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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 (20 September 2022) | Viewed by 38318

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Prof. Dr. Ihn Han

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Plasma Bioscience Research Center, Applied Plasma Medicine Center, Kwangwoon University, Seoul 01897, Republic of Korea
Interests: atmospheric pressure plasma; plasma-treated liquid; p53; MAPK pathway; oriental medicine; in silico drug screening
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Eun Ha Choi

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Guest Editor

Department of Electrical and Biological Physics, Plasma Bioscience Research Center, Kwangwoon University, Seoul 01897, Republic of Korea
Interests: atmospheric pressure plasma; plasma physics; reactive oxygen species; reactive nitrogen species
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In order to develop novel anticancer therapies, it is essential to understand the pathogenesis of cancer and the biological basis of cancer cells. Various adjuvant and alternative therapies recently reported in the literature are attributable to the reduced quality of life associated with traditional cancer treatment. This requires a multidisciplinary approach in biology, physics, chemistry and computer science. Non‑thermal plasma technology has been considered as a new frontier in plasma medicine, in order to aid in the treatment of cancers. Plasma technology is relatively new to the field of medicine. Much experimental work, conducted at several major universities, research centers, and companies around the world over the recent decade, has determined that plasma can be used in a variety of medical applications as a plasma medicine. It is already widely used in surgeries and endoscopic procedures. Recently, a deeper understanding of the various mechanisms by which plasma can interact with biological systems, including the effects of reactive nitrogen species, reactive oxygen species, and charges, has begun to emerge. It was recently reported that this process begins . In addition, it is possible to discover novel lead compounds for cancer treatment, with excellent potential to be applied in the discovery of new natural compounds, through computer simulation and predictive analysis of physiological activity.

For this Special Issue, to be published in the International Journal of Molecular Science, researchers who are active in all aspects of novel applications of cancer therapy and drug development are invited to submit their latest results. Papers covering fundamental studies, as well as papers discussing applications, are welcome.

Prof. Dr. Ihn Han
Prof. Dr. Eun Ha Choi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

cancer biology
drug discovery
atmospheric nonthermal plasma
reactive oxygen species
reactive nitrogen species
redox response
c-myc
p53
p38 MAPK
in silico
microbial inactivation
sterilization
phytochemical
oriental medicine

Published Papers (11 papers)

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Research

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15 pages, 3442 KiB

Open AccessArticle

Effect of Plasma On-Time with a Fixed Duty Ratio on Reactive Species in Plasma-Treated Medium and Its Significance in Biological Applications

by Sohail Mumtaz, Juie Nahushkumar Rana, Jun Sup Lim, Rida Javed, Eun Ha Choi and Ihn Han

Int. J. Mol. Sci. 2023, 24(6), 5289; https://doi.org/10.3390/ijms24065289 - 9 Mar 2023

Cited by 4 | Viewed by 1735

Abstract

Optimizing the therapeutic range of nonthermal atmospheric pressure plasma (NTAPP) for biomedical applications is an active research topic. For the first time, we examined the effect of plasma on-times in this study while keeping the duty ratio and treatment time fixed. We have evaluated the electrical, optical, and soft jet properties for two different duty ratios of 10% and 36%, using the plasma on-times of 25, 50, 75, and 100 ms. Furthermore, the influence of plasma on-time on reactive oxygen and nitrogen species (ROS/RNS) levels in plasma treated medium (PTM) was also investigated. Following treatment, the characteristics of (DMEM media) and PTM (pH, EC, and ORP) were also examined. While EC and ORP rose by raising plasma on-time, pH remained unchanged. Finally, the PTM was used to observe the cell viability and ATP levels in U87-MG brain cancer cells. We found it interesting that, by increasing the plasma on-time, the levels of ROS/RNS dramatically increased in PTM and significantly affected the viability and ATP levels of the U87-MG cell line. The results of this study provide a significant indication of advancement by introducing the optimization of plasma on-time to increase the efficacy of the soft plasma jet for biomedical applications. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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17 pages, 8250 KiB

Open AccessArticle

TRPV4 Promotes Metastasis in Melanoma by Regulating Cell Motility through Cytoskeletal Rearrangement

by Shuai Huang, Suyun Yu, Rui Deng, Huan Liu, Yushi Ding, Yifan Sun, Wenxing Chen, Aiyun Wang, Zhonghong Wei and Yin Lu

Int. J. Mol. Sci. 2022, 23(23), 15155; https://doi.org/10.3390/ijms232315155 - 2 Dec 2022

