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Molecular Mechanisms of Targeted Therapy in Cancer
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Molecular Mechanisms of Targeted Therapy in Cancer

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 (20 August 2023) | Viewed by 13114

Special Issue Editor

Dr. Carmen Cristina Diaconu

E-Mail Website
Guest Editor
Stefan S. Nicolau Institute of Virology, Romanian Academy, 030304 Bucharest, Romania
Interests: cellular pathology; molecular medicine; molecular genetics; epigenetics; signal transduction; targeted therapy; drug resistance

Special Issue Information

Dear Colleagues,

In the “Omics” era, our understanding of the molecular mechanisms involved in the genesis and development of cancer has dramatically increased, and has prompted the discovery of more precise targeted therapies. However, the complex molecular modifications that could potentially be exploited by targeted therapies are still insufficiently explored.

Understanding the intimate molecular basis of different cancers enables us to therapeutically address them, more efficiently, with fewer side effects, possibly eluding multidrug resistance.

In this context, the goal of this Special Issue, to be published in IJMS, is to gather the latest research and ideas on novel avenues to exploit the molecular mechanisms involved in the development of cancer, evaluation of the co-occurrence of multiple pathogenic mechanisms and how these mechanisms are, or might be, used for the development of precision therapeutics.

Dr. Carmen Cristina Diaconu
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 mechanisms of carcinogenesis
  • targeted therapy in cancer
  • multidrug resistance
  • targeted cancer therapy side effects
  • precision therapy in cancer

Published Papers (6 papers)

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Research

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17 pages, 5729 KiB  
Article
Targeting SOX18 Transcription Factor Activity by Small-Molecule Inhibitor Sm4 in Non-Small Lung Cancer Cell Lines
by Olga Rodak, Monika Mrozowska, Agnieszka Rusak, Agnieszka Gomułkiewicz, Aleksandra Piotrowska, Mateusz Olbromski, Marzenna Podhorska-Okołów, Maciej Ugorski and Piotr Dzięgiel
Int. J. Mol. Sci. 2023, 24(14), 11316; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241411316 - 11 Jul 2023
Cited by 1 | Viewed by 1290
Abstract
The transcription factor SOX18 has been shown to play a crucial role in lung cancer progression and metastasis. In this study, we investigated the effect of Sm4, a SOX18 inhibitor, on cell cycle regulation in non-small cell lung cancer (NSCLC) cell lines LXF-289 [...] Read more.
The transcription factor SOX18 has been shown to play a crucial role in lung cancer progression and metastasis. In this study, we investigated the effect of Sm4, a SOX18 inhibitor, on cell cycle regulation in non-small cell lung cancer (NSCLC) cell lines LXF-289 and SK-MES-1, as well as normal human lung fibroblast cell line IMR-90. Our results demonstrated that Sm4 treatment induced cytotoxic effects on all three cell lines, with a greater effect observed in NSCLC adenocarcinoma cells. Sm4 treatment led to S-phase cell accumulation and upregulation of p21, a key regulator of the S-to-G2/M phase transition. While no significant changes in SOX7 or SOX17 protein expression were observed, Sm4 treatment resulted in a significant upregulation of SOX17 gene expression. Furthermore, our findings suggest a complex interplay between SOX18 and p21 in the context of lung cancer, with a positive correlation observed between SOX18 expression and p21 nuclear presence in clinical tissue samples obtained from lung cancer patients. These results suggest that Sm4 has the potential to disrupt the cell cycle and target cancer cell growth by modulating SOX18 activity and p21 expression. Further investigation is necessary to fully understand the relationship between SOX18 and p21 in lung cancer and to explore the therapeutic potential of SOX18 inhibition in lung cancer. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Targeted Therapy in Cancer)
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21 pages, 7422 KiB  
Article
Bcl-2 Family Members Bcl-xL and Bax Cooperatively Contribute to Bortezomib Resistance in Mantle Cell Lymphoma
by Sudjit Luanpitpong, Montira Janan, Juthamas Yosudjai, Jirarat Poohadsuan, Pithi Chanvorachote and Surapol Issaragrisil
Int. J. Mol. Sci. 2022, 23(22), 14474; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214474 - 21 Nov 2022
Cited by 3 | Viewed by 1639
Abstract
Mantle cell lymphoma (MCL) is an aggressive non-Hodgkin lymphoma with poor prognosis, due to the inevitable development of drug resistance. Despite being the first-in-class proteasome inhibitor for relapsed/refractory MCL, resistance to bortezomib (BTZ) in MCL patients remains a major hurdle of effective therapy, [...] Read more.
Mantle cell lymphoma (MCL) is an aggressive non-Hodgkin lymphoma with poor prognosis, due to the inevitable development of drug resistance. Despite being the first-in-class proteasome inhibitor for relapsed/refractory MCL, resistance to bortezomib (BTZ) in MCL patients remains a major hurdle of effective therapy, and relapse following BTZ is frequent. Understanding the mechanisms underlying BTZ resistance is, therefore, important for improving the clinical outcome and developing novel therapeutic strategies. Here, we established de novo BTZ-resistant human MCL-derived cells with the highest resistance index of 300-fold compared to parental cells. We provided compelling evidence that both Bcl-xL and Bax are key mediators in determining BTZ sensitivity in MCL cells. Overexpression of antiapoptotic Bcl-xL and depletion of proapoptotic Bax cooperatively protected MCL cells against BTZ-induced apoptosis, causing acquired BTZ resistance, likely by tilting the balance of Bcl-2 family proteins toward antiapoptotic signaling. Bioinformatics analyses suggested that high BCL2L1 (encoded Bcl-xL) and low BAX were, in part, associated with poor prognosis of MCL patients, e.g., when combined with low OGT, which regulates cellular O-GlcNAcylation. Our findings support recent strategies in small molecule drug discovery co-targeting antiapoptotic Bcl-2 family proteins using BH3 mimetics and Bax using Bax activators to overcome cancer drug resistance. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Targeted Therapy in Cancer)
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Review

