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Novel Therapeutic Targets in Cancers: 3rd Edition
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Novel Therapeutic Targets in Cancers: 3rd Edition

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: 20 January 2025 | Viewed by 5730

Special Issue Editor

Dr. Elena Levantini

E-Mail Website
Guest Editor
Consiglio Nazionale delle Ricerche, Istituto di Tecnologie Biomediche, via Moruzzi 1, 56124 Pisa, Italy
Interests: NSCLC; SCLC; murine models; tumor microenvironment; cancer stem cells; therapy resistance; therapeutic targeting; BMI1; scRNAseq; spatial transcriptomics; single-cell interactomes; gene regulation; transcription factors; KRAS; EGFR; miRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issues “Novel Therapeutic Targets in Cancers” and “Novel Therapeutic Targets in Cancers 2.0”.

In recent decades, we have developed novel precision oncology protocols that are starting to see adoption in routine clinical practice. However, despite major advances, the dream of converting solid tumors into a chronic disease is still unfulfilled, and long-term remission has not yet been achieved.

Starting from preclinical models (cell lines, organoids, and murine models), we can identify oncogenic pathways, mechanisms of resistance, and novel avenues to inhibit tumor growth and metastatic spread that will eventually enter clinical trials. Novel technologies, such as those able to pinpoint the contribution of tumor heterogeneity to transformation and tumor dissemination, as well as tumor evolution during drug response and recurrence, will revolutionize cancer treatment by expanding the therapeutic arsenal at our disposal. State-of-the-art precision medicine protocols require the convergence of multiple interdisciplinary contributions, including the identification of single-cell-specific genetic and epigenetic alterations, the discovery of diagnostic and prognostic biomarkers, the implementation of efficient and specific diagnostic tools, the design of genomic editing protocols, and the planning of well-designed therapeutic strategies that take into consideration the best sequential options to delay/prevent the development of recurrence. This Special Issue welcomes original investigations as well as concise review manuscripts from experts in these relevant research fields. This Special Issue is supervised by Dr. Elena Levantini and assisted by our Topical Advisory Panel Member Dr. Giorgia Maroni.

The topics of interest for our Special Issue include, but are not limited to:

  1. Solid tumor heterogeneity;
  2. Targeted therapy, including target identification and validation;
  3. Immune modulation;
  4. RNA-based therapy;
  5. Epigenetic therapy;
  6. Combination therapy, considering also sequential treatments and drug holidays;
  7. Cancer stem cell targeting;
  8. Recurrence mechanisms;
  9. Tumor evolution as defined by high-resolution transcriptomics;
  10. Preclinical modeling of the heterogeneous tumor milieux.

Please note that manuscripts consisting solely of bioinformatics or the computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section.

Dr. Elena Levantini
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 therapy
  • precision oncology
  • immune modulation
  • cancer stem cell targeting
  • RNA-based therapy

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Published Papers (4 papers)

