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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: 30 June 2024 | Viewed by 9754

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Dr. Julita Kulbacka

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Department of Molecular and Cellular Biology, Wroclaw Medical University, 50-367 Wroclaw, Poland
Interests: drug delivery; drug resistance; electroporation; photodynamic therapy; oxidative stress and free radicals; natural chemotherapeutics; nanotechnology
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of the 2022 Special Issue “Targeted Therapies and Molecular Methods in Cancer”.

This Special Issue of IJMS will examine targeted strategies for dealing with cancer. We welcome articles on new, targeted anticancer methods, new ways for delivering drugs, and entirely new approaches, including, but not limited to: immunotherapy; new aspects of radiotherapy; methods to facilitate drug delivery, such as pulsed electric fields (PEF), sonoporation, magnetic fields (MF), nanotechnology, and nanocarriers; and gene electrotransfer using PEF. Targeted anticancer methods can focus on membrane proteins and ion channel alterations, targets can be specific surface receptors (ER—estrogen receptors, FAR—folic acid receptors, HAR—hyaluronic acid receptors) or cancer biomarkers. Research targeting drug resistance (MDR), aimed at bypassing or modifying the activity of drug transporters, i.e., MDR1/P-gp, MRP1, BCRP, and LRP, etc., will be of interest. We are interested in new and more effective protocols, which could be developed and find potential applications in pharmacy and medical sciences. This Special Issue will cover the latest research concerning targeted therapies and molecular methods against cancer.

Dr. Julita Kulbacka
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.

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Keywords

immunotherapy
radiotherapy
methods using facilitated drug delivery such as electroporation, sonoporation, and magnetic fields
nanotechnology and nanocarriers
gene electrotherapy
intelligent predicting methods with AI

Published Papers (7 papers)

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Research

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18 pages, 2805 KiB

Open AccessArticle

Side-Chain Modified [^99mTc]Tc-DT1 Mimics: A Comparative Study in NTS₁R-Positive Models

by Panagiotis Kanellopoulos, Berthold A. Nock, Maritina Rouchota, George Loudos, Eric P. Krenning and Theodosia Maina

Int. J. Mol. Sci. 2023, 24(21), 15541; https://doi.org/10.3390/ijms242115541 - 24 Oct 2023

Viewed by 781

Abstract

Radiolabeled neurotensin analogs have been developed as candidates for theranostic use against neurotensin subtype 1 receptor (NTS₁R)-expressing cancer. However, their fast degradation by two major peptidases, neprilysin (NEP) and angiotensin-converting enzyme (ACE), has hitherto limited clinical success. We have recently shown that palmitoylation at the ε-amine of Lys⁷ in [^99mTc]Tc-[Lys⁷]DT1 (DT1, N₄-Gly-Arg-Arg-Pro-Tyr-Ile-Leu-OH, N₄ = 6-(carboxy)-1,4,8,11-tetraazaundecane) led to the fully stabilized [^99mTc]Tc-DT9 analog, displaying high uptake in human pancreatic cancer AsPC-1 xenografts but unfavorable pharmacokinetics in mice. Aiming to improve the in vivo stability of [^99mTc]Tc-DT1 without compromising pharmacokinetics, we now introduce three new [^99mTc]Tc-DT1 mimics, carrying different pendant groups at the ε-amine of Lys⁷: MPBA (4-(4-methylphenyl)butyric acid)—[^99mTc]Tc-DT10; MPBA via a PEG4-linker—[^99mTc]Tc-DT11; or a hydrophilic PEG6 chain—[^99mTc]Tc-DT12. The impact of these modifications on receptor affinity and internalization was studied in NTS₁R-positive cells. The effects on stability and AsPC-1 tumor uptake were assessed in mice without or during NEP/ACE inhibition. Unlike [^99mTc]Tc-DT10, the longer-chain modified [^99mTc]Tc-DT11 and [^99mTc]Tc-DT12 were significantly stabilized in vivo, resulting in markedly improved tumor uptake compared to [^99mTc]Tc-DT1. [^99mTc]Tc-DT11 was found to achieve the highest AsPC-1 tumor values and good pharmacokinetics, either without or during NEP inhibition, qualifying for further validation in patients with NTS₁R-positive tumors using SPECT/CT. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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16 pages, 2519 KiB

Open AccessArticle

Murine Breast Cancer Radiosensitization Using Oxygen Microbubbles and Metformin: Vessels Are the Key

by Agnieszka Drzał, Gabriela Dziurman, Paweł Hoła, Jakub Lechowski, Anthony Delalande, Jan Swakoń, Chantal Pichon and Martyna Elas

Int. J. Mol. Sci. 2023, 24(15), 12156; https://doi.org/10.3390/ijms241512156 - 29 Jul 2023