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23 pages, 1798 KiB  
Review
Exploring the JAK/STAT Signaling Pathway in Hepatocellular Carcinoma: Unraveling Signaling Complexity and Therapeutic Implications
by Hyunjung Park, Sangjik Lee, Jaehun Lee, Hyuk Moon and Simon Weonsang Ro
Int. J. Mol. Sci. 2023, 24(18), 13764; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241813764 - 06 Sep 2023
Cited by 3 | Viewed by 1494
Abstract
Hepatocellular Carcinoma (HCC) continues to pose a substantial global health challenge due to its high incidence and limited therapeutic options. In recent years, the Janus Kinase (JAK) and Signal Transducer and Activator of Transcription (STAT) pathway has emerged as a critical signaling cascade [...] Read more.
Hepatocellular Carcinoma (HCC) continues to pose a substantial global health challenge due to its high incidence and limited therapeutic options. In recent years, the Janus Kinase (JAK) and Signal Transducer and Activator of Transcription (STAT) pathway has emerged as a critical signaling cascade in HCC pathogenesis. The review commences with an overview of the JAK/STAT pathway, delving into the dynamic interplay between the JAK/STAT pathway and its numerous upstream activators, such as cytokines and growth factors enriched in pathogenic livers afflicted with chronic inflammation and cirrhosis. This paper also elucidates how the persistent activation of JAK/STAT signaling leads to diverse oncogenic processes during hepatocarcinogenesis, including uncontrolled cell proliferation, evasion of apoptosis, and immune escape. In the context of therapeutic implications, this review summarizes recent advancements in targeting the JAK/STAT pathway for HCC treatment. Preclinical and clinical studies investigating inhibitors and modulators of JAK/STAT signaling are discussed, highlighting their potential in suppressing the deadly disease. The insights presented herein underscore the necessity for continued research into targeting the JAK/STAT signaling pathway as a promising avenue for HCC therapy. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Targeted Therapy in Cancer)
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14 pages, 476 KiB  
Review
Meningiomas and Somatostatin Analogs: A Systematic Scoping Review on Current Insights and Future Perspectives
by Sofie Eline Tollefsen, Ole Solheim, Patricia Mjønes and Sverre Helge Torp
Int. J. Mol. Sci. 2023, 24(5), 4793; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054793 - 01 Mar 2023
Cited by 2 | Viewed by 2002
Abstract
Meningioma is the most frequent brain tumor, and the incidence is ever-increasing. Though often benign and slow growth, recurrence rates are substantial and today’s surgical and radiation-based treatment are not without complications. No drugs specific for meningiomas are hitherto approved and patients with [...] Read more.
Meningioma is the most frequent brain tumor, and the incidence is ever-increasing. Though often benign and slow growth, recurrence rates are substantial and today’s surgical and radiation-based treatment are not without complications. No drugs specific for meningiomas are hitherto approved and patients with inoperable or recurrent meningioma are left with few treatment options. Somatostatin receptors are previously detected in meningiomas and may inhibit growth when stimulated by somatostatin. Hence, somatostatin analogs could provide a targeted drug therapy. The aim of this study was to compile the current insights of somatostatin analogs for patients with meningioma. This paper adheres to the PRISMA extension for Scoping Reviews. A systematic search was conducted in the search databases PubMed, Embase via Ovid, and Web of Science. Seventeen papers adhered to the inclusion and exclusion criteria, and critical appraisal was conducted. The overall quality of evidence is low, as none of the studies were randomized or controlled. Various efficacy of somatostatin analogs is reported, and adverse effects are sparse. Due to the beneficial effects reported by some studies, somatostatin analogs may offer a novel last-option treatment for severely ill-patients. Nonetheless, only a controlled study, preferably a randomized clinical trial, could clarify the efficacy of somatostatin analogs. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Targeted Therapy in Cancer)
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15 pages, 1817 KiB  
Review
