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Molecular Mechanism of Anti-cancer Drugs
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Molecular Mechanism of Anti-cancer Drugs

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 (30 November 2023) | Viewed by 8029

Special Issue Editor

Dr. Elena Andreucci

E-Mail Website
Guest Editor
Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, Section of Experimental Pathology and Oncology, University of Florence, V. le Morgagni, 50, 50134 Florence, Italy
Interests: tumor microenvironment; extracellular acidosis; tumor angiogenesis; tumor-derived extracellular vescicles (exososmes-ectososmes); cancer metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Despite the continuous progress in oncology research, cancer still represents a major health issue worldwide. Preventive medicine and the increasing screening procedures allow to date for diagnosing tumours at their earlier stages, that in this case can be often removed by surgical resection. For advanced and inoperable malignancies instead, pharmacological treatments are needed either as a way to reduce the mass volume and render the tumour eligible for surgery or, when not possible, as an alternative method to the surgical resection. In recent decades, new classes of anti-cancer drugs, such as targeted therapy and immunotherapy, have been introduced in the clinic besides chemo- and radiotherapy, bringing great benefits to cancer patients. Despite these huge advances gained in a few years, the problem of drug resistance onset is still massively present and deserves the attention of the entire scientific community. The understanding of the molecular mechanisms of anti-cancer drugs becomes therefore crucial to identify their weaknesses and strengths so that more and more precise and effective treatments can be developed and offered to cancer patients. Thereby, in this Special Issue research articles, short communications and systematic reviews are welcomed to bring significant contributions to this topic.

Dr. Elena Andreucci
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

  • molecular medicine
  • new anti-cancer targets
  • conventional therapies
  • combined therapies
  • immunotherapy
  • targeted therapy
  • chemotherapy
  • radiotherapy

Published Papers (5 papers)

