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Bioactive Phytochemicals for Cancer Prevention and Treatment 3.0

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

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 6055

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Prof. Dr. Sanjay K. Srivastava

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Department of Immunotherapeutics and Biotechnology, Texas Tech University Health Sciences Center, 1718 Pine Street, Abilene, TX 79601, USA
Interests: development of phytochemicals for cancer prevention and therapeutics; targeting STAT-3, NF-kB, HER2, MCL-1, AKT/FOXO, GLI1/2, and related signaling pathways with agents such as capsaicin, piperlongumine, penfluridol, isothiocyanates, diindolylmethane, panabinostat, cucurbitacin B, and deguelin in pancreatic, ovarian, breast, melanoma, and brain cancer; drug repurposing
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Prof. Dr. Sung-Hoon Kim

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Guest Editor

Cancer Molecular Target Herbal Research Lab, College of Korean Medicine, Kyunghee University, Seoul 02447, Republic of Korea
Interests: cancer biology; tumor immunology; inflammation; angiogenesis; metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Plants have been an important source of bioactive phytochemicals since historic times. Phytochemicals are synthesized by plants as their defensive mechanisms. Several epidemiological studies indicate an inverse correlation between the intake of specific plant foods and cancer incidence. Thousands of phytochemicals have been identified to date, but only a few have been explored in depth for their beneficial roles. Phytochemicals available from dietary plant sources can be classified based on their chemical structures. For example, isothiocyanates, indoles, carotenoids, flavonoids, isoflavones, and terpenoids are some of the major classes studied for their anticancer effects. Phytochemicals are considered to be advantageous over the current chemotherapeutic options available. This is because cancer etiology involves multiple mechanisms, and phytochemicals, being pleiotropic, can counter more procarcinogenic mechanisms. Moreover, being a component of dietary plants, phytochemicals are also relatively nontoxic and generally have broader safety windows. Combination therapy is evitable in clinical practice. Several phytochemicals have been shown to enhance the effects of chemotherapeutic drugs. This Special Issue has been envisaged to document studies on well-known phytochemicals and their role in cancer prevention. The articles in this issue come from eminent researchers in the field of cancer chemoprevention from all around the world. This Issue will be beneficial to all the basic, clinical, and applied researchers and physicians interested in cancer chemoprevention and chemotherapeutics.

Prof. Dr. Sanjay K. Srivastava
Prof. Dr. Sung-Hoon Kim
Guest Editors

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Keywords

Cancer
Chemoprevention
Phytochemicals
Dietary agents
Functional foods
Bioactive agents
Anticancer
Molecular mechanism
Signaling mechanism
Cell cycle
Apoptosis
Combination therapy
Therapeutics

Published Papers (3 papers)

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Research

18 pages, 8012 KiB

Open AccessArticle

Allyl-, Butyl- and Phenylethyl-Isothiocyanate Modulate Akt–mTOR and Cyclin–CDK Signaling in Gemcitabine- and Cisplatin-Resistant Bladder Cancer Cell Lines

by Jochen Rutz, Sebastian Maxeiner, Timothy Grein, Marlon Sonnenburg, Salma El Khadir, Nino Makhatelashvili, Johanna Mann, Hui Xie, Jindrich Cinatl, Anita Thomas, Felix K.-H. Chun, Axel Haferkamp, Roman A. Blaheta and Igor Tsaur

Int. J. Mol. Sci. 2022, 23(19), 10996; https://doi.org/10.3390/ijms231910996 - 20 Sep 2022

Cited by 3 | Viewed by 1674

Abstract

Combined cisplatin–gemcitabine treatment causes rapid resistance development in patients with advanced urothelial carcinoma. The present study investigated the potential of the natural isothiocyanates (ITCs) allyl-isothiocyanate (AITC), butyl-isothiocyanate (BITC), and phenylethyl-isothiocyanate (PEITC) to suppress growth and proliferation of gemcitabine- and cisplatin-resistant bladder cancer cells lines. Sensitive and gemcitabine- and cisplatin-resistant RT112, T24, and TCCSUP cells were treated with the ITCs, and tumor cell growth, proliferation, and clone formation were evaluated. Apoptosis induction and cell cycle progression were investigated as well. The molecular mode of action was investigated by evaluating cell cycle-regulating proteins (cyclin-dependent kinases (CDKs) and cyclins A and B) and the mechanistic target of the rapamycin (mTOR)-AKT signaling pathway. The ITCs significantly inhibited growth, proliferation and clone formation of all tumor cell lines (sensitive and resistant). Cells were arrested in the G2/M phase, independent of the type of resistance. Alterations of both the CDK–cyclin axis and the Akt–mTOR signaling pathway were observed in AITC-treated T24 cells with minor effects on apoptosis induction. In contrast, AITC de-activated Akt–mTOR signaling and induced apoptosis in RT112 cells, with only minor effects on CDK expression. It is concluded that AITC, BITC, and PEITC exert tumor-suppressive properties on cisplatin- and gemcitabine-resistant bladder cancer cells, whereby the molecular action may differ among the cell lines. The integration of these ITCs into the gemcitabine-/cisplatin-based treatment regimen might optimize bladder cancer therapy. Full article

