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Natural Compounds for Cancer and Other Disease Therapeutics

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 27575

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Special Issue Editors

Dr. Vivek K. Bajpai

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Department of Energy & Materials Engineering, Dongguk University-Seoul, Seoul 04620, Republic of Korea
Interests: natural products safety sensing; human diseases
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Prof. Dr. Yun Suk Huh

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Department of Biological Engineering, College of Engineering, Inha University, Incheon 402-751, Korea
Interests: biomaterials; biosensor; ionic liquid; drug delivery system
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Prof. Dr. Shruti Shukla

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TERI-Deakin Nanobiotechnology Centre, The Energy and Resources Institute, Gwal Pahari, Gurugram, Haryana 122003, India
Interests: nano-food technology; food nutrition, food safety; biomaterials; biosensor
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Prof. Dr. MinKyun Na

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College of Pharmacy, Chungnam National University, Daejeon 34134, Korea
Interests: natural products; isolation; structure determination; analysis; NMR spectroscopy

Special Issue Information

Dear Colleagues,

Cancer is a multifactorial disease that arises as a consequence of alterations in many physiological processes that may also initiate other related diseases in the human body. Cancer remains a leading cause of disease-related deaths worldwide. Cancer chemoprevention is the application of natural or synthetic agents to reduce or delay the onset of cancer. With this focus, natural products and their isolated derivatives have proven to be a rich source of therapeutics, particularly in the treatment of infectious diseases and cancer. Over 60% of the current anticancer drugs are derived, in one way or another, from natural sources.

Natural products comprise a large portion of current-day pharmaceutical agents. These structurally unique agents function by novel molecular mechanisms of action against cancer and other associated metabolic diseases. The growing interest in developing multi-targeted cancer therapies may provide another golden opportunity to develop natural products as new cancer therapeutics.

In this context, the goal of this Special Issue is to fully understand the molecular targets and mechanisms of action of natural products and develop them as novel preventive and therapeutic agents against cancer and other associated diseases. The research topic is designed to present recent findings of newly identified anticancer natural products on this platform. We would like to invite review and original articles that focus on understanding the in vitro and in vivo efficacy and pharmacological and toxicological properties of natural products at the molecular level, especially in their role as anticancer agents. In addition, articles pertaining to other associated disease and therapeutic models are also welcome in this Special Issue.

Dr. Vivek K. Bajpai
Prof. Dr. Yun Suk Huh
Prof. Dr. Shruti Shukla
Prof. Dr. MinKyun Na
Guest Editors

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Keywords

Cancer therepy
Anticancer compounds
Molecular targets
Therapeutic models
Clinical studies
In vivo and in vitro models
Natural compound structures
Nanoformulations against cancer therepies

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Published Papers (7 papers)

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Research

14 pages, 9173 KiB

Open AccessArticle

Phytochemicals in Chinese Chive (Allium tuberosum) Induce the Skeletal Muscle Cell Proliferation via PI3K/Akt/mTOR and Smad Pathways in C2C12 Cells

by Mira Oh, Seo-Young Kim, SeonJu Park, Kil-Nam Kim and Seung Hyun Kim

Int. J. Mol. Sci. 2021, 22(5), 2296; https://doi.org/10.3390/ijms22052296 - 25 Feb 2021

Cited by 20 | Viewed by 3562

Abstract

Chinese chive (Allium tuberosum) is a medicinal food that is cultivated and consumed mainly in Asian countries. Its various phytochemicals and physiological effects have been reported, but only a few phytochemicals are available for skeletal muscle cell proliferation. Herein, we isolated a new compound, kaempferol-3-O-(6″-feruloyl)-sophoroside (1), along with one known flavonoid glycoside (2) and six amino acid (3–8) compounds from the water-soluble fraction of the shoot of the Chinese chive. The isolated compounds were identified using extensive spectroscopic methods, including 1D and 2D NMR, and evaluated for their proliferation activity on skeletal muscle cells. Among the tested compounds, newly isolated flavonoid (1) and 5-aminouridine (7) up-regulated PI3K/Akt/mTOR pathways, which implies a positive effect on skeletal muscle growth and differentiation. In particular, compound 1 down-regulated the Smad pathways, which are negative regulators of skeletal muscle growth. Collectively, we suggest that major constituents of Chinese chive, flavonoids and amino acids, might be used in dietary supplements that aid skeletal muscle growth. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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14 pages, 2973 KiB

