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Molecular Targets and Chemoprevention (Tumor Growth and Metastasis)

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A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Oncology".

Deadline for manuscript submissions: closed (20 March 2022) | Viewed by 12519

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Special Issue Editor

Dr. Ram Prasad

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Guest Editor

Department of Ophthalmology and Visual Sciences, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: chronic illness; cancer chemoprevention; UV radiation; DNA damage; immunosuppression; microRNAs; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The COVID-19 pandemic has affected the entire world. Over 82 million people have been infected with the virus, and still the number of new cases is increasing significantly. More than 1.7 million people have died worldwide as a result. The patients with pre-existing medical conditions including diabetes, cardiovascular diseases, and cancer often experience worse outcomes than their healthier counterparts. Studies demonstrate that the death rate is three times higher in cancer patients with COVID-19 than that for COVID-19 patients without cancer. This statistic urges the cancer research community to discover newer molecular targets and effective measures for better management.

The goal of this Special Issue is to emphasize on the identification of newer molecular targets and the development of effective and safe interventional approaches to treat cancer. Despite the extensive knowledge and understanding of molecular signaling, new discoveries are still needed to develop more effective and targeted strategies.

Together with the “Journal of Clinical Medicine”, I want to express my appreciation for your outstanding research and contribution to the CFW (cancer free world) mission, and cordially invite you to publish an article in the Special Issue “Molecular Targets and Chemoprevention (Tumor Growth and Metastasis)”. Original research articles, reviews, and mini reviews are welcome.

Dr. Ram Prasad
Guest Editor

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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

Head and neck cancer
Melanoma and non-melanoma skin cancer
Non-small cell lung cancer
Breast cancer
Prostate cancer
Epithelial–mesenchymal transition
Tumor growth
Small molecule inhibitors
Immuno-oncology
DNA methylation and Histone deacetylases.

Published Papers (5 papers)

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Research

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15 pages, 3595 KiB

Open AccessEditor’s ChoiceArticle

Regular Intake of Green Tea Polyphenols Suppresses the Development of Nonmelanoma Skin Cancer through miR-29-Mediated Epigenetic Modifications

by Vikash Kansal, Anshu Agarwal, Angela Harbour, Humaira Farooqi, Vijay Kumar Singh and Ram Prasad

J. Clin. Med. 2022, 11(2), 398; https://doi.org/10.3390/jcm11020398 - 13 Jan 2022

Cited by 10 | Viewed by 2413

Abstract

Previously, we and others have shown that the regular intake of green tea polyphenols (GTPs) reduces ultraviolet B (UVB) radiation-induced skin cancer by targeting multiple signaling pathways, including DNA damage, DNA repair, immunosuppression, and inflammation. Here, we determine the effect of GTPs on UVB-induced epigenetic changes, emphasizing DNA hypermethylation in UV-exposed skin and tumors and their association with miR-29, a key regulator of DNA methyltransferases (DNMTs). Skin cancer was induced in SKH-1 hairless mice following repeated exposures of UVB radiation (180 mJ/cm², three times/week, 24 weeks) with or without GTPs supplementation (0.2%) in drinking water. Regular intake of GTPs inhibited tumor growth by hindering the cascade of DNA hypermethylation events. GTPs supplementation significantly blocked UVB-induced DNA hypermethylation in the skin (up to 35%; p < 0.0001) and in tumors (up to 50%; p < 0.0001). Experimental results showed that the levels of DNA hypermethylation were higher in GTPs-treated mice than in the control group. The expressions of miR-29a, miR-29b, and miR-29c were markedly decreased in UV-induced skin tumors, and GTPs administration blocked UVB-induced miR-29s depletion. Furthermore, these observations were verified using the in vitro approach in human skin cancer cells (A431) followed by treatment with GTPs or mimics of miR-29c. Increased levels of miR-29 were observed in GTPs-treated A431 cells, resulting in increased TET activity and decreased DNA hypermethylation. In conclusion, UVB-mediated miR-29 depletion promotes DNA hypermethylation and leads to enhanced tumor growth by silencing tumor suppressors. Regular intake of GTPs rescued UVB-induced miR-29 depletion and prevented tumor growth by maintaining reduced DNA hypermethylation and activating tumor suppressors. Our observations suggest that miR-based strategies and regular consumption of GTPs could minimize the risk of UVB-induced skin cancers and contribute to better management of NMSCs. Full article