(This article belongs to the Special Issue Bioactive Phytochemicals for Cancer Prevention and Treatment 3.0)

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14 pages, 4873 KiB

Open AccessArticle

Cellular Regulation of Kynurenic Acid-Induced Cell Apoptosis Pathways in AGS Cells

by Hun Hwan Kim, Se Hyo Jeong, Sang Eun Ha, Min Yeong Park, Pritam Bhagwan Bhosale, Abuyaseer Abusaliya, Chung Kil Won, Jeong Doo Heo, Hyun Wook Kim and Gon Sup Kim

Int. J. Mol. Sci. 2022, 23(16), 8894; https://doi.org/10.3390/ijms23168894 - 10 Aug 2022

Cited by 4 | Viewed by 1967

Abstract

Kynurenic acid was included in the three compounds (caffeic acid, chlorogenic acid, and kynurenic acid) that showed high antioxidant and anti-inflammatory potential among the phenolic compounds contained in Gynura procumbens. In this study, the mechanism of cancer cell death induced by kynurenic acid (KYNA), which has the highest molecular binding affinity, in the gastric cancer cell line AGS was confirmed in molecular docking analysis. KYNA showed the most cancer cell death effect on AGS cells among several gastric cancer cell lines (MKN, AGS, and SNU). AGS cells were used for later experiments, and KYNA concentrations of 0, 150, 200, and 250 µM were used. KYNA inhibited cell migration and proliferation in AGS cells in a concentration-dependent manner. G2/M phase cell cycle arrest and reduction of related proteins (Cdc25C, CDK1 and CyclinB1) were confirmed in KYNA-treated AGS cells. Apoptosis of KYNA-treated AGS cells was confirmed by Annexin V/propidium iodide (PI) staining flow cytometry analysis. As a result of morphological chromatin condensation through DAPI (4′,6-diamidino-2-phenylindole), intense blue fluorescence was confirmed. The mechanism of apoptosis induction of KYNA-treated AGS cells was confirmed by western blotting. In the extrinsic pathway, apoptosis induction markers FasL, Fas, and Caspase-3 and -8 were increased in a concentration-dependent manner upon KYNA treatment. In the intrinsic pathway, the expression of anti-apoptotic factors PI3K, AKT, and Bcl-xL was down-regulated, and the expression of apoptosis-inducing factors BAD, Bak, Bax, Cytochrom C, and Caspase-9 was up-regulated. Therefore, in the present study, we strongly imply that KYNA induces apoptosis in AGS gastric cancer cells. This suggests that KYNA, a natural compound, could be the basis for drug for the treatment of gastric cancer. Full article

(This article belongs to the Special Issue Bioactive Phytochemicals for Cancer Prevention and Treatment 3.0)

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9 pages, 2504 KiB

Open AccessArticle

The Antitumor Effect of Cinnamaldehyde Derivative CB-PIC in Hepatocellular Carcinoma Cells via Inhibition of Pyruvate and STAT3 Signaling

by Hyungjin Kim, Hyo-Jung Lee, Deok Yong Sim, Ji Eon Park, Chi-Hoon Ahn, Su-Yeon Park, Eungyeong Jang, Bonglee Kim and Sung-Hoon Kim

Int. J. Mol. Sci. 2022, 23(12), 6461; https://doi.org/10.3390/ijms23126461 - 09 Jun 2022

Cited by 3 | Viewed by 1740

Abstract

Though cinnamaldehyde derivative (CB-PIC), a major compound of cinnamon, is known to have anticancer activity, its underlying mechanism is not fully understood. In the present study, the anticancer mechanism of CB-PIC was investigated in human hepatocellular carcinoma cells (HCCs) in association with signal transducer and activator of transcription 3 (STAT3) signaling. CB-PIC exerted cytotoxicity in HepG2 and Huh7 cells. CB-PIC increased the sub G1 population and attenuated the expression of pro-poly (ADP-ribose) polymerase (PARP) and pro-Caspase3 in HepG2 and Huh7 cells. Interestingly, CB-PIC significantly abrogated the expression of a glycolytic enzyme pyruvate kinase M2 (PKM2) in HepG2 cells more than in LNCaP, A549, and HCT-116 cells. Consistently, CB-PIC reduced the expression of hexokinase 2 (HK2) and PKM2, along with a reduced production of lactate in HepG2 and Huh7 cells. Notably, CB-PIC suppressed the phosphorylation of STAT3 in HepG2 and Huh7 cells and conversely STAT3 depletion enhanced the capacity of CB-PIC to suppress the expression of HK2, PKM2, and pro-caspase3 and to reduce the viability in Huh7 cells. Furthermore, CB-PIC activated the phosphorylation of AMPK and ERK and suppressed expression of IL-6 as STAT3-related genes in HepG2 and Huh7 cells. Conversely, pyruvate treatment reversed the inhibitory effect of CB-PIC on p-STAT3, HK2, PKM2, and pro-PARP in Huh7 cells. Overall, there findings suggest that CB-PIC exerts an apoptotic effect via inhibition of the Warburg effect mediated by p-STAT3 and pyruvate signaling. Full article

(This article belongs to the Special Issue Bioactive Phytochemicals for Cancer Prevention and Treatment 3.0)

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