Cited by 5 | Viewed by 1490

Abstract

The abnormal expression of Transient Receptor Potential cation channel subfamily V member 4 (TRPV4) is closely related to the progression of multiple tumors. In addition, TRPV4 is increasingly being considered a potential target for cancer therapy, especially in tumor metastasis prevention. However, the biological correlation between TRPV4 and tumor metastasis, as well as the specific role of TRPV4 in malignant melanoma metastasis, is poorly understood. In this study, we aimed to examine the role of TRPV4 in melanoma metastasis through experiments and clinical data analysis, and the underlying anticancer mechanism of Baicalin, a natural compound, and its inhibitory effect on TRPV4 with in vivo and in vitro experiments. Our findings suggested that TRPV4 promotes metastasis in melanoma by regulating cell motility via rearranging the cytoskeletal, and Baicalin can inhibit cancer metastasis, whose mechanisms reverse the recruitment of activated cofilin to leading-edge protrusion and the increasing phosphorylation level of cortactin, which is provoked by TRPV4 activation. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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12 pages, 1557 KiB

Open AccessArticle

Comparison of EMT-Related and Multi-Drug Resistant Gene Expression, Extracellular Matrix Production, and Drug Sensitivity in NSCLC Spheroids Generated by Scaffold-Free and Scaffold-Based Methods

by Xiaoli Qi, Alexandra V. Prokhorova, Alexander V. Mezentsev, Ningfei Shen, Alexander V. Trofimenko, Gleb I. Filkov, Rushan A. Sulimanov, Vladimir A. Makarov and Mikhail O. Durymanov

Int. J. Mol. Sci. 2022, 23(21), 13306; https://doi.org/10.3390/ijms232113306 - 1 Nov 2022

Cited by 4 | Viewed by 2561

Abstract

Multicellular 3D tumor models are becoming a powerful tool for testing of novel drug products and personalized anticancer therapy. Tumor spheroids, a commonly used 3D multicellular tumor model, more closely reproduce the tumor microenvironment than conventional 2D cell cultures. It should be noted that spheroids can be produced using different techniques, which can be subdivided into scaffold-free (SF) and scaffold-based (SB) methods. However, it remains unclear, to what extent spheroid properties depend on the method of their generation. In this study, we aimed to carry out a head-to-head comparison of drug sensitivity and molecular expression profile in SF and SB spheroids along with a monolayer (2D) cell culture. Here, we produced non-small cell lung cancer (NSCLC) spheroids based on human lung adenocarcinoma cell line A549. Drug sensitivity analysis of the tested cell cultures to five different chemotherapeutics resulted in IC₅₀ (A549-SB) > IC₅₀ (A549-SF) > IC₅₀ (A549-2D) trend. It was found that SF and SB A549 spheroids displayed elevated expression levels of epithelial-to-mesenchymal transition (EMT) markers and proteins associated with drug resistance compared with the monolayer A549 cell culture. Enhanced drug resistance of A549-SB spheroids can be a result of larger diameters and elevated deposition of extracellular matrix (ECM) that impairs drug penetration into spheroids. Thus, the choice of the spheroid production method can influence the properties of the generated 3D cell culture and their drug resistance. This fact should be considered for correct interpretation of drug testing results. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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26 pages, 18269 KiB

Open AccessArticle

Repurposing Alone and in Combination of the Antiviral Saquinavir with 5-Fluorouracil in Prostate and Lung Cancer Cells

by Mariana Pereira and Nuno Vale

Int. J. Mol. Sci. 2022, 23(20), 12240; https://doi.org/10.3390/ijms232012240 - 13 Oct 2022

Cited by 9 | Viewed by 1991

Abstract

Prostate and lung cancers are among the most common cancer types, and they still need more therapeutics. For this purpose, saquinavir (SAQ) was tested alone and in combination with 5-fluorouracil (5-FU). PC-3 and A549 cells were exposed to increasing concentrations of both drugs alone or in combination, with simultaneous or sequential administration. Cell viability was obtained using the MTT assay and synergism values using CompuSyn software. Results showed that SAQ was the more cytotoxic of both drugs in PC-3 cells, while 5-FU was the most cytotoxic in A549 cells. When these drugs were used in combination, the more synergistic combination in PC-3 cells was the IC₅₀ of SAQ with various concentrations of 5-FU, particularly when 5-FU was only applied 24 h later. Meanwhile for A549 the most promising combination was 5-FU with delayed SAQ, but with a weaker effect than all combinations demonstrated in PC-3 cells. These results demonstrate that SAQ could be used as a new repurposed drug for the treatment of prostate cancer and this treatment potential could be even greater if SAQ is combined with the anticancer drug 5-FU, while for lung cancer it is not as efficient and, therefore, not of as much interest. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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13 pages, 9684 KiB

