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Anticancer Drugs Activity and Underlying Mechanism
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Anticancer Drugs Activity and Underlying Mechanism

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 (31 May 2023) | Viewed by 19708

Special Issue Editors

Dr. Apostolos E. Papalois

E-Mail Website
Guest Editor
2nd Department of Surgery, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece
Interests: new molecule development; pre-clinical studies; translational research; new technologies in surgery; education and simulation; leadership in research
Special Issues, Collections and Topics in MDPI journals
Dr. Georgios Antonios Margonis

E-Mail Website
Guest Editor
Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
Interests: colorectal liver metastases; colorectal cancer; pancreas cancer; IBD; Artificial Intelligence; precision oncology; precision surgery; targeted therapies; tumor biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The National Cancer Institute defines oncologic precision medicine as the “use of specific information about a person’s tumor to help make a diagnosis, plan treatment, find out how well treatment is working, or make a prognosis.” Specific information about a person’s tumor includes the identification of specific molecules ("molecular targets") that are involved in the growth, progression, and spread of cancer. Examples of conceptually different molecular targets include the overexpression of the normally expressed HER2+ protein and the expression of the abnormal (mutated) BRAF protein. These molecules are then targeted by drugs or other substances which collectively constitute the targeted cancer therapies. Since the advent of the first small molecule targeted agent (the BCR-ABL kinase inhibitor imatinib) three decades ago, the targeted, mechanism-based therapeutics along with immunotherapy have changed the paradigm for cancer treatment, which used to rely on relatively non-specific cytotoxic agents. This special issue invites original and review papers on targeted cancer therapies in any malignancy. Since IJMS is a journal of molecular science, pure clinical studies will not be suitable for this special issue.

Dr. Apostolos E. Papalois
Dr. Georgios Antonios Margonis
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.

Published Papers (4 papers)

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Research

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18 pages, 3866 KiB  
Article
SHP-1/STAT3-Signaling-Axis-Regulated Coupling between BECN1 and SLC7A11 Contributes to Sorafenib-Induced Ferroptosis in Hepatocellular Carcinoma
by Chao-Yuan Huang, Li-Ju Chen, Grace Chen, Tzu-I Chao and Cheng-Yi Wang
Int. J. Mol. Sci. 2022, 23(19), 11092; https://doi.org/10.3390/ijms231911092 - 21 Sep 2022
Cited by 17 | Viewed by 3011
Abstract
Ferroptosis is a type of iron-dependent cell death pertaining to an excess of lipid peroxidation. It has been suggested that sorafenib—an anti-angiogenic medication for hepatocellular carcinoma (HCC)—induces ferroptosis, but the underlying mechanism for this remains largely unknown. We employed siRNA-mediated gene silencing to [...] Read more.
Ferroptosis is a type of iron-dependent cell death pertaining to an excess of lipid peroxidation. It has been suggested that sorafenib—an anti-angiogenic medication for hepatocellular carcinoma (HCC)—induces ferroptosis, but the underlying mechanism for this remains largely unknown. We employed siRNA-mediated gene silencing to investigate the role of Src homology region 2 domain-containing phosphatase-1 (SHP-1), following sorafenib treatment, in cystine/glutamate-antiporter-system-Xc−-regulated cystine uptake. Co-immunoprecipitation was also performed to examine the interactions between MCL1, beclin 1 (BECN1), and solute carrier family 7 member 11 (SLC7A11), which functions as the catalytic subunit of system Xc−. The results of this study showed that sorafenib enhanced the activity of SHP-1, dephosphorylated STAT3, downregulated the expression of MCL1 and, consequently, reduced the association between MCL1 and BECN1. In contrast, increased binding between BECN1 and SLC7A11 was observed following sorafenib treatment. The elevated interaction between BECN1 and SLC7A11 inhibited the activity of system Xc−, whereas BECN1 silencing restored cystine intake and protected cells from ferroptosis. Notably, ectopic expression of MCL1 uncoupled BECN1 from SLC7A11 and rescued cell viability by attenuating lipid peroxidation. The results revealed that ferroptosis could be induced in HCC via SHP-1/STAT3-mediated downregulation of MCL1 and subsequent inhibition of SLC7A11 by increased BECN1 binding. Full article
(This article belongs to the Special Issue Anticancer Drugs Activity and Underlying Mechanism)
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Review

