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Novel Targeted Therapies and Drugs in Cancer
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Novel Targeted Therapies and Drugs in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 5250

Special Issue Editor

Dr. Maria Teresa Vietri

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138 Naples, Italy
Interests: hereditary cancer; molecular diagnosis; clinical pathology; genes related to hereditary cancer; DNA mutations and drug response; BRCA1, BRCA2 genes

Special Issue Information

Dear Colleagues,

During recent years, considerable strides have been made in the understanding and treatment of cancers.

A greater understanding of cancer’s genesis and underlying molecular biology has also influenced the therapeutic landscape. Novel targeted therapies of increasing interest, as evidenced by FDA-approved targeted cancer drugs, block biologic transduction pathways and/or are based on specific cancer proteins to induce the death of cancer cells by means of apoptosis and the stimulation of the immune system, or to minimize undesirable side effects after the use of chemotherapeutic agents.

Poly (ADP-ribose) polymerase (PARP) inhibitors, antiangiogenic therapies, immunotherapy combinations, and targeted agents have changed the standard of care in several cancers, such as breast, ovarian, pancreatic, and prostatic cancer.

The use of PARP inhibitors has shown positive results in patients with BRCA mutations: BRCA protein deficiency, due to mutations, causes this pathway to be inhibited, inducing cell death.

Continued molecular analyses of cancers are leading to the identification of new targetable pathways with the development of drugs, which are being investigated in clinical trials. The aim is to improve the lives of patients impacted by these diseases, but also, in regard to the economic and social spheres, reduce the costs of healthcare systems.

For these reasons, we believe it is important to prepare a Special Issue with the title “Novel Targeted Therapies and Drugs in Cancer”.

It would be a pleasure for us if you agreed to contribute your paper to this Special Issue.

Dr. Maria Teresa Vietri
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. 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

  • targeted therapies
  • genetic mutation
  • PARP inhibitors
  • immunotherapy
  • drug development
  • cancer molecular analysis
  • drug response
  • molecular-targeted therapy

Published Papers (3 papers)

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Research

20 pages, 4001 KiB  
Article
Transcriptome Analysis Reveals Anti-Cancer Effects of Isorhapontigenin (ISO) on Highly Invasive Human T24 Bladder Cancer Cells
by Alex H. Li, Sun Young Park, Peiwei Li, Chaoting Zhou, Thomas Kluz, Jingxia Li, Max Costa and Hong Sun
Int. J. Mol. Sci. 2024, 25(3), 1783; https://doi.org/10.3390/ijms25031783 - 1 Feb 2024
Viewed by 913
Abstract
Bladder cancer, the most common malignancy of the urinary tract, has a poor overall survival rate when the tumor becomes muscle invasive. The discovery and evaluation of new alternative medications targeting high-grade muscle invasive bladder cancer (MIBC) are of tremendous importance in reducing [...] Read more.
Bladder cancer, the most common malignancy of the urinary tract, has a poor overall survival rate when the tumor becomes muscle invasive. The discovery and evaluation of new alternative medications targeting high-grade muscle invasive bladder cancer (MIBC) are of tremendous importance in reducing bladder cancer mortality. Isorhapontigenin (ISO), a stilbene derivative from the Chinese herb Gnetum cleistostachyum, exhibits a strong anti-cancer effect on MIBCs. Here, we report the whole transcriptome profiling of ISO-treated human bladder cancer T24 cells. A total of 1047 differentially expressed genes (DEGs) were identified, including 596 downregulated and 451 upregulated genes. Functional annotation and pathway analysis revealed that ISO treatment induced massive changes in gene expression associated with cell movement, migration, invasion, metabolism, proliferation, and angiogenesis. Additionally, ISO treatment-activated genes involved in the inflammatory response but repressed genes involved in hypoxia signaling, glycolysis, the actin cytoskeleton, and the tumor microenvironment. In summary, our whole transcriptome analysis demonstrated a shift in metabolism and altered actin cytoskeleton in ISO-treated T24 cells, which subsequently contribute to tumor microenvironment remodeling that suppresses tumor growth and progression. Full article
(This article belongs to the Special Issue Novel Targeted Therapies and Drugs in Cancer)
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Figure 1