Open AccessArticle

IDO1 Modulates the Sensitivity of Epithelial Ovarian Cancer Cells to Cisplatin through ROS/p53-Dependent Apoptosis

by Houmei Wang, Yuanyuan Luo, Rui Ran, Xinya Li, Hongjian Ling, Fang Wen and Tinghe Yu

Int. J. Mol. Sci. 2022, 23(19), 12002; https://doi.org/10.3390/ijms231912002 - 9 Oct 2022

Cited by 6 | Viewed by 2047

Abstract

Indoleamine 2,3-dioxygenase 1 (IDO1) is a heme-containing dioxygenase that may play a part in chemoresistance in ovarian cancer. However, its role in cisplatin (DDP) resistance is unclear. Here, the expression level of IDO1 in tumors in platinum-resistant (n = 22) and -sensitive (n = 46) ovarian cancer patients was determined, and then how IDO1 modulated DDP resistance was explored in vitro and in vivo. The IDO1 expression level in platinum-resistant patients was higher than that in -sensitive patients, and a higher IDO1 level was correlated with poor prognosis in type II cancer patients. Up-regulating IDO1 decreased DDP-induced apoptosis in SKOV3 cells via inhibiting the ROS/p53 cell-death pathway, thereby attenuating cytotoxicity of DDP. Silencing IDO1 enhanced p53-dependent apoptosis by increasing ROS accumulation, thereby enhancing DDP against SKOV3 cells. Down-knocking IDO1 augmented the action of DDP in vivo. These data demonstrated that silencing IDO1 enhanced the efficacy of DDP by intensifying p53-dependent apoptosis, and that targeting IDO1 can be a strategy to modulate DDP-based chemotherapy for epithelial ovarian cancer. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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15 pages, 5714 KiB

Open AccessArticle

The Antitumor Effect of Timosaponin A3 through c-Myc Inhibition in Colorectal Cancer Cells and Combined Treatment Effect with 5-FU or Doxorubicin

by Hyun Min Ko, Wona Jee, Do-il Park, Kwan-Il Kim, Ji Hoon Jung and Hyeung-Jin Jang

Int. J. Mol. Sci. 2022, 23(19), 11900; https://doi.org/10.3390/ijms231911900 - 7 Oct 2022

Cited by 4 | Viewed by 1668

Abstract

Timosaponin A3 (TA3), extracted from the rhizome of Anemarrhenaasphodeloides Bunge, has been reported to affect various diseases, such as cancer, Alzheimer’s disease, and allergies. However, the underlying molecular mechanisms and impacts are largely unknown. In the present study, we hypothesized that TA3 induces apoptosis through the inhibition of c-Myc expression via CNOT2 or MID1IP1 in HCT116. An MTT assay and colony formation assay were used to measure cell viability and proliferation. The protein expression of apoptotic markers and oncogenes was measured using immunoblotting and immunofluorescence assays. The interaction between MID1IP1 and c-Myc was confirmed by performing an immunoprecipitation assay. TA3 markedly inhibited colon cancer cell proliferation. Consistently, TA3 regulated the apoptotic proteins pro-PARP and caspase 3. TA3 inhibited the half-life of c-Myc and suppressed its expression in response to serum stimulation. In addition, TA3 enhanced the apoptotic effects of doxorubicin and 5-FU in colon cancer cells. Altogether, our results reveal a mechanism by which TA3 induces apoptosis through inhibiting c-Myc expression via CNOT2 or MID1IP1 in HCT116, which may help in the development of new therapies for colon cancer based on TA3 in the future. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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15 pages, 1572 KiB

Open AccessArticle

Resveratrol Affects Sphingolipid Metabolism in A549 Lung Adenocarcinoma Cells

by Albena Momchilova, Roumen Pankov, Galya Staneva, Stefan Pankov, Plamen Krastev, Evgenia Vassileva, Rusina Hazarosova, Nikolai Krastev, Bozhil Robev, Biliana Nikolova and Adriana Pinkas

Int. J. Mol. Sci. 2022, 23(18), 10870; https://doi.org/10.3390/ijms231810870 - 17 Sep 2022