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26 pages, 803 KiB  
Review
Pharmacological Agents Used in the Prevention and Treatment of Actinic Keratosis: A Review
by Domenico Arcuri, Brandon Ramchatesingh, François Lagacé, Lisa Iannattone, Elena Netchiporouk, Philippe Lefrançois and Ivan V. Litvinov
Int. J. Mol. Sci. 2023, 24(5), 4989; https://doi.org/10.3390/ijms24054989 - 5 Mar 2023
Cited by 7 | Viewed by 5428
Abstract
Actinic keratosis (AK) is among the most commonly diagnosed skin diseases with potentially life-threatening repercussions if left untreated. Usage of pharmacologic agents represents one of many therapeutic strategies that can be used to help manage these lesions. Ongoing research into these compounds continues [...] Read more.
Actinic keratosis (AK) is among the most commonly diagnosed skin diseases with potentially life-threatening repercussions if left untreated. Usage of pharmacologic agents represents one of many therapeutic strategies that can be used to help manage these lesions. Ongoing research into these compounds continues to change our clinical understanding as to which agents most benefit particular patient populations. Indeed, factors such as past personal medical history, lesion location and tolerability of therapy only represent a few considerations that clinicians must account for when prescribing appropriate treatment. This review focuses on specific drugs used in either the prevention or treatment of AKs. Nicotinamide, acitretin and topical 5-fluorouracil (5-FU) continue to be used with fidelity in the chemoprevention of actinic keratosis, although some uncertainty persists in regard to which agents should be used in immunocompetent vs. immunodeficient/immunosuppressed patients. Topical 5-FU, including combination formulations with either calcipotriol or salicylic acid, as well as imiquimod, diclofenac and photodynamic light therapy are all accepted treatment strategies employed to target and eliminate AKs. Five percent of 5-FU is regarded as the most effective therapy in the condition, although the literature has conflictingly shown that lower concentrations of the drug might also be as effective. Topical diclofenac (3%) appears to be less efficacious than 5% 5-FU, 3.75–5% imiquimod and photodynamic light therapy despite its favorable side effect profile. Finally, traditional photodynamic light therapy, while painful, appears to be of higher efficacy in comparison to its more tolerable counterpart, daylight phototherapy. Full article
(This article belongs to the Special Issue Anticancer Drugs Activity and Underlying Mechanism)
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31 pages, 2662 KiB  
Review
The Use of Retinoids for the Prevention and Treatment of Skin Cancers: An Updated Review
by Brandon Ramchatesingh, Amelia Martínez Villarreal, Domenico Arcuri, François Lagacé, Samy Abu Setah, Fadi Touma, Faris Al-Badarin and Ivan V. Litvinov
Int. J. Mol. Sci. 2022, 23(20), 12622; https://doi.org/10.3390/ijms232012622 - 20 Oct 2022
Cited by 11 | Viewed by 7351
Abstract
Retinoids are natural and synthetic vitamin A derivatives that are effective for the prevention and the treatment of non-melanoma skin cancers (NMSC). NMSCs constitute a heterogenous group of non-melanocyte-derived skin cancers that impose substantial burdens on patients and healthcare systems. They include entities [...] Read more.
Retinoids are natural and synthetic vitamin A derivatives that are effective for the prevention and the treatment of non-melanoma skin cancers (NMSC). NMSCs constitute a heterogenous group of non-melanocyte-derived skin cancers that impose substantial burdens on patients and healthcare systems. They include entities such as basal cell carcinoma and cutaneous squamous cell carcinoma (collectively called keratinocyte carcinomas), cutaneous lymphomas and Kaposi’s sarcoma among others. The retinoid signaling pathway plays influential roles in skin physiology and pathology. These compounds regulate diverse biological processes within the skin, including proliferation, differentiation, angiogenesis and immune regulation. Collectively, retinoids can suppress skin carcinogenesis. Both topical and systemic retinoids have been investigated in clinical trials as NMSC prophylactics and treatments. Desirable efficacy and tolerability in clinical trials have prompted health regulatory bodies to approve the use of retinoids for NMSC management. Acceptable off-label uses of these compounds as drugs for skin cancers are also described. This review is a comprehensive outline on the biochemistry of retinoids, their activities in the skin, their effects on cancer cells and their adoption in clinical practice. Full article
(This article belongs to the Special Issue Anticancer Drugs Activity and Underlying Mechanism)
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28 pages, 3467 KiB  
Review
The Role of HDACs in the Response of Cancer Cells to Cellular Stress and the Potential for Therapeutic Intervention
by Rahma K. Alseksek, Wafaa S. Ramadan, Ekram Saleh and Raafat El-Awady
Int. J. Mol. Sci. 2022, 23(15), 8141; https://doi.org/10.3390/ijms23158141 - 24 Jul 2022
Cited by 18 | Viewed by 3105
Abstract
Throughout the process of carcinogenesis, cancer cells develop intricate networks to adapt to a variety of stressful conditions including DNA damage, nutrient deprivation, and hypoxia. These molecular networks encounter genomic instability and mutations coupled with changes in the gene expression programs due to [...] Read more.
Throughout the process of carcinogenesis, cancer cells develop intricate networks to adapt to a variety of stressful conditions including DNA damage, nutrient deprivation, and hypoxia. These molecular networks encounter genomic instability and mutations coupled with changes in the gene expression programs due to genetic and epigenetic alterations. Histone deacetylases (HDACs) are important modulators of the epigenetic constitution of cancer cells. It has become increasingly known that HDACs have the capacity to regulate various cellular systems through the deacetylation of histone and bounteous nonhistone proteins that are rooted in complex pathways in cancer cells to evade death pathways and immune surveillance. Elucidation of the signaling pathways involved in the adaptive responses to cellular stress and the role of HDACs may lead to the development of novel therapeutic agents. In this article, we overview the dominant stress types including metabolic, oxidative, genotoxic, and proteotoxic stress imposed on cancer cells in the context of HDACs, which guide stress adaptation responses. Next, we expose a closer view on the therapeutic interventions and clinical trials that involve HDACs inhibitors, in addition to highlighting the impact of using HDAC inhibitors in combination with stress-inducing agents for the management of cancer and to overcome the resistance to current cancer therapy. Full article
(This article belongs to the Special Issue Anticancer Drugs Activity and Underlying Mechanism)
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