Open AccessArticle

Cudratricusxanthone A Inhibits Lipid Accumulation and Expression of Inducible Nitric Oxide Synthase in 3T3-L1 Preadipocytes

by Hyo-Shin Kwon, Gil-Saeng Jeong and Byeong-Churl Jang

Int. J. Mol. Sci. 2021, 22(2), 505; https://doi.org/10.3390/ijms22020505 - 6 Jan 2021

Cited by 2 | Viewed by 2820

Abstract

Cudratricusxanthone A (CTXA) is a natural bioactive compound extracted from the roots of Cudrania tricuspidata Bureau and has been shown to possess anti-inflammatory, anti-proliferative, and hepatoprotective activities. However, at present, anti-adipogenic and anti-inflammatory effects of CTXA on adipocytes remain unclear. In this study, we investigated the effects of CTXA on lipid accumulation and expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, two known inflammatory enzymes, in 3T3-L1 preadipocytes. Strikingly, CTXA at 10 µM markedly inhibited lipid accumulation and reduced triglyceride (TG) content during 3T3-L1 preadipocyte differentiation with no cytotoxicity. On mechanistic levels, CTXA at 10 µM suppressed not only expression levels of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), fatty acid synthase (FAS), and perilipin A, but also phosphorylation levels of signal transducer and activator of transcription-3 (STAT-3) and STAT-5 during 3T3-L1 preadipocyte differentiation. In addition, CTXA at 10 µM up-regulated phosphorylation levels of cAMP-activated protein kinase (AMPK) while down-regulating expression and phosphorylation levels of acetyl-CoA carboxylase (ACC) during 3T3-L1 preadipocyte differentiation. Moreover, CTXA at 10 µM greatly attenuated tumor necrosis factor (TNF)-α-induced expression of iNOS, but not COX-2, in 3T3-L1 preadipocytes. These results collectively demonstrate that CTXA has strong anti-adipogenic and anti-inflammatory effects on 3T3-L1 cells through control of the expression and phosphorylation levels of C/EBP-α, PPAR-γ, FAS, ACC, perilipin A, STAT-3/5, AMPK, and iNOS. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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22 pages, 8466 KiB

Open AccessArticle

Phorbol 12-Myristate 13-Acetate Induced Toxicity Study and the Role of Tangeretin in Abrogating HIF-1α-NF-κB Crosstalk In Vitro and In Vivo

by Sukkum Ngullie Chang, Debasish Kumar Dey, Seong Taek Oh, Won Ho Kong, Kiu Hyung Cho, Ebtesam M. Al-Olayan, Buyng Su Hwang, Sun Chul Kang and Jae Gyu Park

Int. J. Mol. Sci. 2020, 21(23), 9261; https://doi.org/10.3390/ijms21239261 - 4 Dec 2020

Cited by 38 | Viewed by 5000

Abstract

Phorbol 12-myristate 13-acetate (PMA) is a potent tumor promoter and highly inflammatory in nature. Here, we investigated the toxic effects of PMA on different model system. PMA (10 μg) caused chromosomal aberrations on the Allium cepa root tip and induced mitotic dysfunction. Similarly, PMA caused embryonic and larval deformities and a plummeted survivability rate on zebrafish embryo in a dose-dependent manner. Persistently, PMA treatment on immortalized human keratinocyte human keratinocyte (HaCaT) cells caused massive inflammatory rush at 4 h and a drop in cell survivability at 24 h. Concomitantly, we replicated a cutaneous inflammation similar to human psoriasis induced by PMA. Herein, we used tangeretin (TAN), as an antagonist to counteract the inflammatory response. Results from an in vivo experiment indicated that TAN (10 and 30 mg/kg) significantly inhibited PMA stimulated epidermal hyperplasia and intra-epidermal neutrophilic abscesses. In addition, its treatment effectively neutralized PMA induced elevated reactive oxygen species (ROS) generation on in vitro and in vivo systems, promoting antioxidant response. The association of hypoxia-inducible factor 1-alpha (HIF-1α)-nuclear factor kappa-light-chain-enhancer of activated b cells (NF-κB) crosstalk triggered by PMA enhanced PKCα-ERK1/2-NF-κB pathway; its activation was also significantly counteracted after TAN treatment. Conclusively, we demonstrated TAN inhibited the nuclear translocation of HIF-1α and NF-κB p65. Collectively, TAN treatment ameliorated PMA incited malignant inflammatory response by remodeling the cutaneous microenvironment. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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24 pages, 7577 KiB

Open AccessArticle

Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy

by Mahendra Pal Singh, Tejinder Pal Khaket, Vivek K. Bajpai, Saleh Alfarraj, Se-Gie Kim, Lei Chen, Yun Suk Huh, Young-Kyu Han and Sun Chul Kang