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Research

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19 pages, 4370 KiB  
Article
Identification of Key Molecular Pathways and Associated Genes as Targets to Overcome Radiotherapy Resistance Using a Combination of Radiotherapy and Immunotherapy in Glioma Patients
by Tianqi Zhang, Qiao Zhang, Xinwei He, Yuting Lu, Andrew Shao, Xiaoqiang Sun and Yongzhao Shao
Int. J. Mol. Sci. 2024, 25(5), 3076; https://doi.org/10.3390/ijms25053076 - 6 Mar 2024
Viewed by 1241
Abstract
Recent mechanistic studies have indicated that combinations of radiotherapy (RT) plus immunotherapy (via CSF-1R inhibition) can serve as a strategy to overcome RT resistance and improve the survival of glioma mice. Given the high mortality rate for glioma, including low-grade glioma (LGG) patients, [...] Read more.
Recent mechanistic studies have indicated that combinations of radiotherapy (RT) plus immunotherapy (via CSF-1R inhibition) can serve as a strategy to overcome RT resistance and improve the survival of glioma mice. Given the high mortality rate for glioma, including low-grade glioma (LGG) patients, it is of critical importance to investigate the mechanism of the combination of RT and immunotherapy and further translate the mechanism from mouse studies to improve survival of RT-treated human glioma patients. Using the RNA-seq data from a glioma mouse study, 874 differentially expressed genes (DEGs) between the group of RT-treated mice at glioma recurrence and the group of mice with combination treatment (RT plus CSF-1R inhibition) were translated to the human genome to identify significant molecular pathways using the KEGG enrichment analysis. The enrichment analysis yields statistically significant signaling pathways, including the phosphoinositide 3-kinase (PI3K)/AKT pathway, Hippo pathway, and Notch pathway. Within each pathway, a candidate gene set was selected by Cox regression models as genetic biomarkers for resistance to RT and response to the combination of RT plus immunotherapies. Each Cox model is trained using a cohort of 295 RT-treated LGG patients from The Cancer Genome Atlas (TCGA) database and validated using a cohort of 127 RT-treated LGG patients from the Chinese Glioma Genome Atlas (CGGA) database. A four-DEG signature (ITGB8, COL9A3, TGFB2, JAG1) was identified from the significant genes within the three pathways and yielded the area under time-dependent ROC curve AUC = 0.86 for 5-year survival in the validation set, which indicates that the selected DEGs have strong prognostic value and are potential intervention targets for combination therapies. These findings may facilitate future trial designs for developing combination therapies for glioma patients. Full article
(This article belongs to the Special Issue Molecular Mechanism of Anti-cancer Drugs)
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16 pages, 4722 KiB  
Article
Metallothionein Family Proteins as Regulators of Zinc Ions Synergistically Enhance the Anticancer Effect of Cannabidiol in Human Colorectal Cancer Cells
by In-Seo Kwon, Yu-Na Hwang, Ju-Hee Park, Han-Heom Na, Tae-Hyung Kwon, Jin-Sung Park and Keun-Cheol Kim
Int. J. Mol. Sci. 2023, 24(23), 16621; https://doi.org/10.3390/ijms242316621 - 22 Nov 2023
Cited by 1 | Viewed by 1302
Abstract
Cannabidiol (CBD) is a chemical obtained from Cannabis sativa; it has therapeutic effects on anxiety and cognition and anti-inflammatory properties. Although pharmacological applications of CBD in many types of tumors have recently been reported, the mechanism of action of CBD is not [...] Read more.
Cannabidiol (CBD) is a chemical obtained from Cannabis sativa; it has therapeutic effects on anxiety and cognition and anti-inflammatory properties. Although pharmacological applications of CBD in many types of tumors have recently been reported, the mechanism of action of CBD is not yet fully understood. In this study, we perform an mRNA-seq analysis to identify the target genes of CBD after determining the cytotoxic concentrations of CBD using an MTT assay. CBD treatment regulated the expression of genes related to DNA repair and cell division, with metallothionein (MT) family genes being identified as having highly increased expression levels induced by CBD. It was also found that the expression levels of MT family genes were decreased in colorectal cancer tissues compared to those in normal tissues, indicating that the downregulation of MT family genes might be highly associated with colorectal tumor progression. A qPCR experiment revealed that the expression levels of MT family genes were increased by CBD. Moreover, MT family genes were regulated by CBD or crude extract but not by other cannabinoids, suggesting that the expression of MT family genes was specifically induced by CBD. A synergistic effect between CBD and MT gene transfection or zinc ion treatment was found. In conclusion, MT family genes as novel target genes could synergistically increase the anticancer activity of CBD by regulating the zinc ions in human colorectal cancer cells. Full article
(This article belongs to the Special Issue Molecular Mechanism of Anti-cancer Drugs)
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16 pages, 3505 KiB  
Article
Sodium Butyrate Enhances the Cytotoxic Effect of Etoposide in HDACi-Sensitive and HDACi-Resistant Transformed Cells
by Olga O. Gnedina, Alisa V. Morshneva and Maria V. Igotti
Int. J. Mol. Sci. 2023, 24(21), 15913; https://doi.org/10.3390/ijms242115913 - 2 Nov 2023
Viewed by 901
Abstract
To overcome the problem of antitumor agent toxicity for normal cells, a combined therapy using drugs with synergistic effects seems to be more effective. We investigated the molecular mechanisms of the sensitization of tumor cells resistant and sensitive to histone deacetylase inhibitors (HDACis) [...] Read more.
To overcome the problem of antitumor agent toxicity for normal cells, a combined therapy using drugs with synergistic effects seems to be more effective. We investigated the molecular mechanisms of the sensitization of tumor cells resistant and sensitive to histone deacetylase inhibitors (HDACis) upon etoposide treatment together with the HDACi sodium butyrate (NaBut). We showed that NaBut enhances the cytotoxic effect of etoposide in both HDACi-sensitive and HDACi-resistant cells due to the accumulation of the Bax protein and the dissociation of Ku70–Bax inhibitory complexes. In HDACi-resistant cells, NaBut causes the cytoplasmic accumulation of Bax dissociated from mitochondria in complexes with Ku70 proteins. The increased phosphorylation of the pro-apoptotic Bad protein due to the NaBut-induced activation of Erk and Akt kinases is one of the possible reasons for the accumulation of Bax in the cytoplasm. Despite the inactivation of Bax in HDACi-resistant cells, its accumulation in the cytoplasm upon NaBut treatment makes it possible to enhance the apoptotic response against agents activating the intrinsic pathway of apoptosis. Thus, HDACis involved in combined therapy mediate the sensitization of tumor cells to genotoxic drugs, regardless of the cells’ resistance to HDACis. Full article
(This article belongs to the Special Issue Molecular Mechanism of Anti-cancer Drugs)
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13 pages, 3245 KiB  
Article
TP5: A Novel Therapeutic Approach Targeting Aberrant and Hyperactive CDK5/p25 for the Treatment of Colorectal Carcinoma
by Niranjana Amin, Herui Wang, Qi Song, Manju Bhaskar, Sharda Prasad Yadav, Mark R. Gilbert, Harish Pant, Emeline Tabouret and Zhengping Zhuang
Int. J. Mol. Sci. 2023, 24(14), 11733; https://doi.org/10.3390/ijms241411733 - 21 Jul 2023
Viewed by 1488
Abstract
Colorectal carcinoma (CRC) is a prevalent cancer worldwide with a high mortality rate. Evidence suggests that increased expression of Cyclin-dependent kinase 5 (CDK5) contributes to cancer progression, making it a promising target for treatment. This study examined the efficacy of selectively [...] Read more.
Colorectal carcinoma (CRC) is a prevalent cancer worldwide with a high mortality rate. Evidence suggests that increased expression of Cyclin-dependent kinase 5 (CDK5) contributes to cancer progression, making it a promising target for treatment. This study examined the efficacy of selectively inhibiting CDK5 in colorectal carcinoma using TP5, a small peptide that selectively inhibits the aberrant and hyperactive CDK5/p25 complex while preserving physiological CDK5/p35 functions. We analyzed TP5’s impact on CDK5 activity, cell survival, apoptosis, the cell cycle, DNA damage, ATM phosphorylation, and reactive oxygen species (ROS) signaling in mitochondria, in CRC cell lines, both alone and in combination with chemotherapy. We also assessed TP5’s efficacy on a xenograft mouse model with HCT116 cells. Our results showed that TP5 decreased CDK5 activity, impaired cell viability and colony formation, induced apoptosis, increased DNA damage, and led to the G1 phase arrest of cell cycle progression. In combination with irinotecan, TP5 demonstrated a synergy by leading to the accumulation of DNA damage, increasing the γH2A.X foci number, and inhibiting G2/M arrest induced by Sn38 treatment. TP5 alone or in combination with irinotecan increased mitochondrial ROS levels and inhibited tumor growth, prolonging mouse survival in the CRC xenograft animal model. These results suggest that TP5, either alone or in combination with irinotecan, is a promising therapeutic option for colorectal carcinoma. Full article
(This article belongs to the Special Issue Molecular Mechanism of Anti-cancer Drugs)
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Review

