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Recent Advances in Anticancer Drugs III
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Recent Advances in Anticancer Drugs III

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 9332

Special Issue Editors

Prof. Dr. Simona Collina

E-Mail Website
Guest Editor
Department of Drug Sciences, Medicinal Chemistry and Pharmaceutical Technology Section, University of Pavia, Viale Taramelli 12, 27100 Pavia, Italy
Interests: rational drug design, synthesis and structure–activity relationships of biologically active compounds (small molecules and peptides); preparation and characterization of chiral compounds; discovery of new modulators of sigma receptors as well as of small molecules able to affect the protein kinase C (PKC)/ELAV proteins/mRNA system
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Mariarosaria Miloso

E-Mail Website
Guest Editor
School of Medicine and Surgery, University of Milano-Bicocca, Via Cadore 48, 20900 Monza, Italy
Interests: evaluation of antitumorigenic effects of natural and synthetic compounds; characterization of biological properties of mesenchymal stem cells from different sources
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Considering the wide interest in the previous editions, we announce with great pleasure the third edition of “Recent Advances in Anticancer Drugs”. 

Cancer is the second leading cause of death, responsible for almost one in six deaths globally. The aim of technological and scientific advances is to improve the survival and quality of life of people living with the disease. Oncology drug discovery and development, and the identification of biomarkers useful for early diagnosis, remain a challenge for all scientists working in this field. 

This Special Issue of Molecules will cover the major advancements and challenges in cancer drug discovery. It will report on the identification and evaluation of novel anticancer agents, biological targets, therapeutic approaches for exploring antitumor drugs, and anticancer drug delivery systems. We cordially invite researchers working in this field to contribute original research articles, short communications, and critical review articles. Short papers on one compound will be also welcome.

Prof. Dr. Simona Collina
Prof. Dr. Mariarosaria Miloso
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. Molecules 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 2700 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

  • anticancer drugs
  • drug discovery
  • biological targets
  • therapeutic approaches
  • biomarkers

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Published Papers (3 papers)