Int. J. Mol. Sci. 2020, 21(21), 8253; https://doi.org/10.3390/ijms21218253 - 4 Nov 2020

Cited by 17 | Viewed by 3516

Abstract

The cross-talk between apoptosis and autophagy influences anticancer drug sensitivity and cellular death in various cancer cell lines. However, the fundamental mechanisms behind this phenomenon are still unidentified. We demonstrated anti-cancerous role of cisplatin (CP) and morin hydrate (Mh) as an individual and/or in combination (CP-Mh) in hepatoma cells and tumor model. Exposure of CP resulted in the production of intracellular reactive oxygen species (ROS)-mediated cellular vacuolization, expansion of mitochondria membrane and activation of endoplasmic reticulum (ER)-stress. Consequently, Cyt c translocation led to the increase of Bax/Bcl-2 ratio, which simultaneously triggered caspase-mediated cellular apoptosis. In addition, CP-induced PARP-1 activation led to ADP-ribosylation of HMGB1, which consequently developed autophagy as evident by the LC3I/II ratio. Chemically-induced inhibition of autophagy marked by increased cell death signified a protective role of autophagy against CP treatment. CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation. In the absence of PARP-1, a reduced HMGB1 mediated autophagy was observed followed by induced caspase-dependent apoptosis. To confirm the role of PARP-1-HMGB1 signaling in autophagy, we used the PARP-1 inhibitor, 4-amino-1,8-naphthalimide (ANI), HMGB1 inhibitor, ethyl pyruvate (EP), autophagy inhibitors, 3-methyl adenine (3-MA) and bafilomycin (baf) and small interfering RNAs (siRNA) to target Atg5 in combination of CP and Mh. Exposure to these inhibitors enhanced the sensitivity of HepG2 cells to CP. Collectively, our findings indicate that CP-Mh in combination served as a prominent regulator of autophagy and significant inducer of apoptosis that maintains a homeostatic balance towards HepG2 cells and the subcutaneous tumor model. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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26 pages, 9752 KiB

Open AccessArticle

In Vivo Studies of Inoculated Plants and In Vitro Studies Utilizing Methanolic Extracts of Endophytic Streptomyces sp. Strain DBT34 Obtained from Mirabilis jalapa L. Exhibit ROS-Scavenging and Other Bioactive Properties

by Ajit Kumar Passari, Vincent Vineeth Leo, Garima Singh, Loknath Samanta, Heera Ram, Chandra Nayak Siddaiah, Abeer Hashem, Al-Bandari Fahad Al-Arjani, Abdulaziz A. Alqarawi, Elsayed Fathi Abd_Allah and Bhim Pratap Singh

Int. J. Mol. Sci. 2020, 21(19), 7364; https://doi.org/10.3390/ijms21197364 - 6 Oct 2020

Cited by 15 | Viewed by 4432

Abstract

Reactive oxygen species (ROS) and other free radicals cause oxidative damage in cells under biotic and abiotic stress. Endophytic microorganisms reside in the internal tissues of plants and contribute to the mitigation of such stresses by the production of antioxidant enzymes and compounds. We hypothesized that the endophytic actinobacterium Streptomyces sp. strain DBT34, which was previously demonstrated to have plant growth-promoting (PGP) and antimicrobial properties, may also have a role in protecting plants against several stresses through the production of antioxidants. The present study was designed to characterize catalase and superoxide dismutase (SOD), two enzymes involved in the detoxification of ROS, in methanolic extracts derived from six endophytic actinobacterial isolates obtained from the traditional medicinal plant Mirabilis jalapa. The results of a preliminary screen indicated that Streptomyces sp. strain DBT34 was the best overall strain and was therefore used in subsequent detailed analyses. A methanolic extract of DBT34 exhibited significant antioxidant potential in 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2′-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS) assays. The cytotoxicity of DBT34 against liver hepatocellular cells (HepG2) was also determined. Results indicated that methanolic extract of Streptomyces sp. strain DBT34 exhibited significant catalase and SOD-like activity with 158.21 U resulting in a 55.15% reduction in ROS. The IC₅₀ values of a crude methanolic extract of strain DBT34 on DPPH radical scavenging and ABTS radical cation decolorization were 41.5 µg/mL and 47.8 µg/mL, respectively. Volatile compounds (VOC) were also detected in the methanolic extract of Streptomyces sp. strain DBT34 using GC-MS analysis to correlate their presence with bioactive potential. Treatments of rats with DBT34 extract and sitagliptin resulted in a significant (p ≤ 0.001) reduction in total cholesterol, LDL-cholesterol, and VLDL-cholesterol, relative to the vehicle control and a standard diabetic medicine. The pancreatic histoarchitecture of vehicle control rats exhibited a compact volume of isolated clusters of Langerhans cells surrounded by acinies with proper vaculation. An in-vivo study of Streptomyces sp. strain DBT34 on chickpea seedlings revealed an enhancement in its antioxidant potential as denoted by lower IC₅₀ values for DPPH and ABTS radical scavenging activity under greenhouse conditions in relative comparison to control plants. Results of the study indicate that strain DBT34 provides a defense mechanism to its host through the production of antioxidant therapeutic agents that mitigate ROS in hosts subjected to biotic and abiotic stresses. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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15 pages, 4132 KiB