Viewed by 1138

Abstract

Radiotherapy is a cornerstone of cancer treatment, but tumor hypoxia and resistance to radiation remain significant challenges. Vascular normalization has emerged as a strategy to improve oxygenation and enhance therapeutic outcomes. In this study, we examine the radiosensitization potential of vascular normalization using metformin, a widely used anti-diabetic drug, and oxygen microbubbles (OMBs). We investigated the synergistic action of metformin and OMBs and the impact of this therapeutic combination on the vasculature, oxygenation, invasiveness, and radiosensitivity of murine 4T1 breast cancer. We employed in vivo Doppler ultrasonographic imaging for vasculature analysis, electron paramagnetic resonance oximetry, and immunohistochemical assessment of microvessels, perfusion, and invasiveness markers. Our findings demonstrate that both two-week metformin therapy and oxygen microbubble treatment normalize abnormal cancer vasculature. The combination of metformin and OMB yielded more pronounced and sustained effects than either treatment alone. The investigated therapy protocols led to nearly twice the radiosensitivity of 4T1 tumors; however, no significant differences in radiosensitivity were observed between the various treatment groups. Despite these improvements, resistance to treatment inevitably emerged, leading to the recurrence of hypoxia and an increased incidence of metastasis. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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Review

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31 pages, 2259 KiB

Open AccessReview

Experimental Tumor Induction and Evaluation of Its Treatment in the Chicken Embryo Chorioallantoic Membrane Model: A Systematic Review

by Cristina Mesas, Maria Angeles Chico, Kevin Doello, Patricia Lara, Javier Moreno, Consolación Melguizo, Gloria Perazzoli and Jose Prados

Int. J. Mol. Sci. 2024, 25(2), 837; https://doi.org/10.3390/ijms25020837 - 09 Jan 2024

Viewed by 1397

Abstract

The chorioallantoic membrane (CAM) model, generated during avian development, can be used in cancer research as an alternative in vivo model to perform tumorigenesis in ovo due to advantages such as simplicity, low cost, rapid growth, and being naturally immunodeficient. The aim of this systematic review has been to compile and analyze all studies that use the CAM assay as a tumor induction model. For that, a systematic search was carried out in four different databases: PubMed, Scopus, Cochrane, and WOS. After eliminating duplicates and following the established inclusion and exclusion criteria, a total of 74 articles were included. Of these, 62% use the in ovo technique, 13% use the ex ovo technique, 9% study the formation of metastasis, and 16% induce tumors from patient biopsies. Regarding the methodology followed, the main species used is chicken (95%), although some studies use quail eggs (4%), and one article uses ostrich eggs. Therefore, the CAM assay is a revolutionary technique that allows a simple and effective way to induce tumors, test the effectiveness of treatments, carry out metastasis studies, perform biopsy grafts of patients, and carry out personalized medicine. However, unification of the methodology used is necessary. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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14 pages, 1958 KiB

Open AccessReview

Role of the Mitochondrial E3 Ubiquitin Ligases as Possible Therapeutic Targets in Cancer Therapy

by Jacopo Di Gregorio, Martina Appignani and Vincenzo Flati

Int. J. Mol. Sci. 2023, 24(24), 17176; https://doi.org/10.3390/ijms242417176 - 06 Dec 2023

Viewed by 1079

Abstract

Ubiquitination is a post-translational modification that targets specific proteins on their lysine residues. Depending on the type of ubiquitination, this modification ultimately regulates the stability or degradation of the targeted proteins. Ubiquitination is mediated by three different classes of enzymes: the E1 ubiquitin-activating enzymes, the E2 ubiquitin-conjugating enzymes and, most importantly, the E3 ubiquitin ligases. E3 ligases are responsible for the final step of the ubiquitin cascade, interacting directly with the target proteins. E3 ligases can also be involved in DNA repair, cell cycle regulation and response to stress; alteration in their levels can be involved in oncogenic transformation and cancer progression. Of all the six hundred E3 ligases of the human genome, only three of them are specific to the mitochondrion: MARCH5, RNF185 and MUL1. Their alterations (that reflect on the alteration of the mitochondria functions) can be related to cancer progression, as underlined by the increasing research performed in recent years on these three mitochondrial enzymes. This review will focus on the function and mechanisms of the mitochondrial E3 ubiquitin ligases, as well as their important targets, in cancer development and progression, also highlighting their potential use for cancer therapy. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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29 pages, 23403 KiB

Open AccessReview

Galectin-1 in Pancreatic Ductal Adenocarcinoma: Bridging Tumor Biology, Immune Evasion, and Therapeutic Opportunities

by Ana Bogut, Bojan Stojanovic, Marina Jovanovic, Milica Dimitrijevic Stojanovic, Nevena Gajovic, Bojana S. Stojanovic, Goran Balovic, Milan Jovanovic, Aleksandar Lazovic, Milos Mirovic, Milena Jurisevic, Ivan Jovanovic and Violeta Mladenovic