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19 pages, 2429 KiB  
Review
Edaravone: A Novel Possible Drug for Cancer Treatment?
by Elisa Duranti, Nicoletta Cordani and Chiara Villa
Int. J. Mol. Sci. 2024, 25(3), 1633; https://doi.org/10.3390/ijms25031633 - 29 Jan 2024
Viewed by 2159
Abstract
Despite significant advancements in understanding the causes and progression of tumors, cancer remains one of the leading causes of death worldwide. In light of advances in cancer therapy, there has been a growing interest in drug repurposing, which involves exploring new uses for [...] Read more.
Despite significant advancements in understanding the causes and progression of tumors, cancer remains one of the leading causes of death worldwide. In light of advances in cancer therapy, there has been a growing interest in drug repurposing, which involves exploring new uses for medications that are already approved for clinical use. One such medication is edaravone, which is currently used to manage patients with cerebral infarction and amyotrophic lateral sclerosis. Due to its antioxidant and anti-inflammatory properties, edaravone has also been investigated for its potential activities in treating cancer, notably as an anti-proliferative and cytoprotective drug against side effects induced by traditional cancer therapies. This comprehensive review aims to provide updates on the various applications of edaravone in cancer therapy. It explores its potential as a standalone antitumor drug, either used alone or in combination with other medications, as well as its role as an adjuvant to mitigate the side effects of conventional anticancer treatments. Full article
(This article belongs to the Special Issue Molecular Mechanism of Anti-cancer Drugs)
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