Open AccessArticle

Dihydromyricetin Improves Endothelial Dysfunction in Diabetic Mice via Oxidative Stress Inhibition in a SIRT3-Dependent Manner

by Yu-Yun Hua, Yue Zhang, Wei-Wei Gong, Yue Ding, Jie-Ru Shen, Hua Li, Yun Chen and Guo-Liang Meng

Int. J. Mol. Sci. 2020, 21(18), 6699; https://doi.org/10.3390/ijms21186699 - 13 Sep 2020

Cited by 30 | Viewed by 3217

Abstract

Dihydromyricetin (DHY), a flavonoid component isolated from Ampelopsis grossedentata, exerts versatile pharmacological activities. However, the possible effects of DHY on diabetic vascular endothelial dysfunction have not yet been fully elucidated. In the present study, male C57BL/6 mice, wild type (WT) 129S1/SvImJ mice and sirtuin 3 (SIRT3) knockout (SIRT3^-/-) mice were injected with streptozotocin (STZ, 60 mg/kg/day) for 5 consecutive days. Two weeks later, DHY were given at the doses of 250 mg/kg by gavage once daily for 12 weeks. Fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) level, endothelium-dependent relaxation of thoracic aorta, reactive oxygen species (ROS) production, SIRT3, and superoxide dismutase 2 (SOD2) protein expressions, as well as mitochondrial Deoxyribonucleic Acid (mtDNA) copy number, in thoracic aorta were detected. Our study found that DHY treatment decreased FBG and HbA1c level, improved endothelium-dependent relaxation of thoracic aorta, inhibited oxidative stress and ROS production, and enhanced SIRT3 and SOD2 protein expression, as well as mtDNA copy number, in thoracic aorta of diabetic mice. However, above protective effects of DHY were unavailable in SIRT3^-/- mice. The study suggested DHY improved endothelial dysfunction in diabetic mice via oxidative stress inhibition in a SIRT3-dependent manner. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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15 pages, 2845 KiB

Open AccessArticle

Consumption of Wild Rice (Zizania latifolia) Prevents Metabolic Associated Fatty Liver Disease through the Modulation of the Gut Microbiota in Mice Model

by Xiao-Dong Hou, Ning Yan, Yong-Mei Du, Hui Liang, Zhong-Feng Zhang and Xiao-Long Yuan

Int. J. Mol. Sci. 2020, 21(15), 5375; https://doi.org/10.3390/ijms21155375 - 29 Jul 2020

Cited by 13 | Viewed by 3936

Abstract

Metabolic associated fatty liver disease (MAFLD) due to excess weight and obesity threatens public health worldwide. Gut microbiota dysbiosis contributes to obesity and related diseases. The cholesterol-lowering, anti-inflammatory, and antioxidant effects of wild rice have been reported in several studies; however, whether it has beneficial effects on the gut microbiota is unknown. Here, we show that wild rice reduces body weight, liver steatosis, and low-grade inflammation, and improves insulin resistance in high-fat diet (HFD)-fed mice. High-throughput 16S rRNA pyrosequencing demonstrated that wild rice treatment significantly changed the gut microbiota composition in mice fed an HFD. The richness and diversity of the gut microbiota were notably decreased upon wild rice consumption. Compared with a normal chow diet (NCD), HFD feeding altered 117 operational taxonomic units (OTUs), and wild rice supplementation reversed 90 OTUs to the configuration in the NCD group. Overall, our results suggest that wild rice may be used as a probiotic agent to reverse HFD-induced MAFLD through the modulation of the gut microbiota. Full article

(This article belongs to the Special Issue Natural Compounds for Cancer and Other Disease Therapeutics)

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