Cited by 10 | Viewed by 2011

Abstract

Resveratrol is a naturally occurring polyphenol which has various beneficial effects, such as anti-inflammatory, anti-tumor, anti-aging, antioxidant, and neuroprotective effects, among others. The anti-cancer activity of resveratrol has been related to alterations in sphingolipid metabolism. We analyzed the effect of resveratrol on the enzymes responsible for accumulation of the two sphingolipids with highest functional activity—apoptosis promoting ceramide (CER) and proliferation-stimulating sphingosine-1-phosphate (S1P)—in human lung adenocarcinoma A549 cells. Resveratrol treatment induced an increase in CER and sphingosine (SPH) and a decrease in sphingomyelin (SM) and S1P. Our results showed that the most common mode of CER accumulation, through sphingomyelinase-induced hydrolysis of SM, was not responsible for a CER increase despite the reduction in SM in A549 plasma membranes. However, both the activity and the expression of CER synthase 6 were upregulated in resveratrol-treated cells, implying that CER was accumulated as a result of stimulated de novo synthesis. Furthermore, the enzyme responsible for CER hydrolysis, alkaline ceramidase, was not altered, suggesting that it was not related to changes in the CER level. The enzyme maintaining the balance between apoptosis and proliferation, sphingosine kinase 1 (SK1), was downregulated, and its expression was reduced, resulting in a decrease in S1P levels in resveratrol-treated lung adenocarcinoma cells. In addition, incubation of resveratrol-treated A549 cells with the SK1 inhibitors DMS and fingolimod additionally downregulated SK1 without affecting its expression. The present studies provide information concerning the biochemical processes underlying the influence of resveratrol on sphingolipid metabolism in A549 lung cancer cells and reveal possibilities for combined use of polyphenols with specific anti-proliferative agents that could serve as the basis for the development of complex therapeutic strategies. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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21 pages, 5602 KiB

Open AccessArticle

Hypoxia Triggers TAZ Phosphorylation in Basal A Triple Negative Breast Cancer Cells

by Qiuyu Liu, Wanda van der Stel, Vera E. van der Noord, Hanneke Leegwater, Bircan Coban, Kim Elbertse, Joannes T. M. Pruijs, Olivier J. M. Béquignon, Gerard van Westen, Sylvia E. Le Dévédec and Erik H. J. Danen

Int. J. Mol. Sci. 2022, 23(17), 10119; https://doi.org/10.3390/ijms231710119 - 4 Sep 2022

Cited by 2 | Viewed by 2235

Abstract

Hypoxia and HIF signaling drive cancer progression and therapy resistance and have been demonstrated in breast cancer. To what extent breast cancer subtypes differ in their response to hypoxia has not been resolved. Here, we show that hypoxia similarly triggers HIF1 stabilization in luminal and basal A triple negative breast cancer cells and we use high throughput targeted RNA sequencing to analyze its effects on gene expression in these subtypes. We focus on regulation of YAP/TAZ/TEAD targets and find overlapping as well as distinct target genes being modulated in luminal and basal A cells under hypoxia. We reveal a HIF1 mediated, basal A specific response to hypoxia by which TAZ, but not YAP, is phosphorylated at Ser89. While total YAP/TAZ localization is not affected by hypoxia, hypoxia drives a shift of [p-TAZ(Ser89)/p-YAP(Ser127)] from the nucleus to the cytoplasm in basal A but not luminal breast cancer cells. Cell fractionation and YAP knock-out experiments confirm cytoplasmic sequestration of TAZ(Ser89) in hypoxic basal A cells. Pharmacological and genetic interference experiments identify c-Src and CDK3 as kinases involved in such phosphorylation of TAZ at Ser89 in hypoxic basal A cells. Hypoxia attenuates growth of basal A cells and the effect of verteporfin, a disruptor of YAP/TAZ-TEAD–mediated transcription, is diminished under those conditions, while expression of a TAZ-S89A mutant does not confer basal A cells with a growth advantage under hypoxic conditions, indicating that other hypoxia regulated pathways suppressing cell growth are dominant. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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22 pages, 6760 KiB

Open AccessArticle

Compound C Inhibits Renca Renal Epithelial Carcinoma Growth in Syngeneic Mouse Models by Blocking Cell Cycle Progression, Adhesion and Invasion

by Myungyeon Lee, Na Yeon Ham, Chi Yeon Hwang, Jiwon Jang, Boram Lee, Joo-Won Jeong, Insug Kang and Eui-Ju Yeo

Int. J. Mol. Sci. 2022, 23(17), 9675; https://doi.org/10.3390/ijms23179675 - 26 Aug 2022