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Research

10 pages, 1830 KiB  
Article
Anti-Cancer Effects of Queen Bee Acid (10-Hydroxy-2-Decenoic Acid) and Its Cellular Mechanisms against Human Hepatoma Cells
by Zafer Saad Al Shehri, Abdullah D. Alanazi and Sultan F. Alnomasy
Molecules 2023, 28(4), 1972; https://doi.org/10.3390/molecules28041972 - 19 Feb 2023
Cited by 7 | Viewed by 3471
Abstract
Background: Hepatocellular carcinoma (HCC) is the most common form of liver cancer that occurs in hepatocytes. Although many chemical drugs, e.g., cisplatin, methotrexate, taxis, and doxorubicin are used to treat HCC, there have been numerous reports related to the side effects of these [...] Read more.
Background: Hepatocellular carcinoma (HCC) is the most common form of liver cancer that occurs in hepatocytes. Although many chemical drugs, e.g., cisplatin, methotrexate, taxis, and doxorubicin are used to treat HCC, there have been numerous reports related to the side effects of these drugs (e.g., emerging drug resistance, bone marrow failure, and gastrointestinal disorders). These issues led scientists to search for the novel anti-cancer drugs, mainly in natural products with greater efficiency and less toxicity. The current survey was intended to assess the anti-cancer effects of queen bee acid (10-Hydroxy-2-Decenoic Acid, 10-HDA) and its cellular mechanisms against the human hepatoma cell line HepG2. Materials and Methods: The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay was used to evaluate the effect of 10-HDA on the viability of HepG2 cells. The initial and late apoptosis in the HepG2 cells treated with 10-HDA were assessed by the Annexin-V (AV) assay. The level of the gene and protein expression of some apoptosis genes (e.g., caspase-3, Bcl-2-associated X protein (BAX), and B-cell lymphoma protein 2 (Bcl-2)), Poly (ADP-ribose) polymerases (PARP), and miRNA-34a (miR-34a), were measured by real-time PCR and Western blot. Results: The obtained findings revealed that HepG2 cell viability was markedly reduced (p < 0.01) following exposure to 10-HDA in a dose-dependent matter. The calculated half maximal cytotoxic concentration (CC50) value of 10-HDA was 59.6 µg/mL for HepG2 cells, while this value for normal THLE-3 cells was 106.4 µg/mL. We found that 10-HDA markedly elevated (p < 0.01) the percentage of necrotic and apoptotic cells from 0.94 to 9.7 and 27.6%, respectively. The real-time PCR results showed that the expression levels of the caspase-3, Bax, and miR-34a genes were significantly (p < 0.001) elevated. Contrary to these results, a significant (p < 0.01) reduction in the expression level of the Bcl2 gene was observed. The levels of protein expression of Caspase-3, PARP, and Bax were markedly elevated following exposure of HepG2 cells to 10-HDA at ¼ CC50, ½ CC50, and CC50. The level of protein expression of Bcl-2 was markedly reduced following exposure of HepG2 cells to 10-HDA at ¼ CC50, ½ CC50, and CC50 (p < 0.01). Conclusion: The current results confirmed the potent in vitro cytotoxic effects of 10-HDA on HepG2 cells with no significant cytotoxic effects on normal cells. Although its mechanisms of action have not been fully studied, the induction of apoptosis via different pathways was determined as one of the principle mechanisms of action of 10-HDA against HepG2 cells. Nevertheless, additional surveys must be performed to clearly understand the mechanisms of action and safety of this fatty acid. Full article
(This article belongs to the Special Issue Recent Advances in Anticancer Drugs III)
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21 pages, 2713 KiB  
Article
Anticancer Cytotoxic Activity of Bispidine Derivatives Associated with the Increasing Catabolism of Polyamines
by Ekaterina V. Neborak, Altynay B. Kaldybayeva, Lylia Bey, Aigul Y. Malmakova, Anna S. Tveritinova, Abdullah Hilal, Valentina K. Yu, Maria V. Ploskonos, Marina V. Komarova, Enzo Agostinelli and Dmitry D. Zhdanov
Molecules 2022, 27(12), 3872; https://doi.org/10.3390/molecules27123872 - 16 Jun 2022
Cited by 3 | Viewed by 2875
Abstract
Polyamine (PA) catabolism is often reduced in cancer cells. The activation of this metabolic pathway produces cytotoxic substances that might cause apoptosis in cancer cells. Chemical compounds able to restore the level of PA catabolism in tumors could become potential antineoplastic agents. The [...] Read more.
Polyamine (PA) catabolism is often reduced in cancer cells. The activation of this metabolic pathway produces cytotoxic substances that might cause apoptosis in cancer cells. Chemical compounds able to restore the level of PA catabolism in tumors could become potential antineoplastic agents. The search for activators of PA catabolism among bicyclononan-9-ones is a promising strategy for drug development. The aim of the study was to evaluate the biological activity of new 3,7-diazabicyclo[3.3.1]nonan-9-one derivatives that have antiproliferative properties by accelerating PA catabolism. Eight bispidine derivatives were synthetized and demonstrated the ability to activate PA catabolism in regenerating rat liver homogenates. However, only three of them demonstrated a potent ability to decrease the viability of cancer cells in the MTT assay. Compounds 4c and 4e could induce apoptosis more effectively in cancer HepG2 cells rather than in normal WI-38 fibroblasts. The lead compound 4e could significantly enhance cancer cell death, but not the death of normal cells if PAs were added to the cell culture media. Thus, the bispidine derivative 4e 3-(3-methoxypropyl)-7-[3-(1H-piperazin-1-yl)ethyl]-3,7-diazabicyclo[3.3.1]nonane could become a potential anticancer drug substance whose mechanism relies on the induction of PA catabolism in cancer cells. Full article
(This article belongs to the Special Issue Recent Advances in Anticancer Drugs III)
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13 pages, 738 KiB  
Article
Expression of Growth Hormone-Releasing Hormone and Its Receptor Splice Variants in Primary Human Endometrial Carcinomas: Novel Therapeutic Approaches
by Zsuzsanna Szabo, Eva Juhasz, Andrew V. Schally, Balazs Dezso, Sandor Huga, Zoltan Hernadi, Gabor Halmos and Csongor Kiss
Molecules 2022, 27(9), 2671; https://doi.org/10.3390/molecules27092671 - 21 Apr 2022
Cited by 7 | Viewed by 2088
Abstract
Antagonists of growth hormone-releasing hormone (GHRH) inhibit the growth of various tumors, including endometrial carcinomas (EC). However, tumoral receptors that mediate the antiproliferative effects of GHRH antagonists in human ECs have not been fully characterized. In this study, we investigated the expression of [...] Read more.
Antagonists of growth hormone-releasing hormone (GHRH) inhibit the growth of various tumors, including endometrial carcinomas (EC). However, tumoral receptors that mediate the antiproliferative effects of GHRH antagonists in human ECs have not been fully characterized. In this study, we investigated the expression of mRNA for GHRH and splice variants (SVs) of GHRH receptors (GHRH-R) in 39 human ECs and in 7 normal endometrial tissue samples using RT-PCR. Primers designed for the PCR amplification of mRNA for the full length GHRH-R and SVs were utilized. The PCR products were sequenced, and their specificity was confirmed. Nine ECs cancers (23%) expressed mRNA for SV1, three (7.7%) showed SV2 and eight (20.5%) revealed mRNA for SV4. The presence of SVs for GHRH-Rs could not be detected in any of the normal endometrial tissue specimens. The presence of specific, high affinity GHRH-Rs was also demonstrated in EC specimens using radioligand binding studies. Twenty-four of the investigated thirty-nine tumor samples (61.5%) and three of the seven corresponding normal endometrial tissues (42.9%) expressed mRNA for GHRH ligand. Our findings suggest the possible existence of an autocrine loop in EC based on GHRH and its tumoral SV receptors. The antiproliferative effects of GHRH antagonists on EC are likely to be exerted in part by the local SVs and GHRH system. Full article
(This article belongs to the Special Issue Recent Advances in Anticancer Drugs III)
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