(This article belongs to the Special Issue Molecular Targets and Chemoprevention (Tumor Growth and Metastasis))

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9 pages, 1811 KiB

Open AccessArticle

Immunohistochemical Expression of Wnt-4 Protein in Clear Cell Renal Carcinoma

by Oliver Pavlovic, Tvrtko Hudolin, Ivan Miskulin, Stela Bulimbasic, Marijana Coric, Josip Perkovic and Toni Zekulic

J. Clin. Med. 2021, 10(24), 5795; https://doi.org/10.3390/jcm10245795 - 11 Dec 2021

Viewed by 1813

Abstract

Wingless binding integration site proteins (Wnt) have an important role in normal kidney development and in various kidney diseases. They are required for complete epithelial differentiation and normal nephron formation. Changes in these proteins could also have important role in carcinogenesis. This study included 185 patients with clear cell renal carcinoma (ccRCC) in whom immunohistochemical expression of Wnt-4 protein in healthy and tumorous tissue after surgery was investigated. There was higher expression of Wnt-4 in healthy than in tumor tissue. No difference between Fuhrman’s grade and Wnt-4 expression was found. A poor negative correlation between tumor size and Wnt-4 expression was found. Patients with suspected metastatic diseases had higher Wnt-4 expression. There was no difference in survival rates between Wnt-4 negative and positive groups. In our study we have shown that high Wnt-4 expression in healthy tissue decreases in low-grade tumors but then increases in high-grade tumors, suggesting that tumor progression requires Wnt-4 activation or reactivation. Full article

(This article belongs to the Special Issue Molecular Targets and Chemoprevention (Tumor Growth and Metastasis))

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15 pages, 2088 KiB

Open AccessArticle

Diosmetin Induces Modulation of Igf-1 and Il-6 Levels to Alter Rictor-Akt-PKCα Cascade in Inhibition of Prostate Cancer

by Rebecca Pakradooni, Nishka Shukla, Kalpana Gupta, Jatinder Kumar, Ilaha Isali, Ahmed O. Khalifa and Sanjeev Shukla

J. Clin. Med. 2021, 10(20), 4741; https://doi.org/10.3390/jcm10204741 - 15 Oct 2021

Cited by 4 | Viewed by 1629

Abstract

Growth signals, which typically originate from the surrounding microenvironment, are important for cells. However, when stimulation by growth factors becomes excessive and exceeds their threshold limit, deleterious effects may ensue. In patients with cancer, maintenance of tumors depends, at least in part, on growth factor stimulation, which can also facilitate cancer progression into advanced stages. This is particularly important when the tumor grows beyond its tissue boundaries or when it invades and colonizes other tissues. These aforementioned malignant events are known to be partly supported by elevated cytokine levels. Among the currently known growth signals, insulin-like growth factor (IGF)-1 and IL-6 have been previously studied for their roles in prostate cancer. Both IGF-1 and IL-6 have been reported to activate the RAPTOR independent companion of MTOR complex 2 (Rictor)/AKT/protein kinase C α (PKCα) signaling pathway as one of their downstream mechanisms. At present, research efforts are mainly focused on the exploration of agents that alter growth factor (such as IGF-1) and cytokine (such as IL-6) signaling for their potential application as therapeutic agents, as both of these have been reported to modulate disease outcome. In the present study, IGF-1 and IL-6 served distinct roles in the androgen responsive LNCaP cell line and in the androgen refractory PC-3 cell line in a dose- and time-dependent manner. Increased phosphorylation of Rictor at the Thr-1135 residue, AKT at the Ser-473 residue and PKCα at the Ser-657 residue were observed after treatment with IGF-1 and IL-6. Subsequently, it was found that diosmetin, a natural plant aglycone, had the potential to modulate the downstream signaling cascade of Rictor/AKT/PKCα to inhibit the progression of prostate cancer. Treatment of LNCaP and PC-3 cells with diosmetin inhibited the phosphorylation of Rictor (Thr-1135), AKT (Ser-473) and PKCα (Ser-657) in a dose-dependent manner. Furthermore, the Bax/Bcl-2 expression ratio was increased in response to diosmetin treatment, which would result in increased apoptosis. Based on these observations, diosmetin may represent a novel therapeutic target for prostate cancer. Full article

(This article belongs to the Special Issue Molecular Targets and Chemoprevention (Tumor Growth and Metastasis))