Cited by 2 | Viewed by 1799

Abstract

Compound C (CompC), an inhibitor of AMP-activated protein kinase, reduces the viability of various renal carcinoma cells. The molecular mechanism underlying anti-proliferative effect was investigated by flow cytometry and western blot analysis in Renca cells. Its effect on the growth of Renca xenografts was also examined in a syngeneic BALB/c mouse model. Subsequent results demonstrated that CompC reduced platelet-derived growth factor receptor signaling pathways and increased ERK1/2 activation as well as reactive oxygen species (ROS) production. CompC also increased the level of active Wee1 tyrosine kinase (P-Ser⁶⁴²-Wee1) and the inactive form of Cdk1 (P-Tyr¹⁵-Cdk1) while reducing the level of active histone H3 (P-Ser¹⁰-H3). ROS-dependent ERK1/2 activation and sequential alterations in Wee1, Cdk1, and histone H3 might be responsible for the CompC-induced G2/M cell cycle arrest and cell viability reduction. In addition, CompC reduced the adhesion, migration, and invasion of Renca cells in the in vitro cell systems, and growth of Renca xenografts in the BALB/c mouse model. Taken together, the inhibition of in vivo tumor growth by CompC may be attributed to the blockage of cell cycle progression, adhesion, migration, and invasion of tumor cells. These findings suggest the therapeutic potential of CompC against tumor development and progression. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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Review

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26 pages, 5500 KiB

Open AccessReview

Microwave Radiation and the Brain: Mechanisms, Current Status, and Future Prospects

by Sohail Mumtaz, Juie Nahushkumar Rana, Eun Ha Choi and Ihn Han

Int. J. Mol. Sci. 2022, 23(16), 9288; https://doi.org/10.3390/ijms23169288 - 18 Aug 2022

Cited by 63 | Viewed by 17509

Abstract

Modern humanity wades daily through various radiations, resulting in frequent exposure and causing potentially important biological effects. Among them, the brain is the organ most sensitive to electromagnetic radiation (EMR) exposure. Despite numerous correlated studies, critical unknowns surround the different parameters used, including operational frequency, power density (i.e., energy dose), and irradiation time that could permit reproducibility and comparability between analyses. Furthermore, the interactions of EMR with biological systems and its precise mechanisms remain poorly characterized. In this review, recent approaches examining the effects of microwave radiations on the brain, specifically learning and memory capabilities, as well as the mechanisms of brain dysfunction with exposure as reported in the literature, are analyzed and interpreted to provide prospective views for future research directed at this important and novel medical technology for developing preventive and therapeutic strategies on brain degeneration caused by microwave radiation. Additionally, the interactions of microwaves with biological systems and possible mechanisms are presented in this review. Treatment with natural products and safe techniques to reduce harm to organs have become essential components of daily life, and some promising techniques to treat cancers and their radioprotective effects are summarized as well. This review can serve as a platform for researchers to understand the mechanism and interactions of microwave radiation with biological systems, the present scenario, and prospects for future studies on the effect of microwaves on the brain. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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13 pages, 1430 KiB

Open AccessReview

Stem Cell Models for Breast and Colon Cancer: Experimental Approach for Drug Discovery

by Nitin T. Telang

Int. J. Mol. Sci. 2022, 23(16), 9223; https://doi.org/10.3390/ijms23169223 - 17 Aug 2022

Cited by 3 | Viewed by 1933

Abstract

The progression of the early stages of female breast and colon cancer to metastatic disease represents a major cause of mortality in women. Multi-drug chemotherapy and/or pathway selective targeted therapy are notable for their off-target effects and are associated with spontaneous and/or acquired chemotherapy resistance and the emergence of premalignant chemo-resistant cancer-initiating stem cells. The stem cell populations are responsible for the evolution of therapy-resistant metastatic disease. These limitations emphasize an unmet need to develop reliable drug-resistant cancer stem cell models as novel experimental approaches for therapeutic alternatives in drug discovery platforms. Drug-resistant stem cell models for breast and colon cancer subtypes exhibit progressive growth in the presence of cytotoxic chemo-endocrine therapeutics. The resistant cells exhibit upregulated expressions of stem cell-selective cellular and molecular markers. Dietary phytochemicals, nutritional herbs and their constituent bioactive compounds have documented growth inhibitory efficacy for cancer stem cells. The mechanistic leads for the stem cell-targeted efficacy of naturally occurring agents validates the present experimental approaches for new drug discovery as therapeutic alternatives for therapy-resistant breast and colon cancer. The present review provides a systematic discussion of published evidence on (i) conventional/targeted therapy for breast and colon cancer, (ii) cellular and molecular characterization of stem cell models and (iii) validation of the stem cell models as an experimental approach for novel drug discovery of therapeutic alternatives for therapy-resistant cancers. Full article

(This article belongs to the Special Issue Cancer Cell Biology and Drug Discovery)

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