cited by 34 | Viewed by 6515

Abstract

Despite the development of more advanced medical therapies, cancer management remains a problem. Head and neck squamous cell carcinoma (HNSCC) is a particularly challenging malignancy and requires more effective treatment strategies and a reduction in the debilitating morbidities associated with the therapies. Phytochemicals have long been used in ancient systems of medicine, and non-toxic phytochemicals are being considered as new options for the effective management of cancer. Here, we discuss the growth inhibitory and anti-cell migratory actions of proanthocyanidins from grape seeds (GSPs), polyphenols in green tea and honokiol, derived from the Magnolia species. Studies of these phytochemicals using human HNSCC cell lines from different sub-sites have demonstrated significant protective effects against HNSCC in both in vitro and in vivo models. Treatment of human HNSCC cell lines with GSPs, (−)-epigallocatechin-3-gallate (EGCG), a polyphenolic component of green tea or honokiol reduced cell viability and induced apoptosis. These effects have been associated with inhibitory effects of the phytochemicals on the epidermal growth factor receptor (EGFR), and cell cycle regulatory proteins, as well as other major tumor-associated pathways. Similarly, the cell migration capacity of HNSCC cell lines was inhibited. Thus, GSPs, honokiol and EGCG appear to be promising bioactive phytochemicals for the management of head and neck cancer. Full article

(This article belongs to the Special Issue Cancer Chemoprevention)

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