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17 pages, 7116 KiB

Open AccessArticle

Assessment of Histological Features in Squamous Cell Carcinoma Involving Head and Neck Skin and Mucosa

by Ana Caruntu, Liliana Moraru, Mihai Lupu, Diana Alina Ciubotaru, Marius Dumitrescu, Lucian Eftimie, Radu Hertzog, Sabina Zurac, Constantin Caruntu and Oana Cristina Voinea

J. Clin. Med. 2021, 10(11), 2343; https://doi.org/10.3390/jcm10112343 - 27 May 2021

Cited by 15 | Viewed by 3201

Abstract

Background: squamous cell carcinoma (SCC) is the second most common type of malignancy worldwide. Skin and mucosa of the head and neck areas are the most frequently affected. An aggressive behavior in SCC is not easily detected, and despite all efforts, mortality in these types of cancer did not show major improvements during recent decades. In this study, we aim to determine the role of histological features available through standard pathology assessment in SCC and their relation with tumor behavior and patients’ survival. Method: in a group of one hundred patients diagnosed with SCC involving the head and neck areas, we assessed the presence of four histological features (tumor/stroma ratio, immune infiltration at the front of invasion, tumor-budding activity, and tumor necrosis), their correlations with tumor type (mucosal or cutaneous), tumor clinicopathological characteristics, and their prognostic potential. Results: the comparison between histological features in cutaneous versus mucosal SCC reveals no significant differences for any of the four parameters assessed. We found significant correlations between tumor/stroma ratio and lymphatic metastasis (p = 0.0275), perineural invasion (p = 0.0006), and clinical staging (p = 0.0116). Immune infiltration at the front of invasion revealed similar correlations with lymph node involvement (p = 0.002), perineural invasion (p = 0.0138), and clinical staging (p = 0.0043). Tumor budding and tumor necrosis correlated with the size of the tumor (p = 0.0077 and p = 0.0004) and the clinical staging (p = 0.0039 and p = 0.0143). In addition, tumor budding was significantly correlated with perineural invasion (p = 0.0454). In mucosal SCC, patients with improved outcome revealed high values for the tumor/stroma ratio (p = 0.0159) and immune infiltration at the front of invasion (p = 0.0274). However, the multivariate analysis did not confirm their independent prognostic roles. Conclusions: extended histological assessments that include features such as tumor/stroma ratio, immune infiltration at the front of invasion, tumor budding, and tumor necrosis can be an easy, accessible method to collect additional information on tumor aggressiveness in skin and mucosa SCC affecting the head and neck areas. Full article

(This article belongs to the Special Issue Molecular Targets and Chemoprevention (Tumor Growth and Metastasis))

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Review

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13 pages, 700 KiB

Open AccessReview

Updates on Molecular and Biochemical Development and Progression of Prostate Cancer

by Omar Fahmy, Nabil A. Alhakamy, Waleed Y. Rizg, Alaa Bagalagel, Abdulmohsin J. Alamoudi, Hibah M. Aldawsari, Aiah M. Khateb, Basmah M. Eldakhakhny, Usama A. Fahmy, Wesam H. Abdulaal, Claudia G. Fresta and Giuseppe Caruso

J. Clin. Med. 2021, 10(21), 5127; https://doi.org/10.3390/jcm10215127 - 31 Oct 2021

Cited by 7 | Viewed by 2421

Abstract

Prostate cancer (PCa) represents the most commonly non-cutaneous diagnosed cancer in men worldwide and occupies a very wide area of preclinical and clinical research. Targeted therapy for any cancer depends on the understanding of the molecular bases and natural behaviour of the diseases. Despite the well-known effect of androgen deprivation on PCa, many patients develop resistance either for antiandrogen therapy or other new treatment modalities such as checkpoint inhibitors and chemotherapy. Comprehensive understanding of the development of PCa as well as of the mechanisms underlying its progression is mandatory to maximise the benefit of the current approved medications or to guide the future research for targeted therapy of PCa. The aim of this review was to provide updates on the most recent mechanisms regarding the development and the progression of PCa. According to the current understanding, future treatment strategies should include more predictive genetic and biomarker analysis to assign different patients to the expected most appropriate and effective treatment. Full article

(This article belongs to the Special Issue Molecular Targets and Chemoprevention (Tumor Growth and Metastasis))

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