Int. J. Mol. Sci. 2023, 24(21), 15500; https://doi.org/10.3390/ijms242115500 - 24 Oct 2023

Viewed by 1128

Abstract

Pancreatic Ductal Adenocarcinoma (PDAC) remains one of the most challenging malignancies to treat, with a complex interplay of molecular pathways contributing to its aggressive nature. Galectin-1 (Gal-1), a member of the galectin family, has emerged as a pivotal player in the PDAC microenvironment, influencing various aspects from tumor growth and angiogenesis to immune modulation. This review provides a comprehensive overview of the multifaceted role of Galectin-1 in PDAC. We delve into its contributions to tumor stroma remodeling, angiogenesis, metabolic reprogramming, and potential implications for therapeutic interventions. The challenges associated with targeting Gal-1 are discussed, given its pleiotropic functions and complexities in different cellular conditions. Additionally, the promising prospects of Gal-1 inhibition, including the utilization of nanotechnology and theranostics, are highlighted. By integrating recent findings and shedding light on the intricacies of Gal-1’s involvement in PDAC, this review aims to provide insights that could guide future research and therapeutic strategies. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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15 pages, 1103 KiB

Open AccessReview

Alternations of NF-κB Signaling by Natural Compounds in Muscle-Derived Cancers

by Justyna Radzka, Zofia Łapińska, Urszula Szwedowicz, Agnieszka Gajewska-Naryniecka, Agnieszka Gizak and Julita Kulbacka

Int. J. Mol. Sci. 2023, 24(15), 11900; https://doi.org/10.3390/ijms241511900 - 25 Jul 2023

Cited by 2 | Viewed by 1587

Abstract

The NF-κB-signaling pathway plays a crucial role in cancer progression, including muscle-derived cancers such as rhabdomyosarcoma or sarcoma. Several natural compounds have been studied for their ability to alter NF-κB signaling in these types of cancers. This review paper summarizes the current knowledge on the effects of natural compounds, including curcumin, resveratrol, quercetin, epigallocatechin-3-gallate, and berberine, on NF-κB signaling in muscle-derived cancers. These compounds have been shown to inhibit NF-κB signaling in rhabdomyosarcoma cells through various mechanisms, such as inhibiting the activation of the IKK complex and the NF-κB transcription factor. These findings suggest that natural compounds could be potential therapeutic agents for muscle-derived cancers. However, further research is needed to fully understand their mechanisms of action and potential clinical applications. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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18 pages, 1375 KiB

Open AccessReview

Comprehensive Review: Unveiling the Pro-Oncogenic Roles of IL-1ß and PD-1/PD-L1 in NSCLC Development and Targeting Their Pathways for Clinical Management

by Dani Ran Castillo, Won Jin Jeon, Daniel Park, Bryan Pham, Chieh Yang, Bowon Joung, Jin Hyun Moon, Jae Lee, Esther G. Chong, Kiwon Park, Mark E. Reeves, Penelope Duerksen-Hughes, Hamid R. Mirshahidi and Saied Mirshahidi

Int. J. Mol. Sci. 2023, 24(14), 11547; https://doi.org/10.3390/ijms241411547 - 17 Jul 2023

Cited by 1 | Viewed by 1697

Abstract

In the past decade, targeted therapies for solid tumors, including non-small cell lung cancer (NSCLC), have advanced significantly, offering tailored treatment options for patients. However, individuals without targetable mutations pose a clinical challenge, as they may not respond to standard treatments like immune-checkpoint inhibitors (ICIs) and novel targeted therapies. While the mechanism of action of ICIs seems promising, the lack of a robust response limits their widespread use. Although the expression levels of programmed death ligand 1 (PD-L1) on tumor cells are used to predict ICI response, identifying new biomarkers, particularly those associated with the tumor microenvironment (TME), is crucial to address this unmet need. Recently, inflammatory cytokines such as interleukin-1 beta (IL-1β) have emerged as a key area of focus and hold significant potential implications for future clinical practice. Combinatorial approaches of IL-1β inhibitors and ICIs may provide a potential therapeutic modality for NSCLC patients without targetable mutations. Recent advancements in our understanding of the intricate relationship between inflammation and oncogenesis, particularly involving the IL-1β/PD-1/PD-L1 pathway, have shed light on their application in lung cancer development and clinical outcomes of patients. Targeting these pathways in cancers like NSCLC holds immense potential to revolutionize cancer treatment, particularly for patients lacking targetable genetic mutations. However, despite these promising prospects, there remain certain aspects of this pathway that require further investigation, particularly regarding treatment resistance. Therefore, the objective of this review is to delve into the role of IL-1β in NSCLC, its participation in inflammatory pathways, and its intricate crosstalk with the PD-1/PD-L1 pathway. Additionally, we aim to explore the potential of IL-1β as a therapeutic target for NSCLC treatment. Full article

(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer 2.0)

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