Collagen Family as Promising Biomarkers and Therapeutic Targets in Cancer
by Laura Necula, Lilia Matei, Denisa Dragu, Ioana Pitica, Ana Neagu, Coralia Bleotu, Carmen C. Diaconu and Mihaela Chivu-Economescu
Int. J. Mol. Sci. 2022, 23(20), 12415; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012415 - 17 Oct 2022
Cited by 14 | Viewed by 2537
Abstract
Despite advances in cancer detection and therapy, it has been estimated that the incidence of cancers will increase, while the mortality rate will continue to remain high, a fact explained by the large number of patients diagnosed in advanced stages when therapy is [...] Read more.
Despite advances in cancer detection and therapy, it has been estimated that the incidence of cancers will increase, while the mortality rate will continue to remain high, a fact explained by the large number of patients diagnosed in advanced stages when therapy is often useless. Therefore, it is necessary to invest knowledge and resources in the development of new non-invasive biomarkers for the early detection of cancer and new therapeutic targets for better health management. In this review, we provided an overview on the collagen family as promising biomarkers and on how they may be exploited as therapeutic targets in cancer. The collagen family tridimensional structure, organization, and functions are very complex, being in a tight relationship with the extracellular matrix, tumor, and immune microenvironment. Moreover, accumulating evidence underlines the role of collagens in promoting tumor growth and creating a permissive tumor microenvironment for metastatic dissemination. Knowledge of the molecular basis of these interactions may help in cancer diagnosis and prognosis, in overcoming chemoresistance, and in providing new targets for cancer therapies. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Targeted Therapy in Cancer)
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39 pages, 2830 KiB  
Review
Unraveling the Potential Role of NEDD4-like E3 Ligases in Cancer
by Sujitha Jayaprakash, Mangala Hegde, Bandari BharathwajChetty, Sosmitha Girisa, Mohammed S. Alqahtani, Mohamed Abbas, Gautam Sethi and Ajaikumar B. Kunnumakkara
Int. J. Mol. Sci. 2022, 23(20), 12380; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012380 - 16 Oct 2022
Cited by 4 | Viewed by 3514
Abstract
Cancer is a deadly disease worldwide, with an anticipated 19.3 million new cases and 10.0 million deaths occurring in 2020 according to GLOBOCAN 2020. It is well established that carcinogenesis and cancer development are strongly linked to genetic changes and post-translational modifications (PTMs). [...] Read more.
Cancer is a deadly disease worldwide, with an anticipated 19.3 million new cases and 10.0 million deaths occurring in 2020 according to GLOBOCAN 2020. It is well established that carcinogenesis and cancer development are strongly linked to genetic changes and post-translational modifications (PTMs). An important PTM process, ubiquitination, regulates every aspect of cellular activity, and the crucial enzymes in the ubiquitination process are E3 ubiquitin ligases (E3s) that affect substrate specificity and must therefore be carefully regulated. A surfeit of studies suggests that, among the E3 ubiquitin ligases, neuronal precursor cell-expressed developmentally downregulated 4 (NEDD4)/NEDD4-like E3 ligases show key functions in cellular processes by controlling subsequent protein degradation and substrate ubiquitination. In addition, it was demonstrated that NEDD4 mainly acts as an oncogene in various cancers, but also plays a tumor-suppressive role in some cancers. In this review, to comprehend the proper function of NEDD4 in cancer development, we summarize its function, both its tumor-suppressive and oncogenic role, in multiple types of malignancies. Moreover, we briefly explain the role of NEDD4 in carcinogenesis and progression, including cell survival, cell proliferation, autophagy, cell migration, invasion, metastasis, epithelial-mesenchymal transition (EMT), chemoresistance, and multiple signaling pathways. In addition, we briefly explain the significance of NEDD4 as a possible target for cancer treatment. Therefore, we conclude that targeting NEDD4 as a therapeutic method for treating human tumors could be a practical possibility. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Targeted Therapy in Cancer)
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