27 pages, 10164 KiB  
Article
A Novel Tri-Hydroxy-Methylated Chalcone Isolated from Chromolaena tacotana with Anti-Cancer Potential Targeting Pro-Survival Proteins
by Gina Mendez-Callejas, Marco Piñeros-Avila, Juvenal Yosa-Reyes, Roberto Pestana-Nobles, Ruben Torrenegra, María F. Camargo-Ubate, Andrea E. Bello-Castro and Crispin A. Celis
Int. J. Mol. Sci. 2023, 24(20), 15185; https://doi.org/10.3390/ijms242015185 - 14 Oct 2023
Cited by 1 | Viewed by 1619
Abstract
Chromolaena tacotana (Klatt) R. M. King and H. Rob (Ch. tacotana) contains bioactive flavonoids that may have antioxidant and/or anti-cancer properties. This study investigated the potential anti-cancer properties of a newly identified chalcone isolated from the inflorescences of the [...] Read more.
Chromolaena tacotana (Klatt) R. M. King and H. Rob (Ch. tacotana) contains bioactive flavonoids that may have antioxidant and/or anti-cancer properties. This study investigated the potential anti-cancer properties of a newly identified chalcone isolated from the inflorescences of the plant Chromolaena tacotana (Klatt) R. M. King and H. Rob (Ch. tacotana). The chalcone structure was determined using HPLC/MS (QTOF), UV, and NMR spectroscopy. The compound cytotoxicity and selectivity were evaluated on prostate, cervical, and breast cancer cell lines using the MTT assay. Apoptosis and autophagy induction were assessed through flow cytometry by detecting annexin V/7-AAD, active Casp3/7, and LC3B proteins. These results were supported by Western blot analysis. Mitochondrial effects on membrane potential, as well as levels of pro- and anti-apoptotic proteins were analyzed using flow cytometry, fluorescent microscopy, and Western blot analysis specifically on a triple-negative breast cancer (TNBC) cell line. Furthermore, molecular docking (MD) and molecular dynamics (MD) simulations were performed to evaluate the interaction between the compounds and pro-survival proteins. The compound identified as 2′,3,4-trihydroxy-4′,6′-dimethoxy chalcone inhibited the cancer cell line proliferation and induced apoptosis and autophagy. MDA-MB-231, a TNBC cell line, exhibited the highest sensitivity to the compound with good selectivity. This activity was associated with the regulation of mitochondrial membrane potential, activation of the pro-apoptotic proteins, and reduction of anti-apoptotic proteins, thereby triggering the intrinsic apoptotic pathway. The chalcone consistently interacted with anti-apoptotic proteins, particularly the Bcl-2 protein, throughout the simulation period. However, there was a noticeable conformational shift observed with the negative autophagy regulator mTOR protein. Future studies should focus on the molecular mechanisms underlying the anti-cancer potential of the new chalcone and other flavonoids from Ch. tacotana, particularly against predominant cancer cell types. Full article
(This article belongs to the Special Issue Novel Targeted Therapies and Drugs in Cancer)
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26 pages, 41378 KiB  
Article
Evolution of Resistance to Irinotecan in Cancer Cells Involves Generation of Topoisomerase-Guided Mutations in Non-Coding Genome That Reduce the Chances of DNA Breaks
by Santosh Kumar, Valid Gahramanov, Shivani Patel, Julia Yaglom, Lukasz Kaczmarczyk, Ivan A. Alexandrov, Gabi Gerlitz, Mali Salmon-Divon and Michael Y. Sherman
Int. J. Mol. Sci. 2023, 24(10), 8717; https://doi.org/10.3390/ijms24108717 - 13 May 2023
Cited by 2 | Viewed by 1802
Abstract
Resistance to chemotherapy is a leading cause of treatment failure. Drug resistance mechanisms involve mutations in specific proteins or changes in their expression levels. It is commonly understood that resistance mutations happen randomly prior to treatment and are selected during the treatment. However, [...] Read more.
Resistance to chemotherapy is a leading cause of treatment failure. Drug resistance mechanisms involve mutations in specific proteins or changes in their expression levels. It is commonly understood that resistance mutations happen randomly prior to treatment and are selected during the treatment. However, the selection of drug-resistant mutants in culture could be achieved by multiple drug exposures of cloned genetically identical cells and thus cannot result from the selection of pre-existent mutations. Accordingly, adaptation must involve the generation of mutations de novo upon drug treatment. Here we explored the origin of resistance mutations to a widely used Top1 inhibitor, irinotecan, which triggers DNA breaks, causing cytotoxicity. The resistance mechanism involved the gradual accumulation of recurrent mutations in non-coding regions of DNA at Top1-cleavage sites. Surprisingly, cancer cells had a higher number of such sites than the reference genome, which may define their increased sensitivity to irinotecan. Homologous recombination repairs of DNA double-strand breaks at these sites following initial drug exposures gradually reverted cleavage-sensitive “cancer” sequences back to cleavage-resistant “normal” sequences. These mutations reduced the generation of DNA breaks upon subsequent exposures, thus gradually increasing drug resistance. Together, large target sizes for mutations and their Top1-guided generation lead to their gradual and rapid accumulation, synergistically accelerating the development of resistance. Full article
(This article belongs to the Special Issue Novel Targeted Therapies and Drugs in Cancer)
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