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17 pages, 2562 KiB  
Article
Polθ Inhibitor (ART558) Demonstrates a Synthetic Lethal Effect with PARP and RAD52 Inhibitors in Glioblastoma Cells
by Gabriela Barszczewska-Pietraszek, Piotr Czarny, Małgorzata Drzewiecka, Maciej Błaszczyk, Maciej Radek, Ewelina Synowiec, Paulina Wigner-Jeziorska, Przemysław Sitarek, Janusz Szemraj, Tomasz Skorski and Tomasz Śliwiński
Int. J. Mol. Sci. 2024, 25(17), 9134; https://doi.org/10.3390/ijms25179134 - 23 Aug 2024
Viewed by 1077
Abstract
DNA repair proteins became the popular targets in research on cancer treatment. In our studies we hypothesized that inhibition of DNA polymerase theta (Polθ) and its combination with Poly (ADP-ribose) polymerase 1 (PARP1) or RAD52 inhibition and the alkylating drug temozolomide (TMZ) has [...] Read more.
DNA repair proteins became the popular targets in research on cancer treatment. In our studies we hypothesized that inhibition of DNA polymerase theta (Polθ) and its combination with Poly (ADP-ribose) polymerase 1 (PARP1) or RAD52 inhibition and the alkylating drug temozolomide (TMZ) has an anticancer effect on glioblastoma cells (GBM21), whereas it has a low impact on normal human astrocytes (NHA). The effect of the compounds was assessed by analysis of cell viability, apoptosis, proliferation, DNA damage and cell cycle distribution, as well as gene expression. The main results show that Polθ inhibition causes a significant decrease in glioblastoma cell viability. It induces apoptosis, which is accompanied by a reduction in cell proliferation and DNA damage. Moreover, the effect was stronger when dual inhibition of Polθ with PARP1 or RAD52 was applied, and it is further enhanced by addition of TMZ. The impact on normal cells is much lower, especially when considering cell viability and DNA damage. In conclusion, we would like to highlight that Polθ inhibition used in combination with PARP1 or RAD52 inhibition has great potential to kill glioblastoma cells, and shows a synthetic lethal effect, while sparing normal astrocytes. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets in Cancers: 3rd Edition)
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17 pages, 2432 KiB  
Article
LncRNA PTENP1/miR-21/PTEN Axis Modulates EMT and Drug Resistance in Cancer: Dynamic Boolean Modeling for Cell Fates in DNA Damage Response
by Shantanu Gupta, Daner A. Silveira, Pedro R. Lorenzoni, Jose Carlos M. Mombach and Ronaldo F. Hashimoto
Int. J. Mol. Sci. 2024, 25(15), 8264; https://doi.org/10.3390/ijms25158264 - 29 Jul 2024
Cited by 1 | Viewed by 1151
Abstract
It is well established that microRNA-21 (miR-21) targets phosphatase and tensin homolog (PTEN), facilitating epithelial-to-mesenchymal transition (EMT) and drug resistance in cancer. Recent evidence indicates that PTEN activates its pseudogene-derived long non-coding RNA, PTENP1, which in turn inhibits miR-21. However, the dynamics of [...] Read more.
It is well established that microRNA-21 (miR-21) targets phosphatase and tensin homolog (PTEN), facilitating epithelial-to-mesenchymal transition (EMT) and drug resistance in cancer. Recent evidence indicates that PTEN activates its pseudogene-derived long non-coding RNA, PTENP1, which in turn inhibits miR-21. However, the dynamics of PTEN, miR-21, and PTENP1 in the DNA damage response (DDR) remain unclear. Thus, we propose a dynamic Boolean network model by integrating the published literature from various cancers. Our model shows good agreement with the experimental findings from breast cancer, hepatocellular carcinoma (HCC), and oral squamous cell carcinoma (OSCC), elucidating how DDR activation transitions from the intra-S phase to the G2 checkpoint, leading to a cascade of cellular responses such as cell cycle arrest, senescence, autophagy, apoptosis, drug resistance, and EMT. Model validation underscores the roles of PTENP1, miR-21, and PTEN in modulating EMT and drug resistance. Furthermore, our analysis reveals nine novel feedback loops, eight positive and one negative, mediated by PTEN and implicated in DDR cell fate determination, including pathways related to drug resistance and EMT. Our work presents a comprehensive framework for investigating cellular responses following DDR, underscoring the therapeutic potential of targeting PTEN, miR-21, and PTENP1 in cancer treatment. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets in Cancers: 3rd Edition)
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18 pages, 4203 KiB  
Article
Deciphering the Interplay: Thieno[2,3-b]pyridine’s Impact on Glycosphingolipid Expression, Cytotoxicity, Apoptosis, and Metabolomics in Ovarian Tumor Cell Lines
by Zdravko Odak, Sandra Marijan, Mila Radan, Lisa I. Pilkington, Monika Čikeš Botić, David Barker, Jóhannes Reynisson, Euphemia Leung and Vedrana Čikeš Čulić
Int. J. Mol. Sci. 2024, 25(13), 6954; https://doi.org/10.3390/ijms25136954 - 25 Jun 2024
Cited by 1 | Viewed by 1299
Abstract
Ovarian cancer is among the most prevalent causes of mortality among women. Despite improvements in diagnostic methods, non-specific symptoms and delayed gynecological exams can lead to late-stage ovarian tumor discovery. In this study, the effect of an anti-cancer compound, 3-amino-N-(3-chloro-2-methylphenyl)-5-oxo-5,6,7,8-tetrahydrothieno[2,3-b [...] Read more.
Ovarian cancer is among the most prevalent causes of mortality among women. Despite improvements in diagnostic methods, non-specific symptoms and delayed gynecological exams can lead to late-stage ovarian tumor discovery. In this study, the effect of an anti-cancer compound, 3-amino-N-(3-chloro-2-methylphenyl)-5-oxo-5,6,7,8-tetrahydrothieno[2,3-b]quinoline-2-carboxamide (Compound 1), was examined. The impacts of cytotoxicity, apoptosis, and metabolomic changes in ovarian cancer cell lines SK-OV-3 and OVCAR-3, as well as glycosphingolipid (GSL) expression, on cancer stem cells (CSCs), marked as CD49f+, and non-CSCs (CD49f−) were explored. Treatment with Compound 1 reduced the percentage of CSCs compared to non-treated cells (p < 0.001). The functional impact of eight GSLs on CSCs and non-CSCs was examined using flow cytometry. The glycophenotype changed in both cell lines, with increases or decreases in its expression, after the treatment. These findings raise the possibility of specifically targeting CSCs in ovarian cancer therapy. Additionally, treatment with Compound 1 resulted in statistically meaningful increased apoptosis, including both early and late apoptosis (p < 0.001), suggesting a pivotal role in initiating programmed cell death by the apoptotic pathway. The analysis revealed that the metabolic activity of treated cancer cells was lower compared to those of the control group (p < 0.001). Full article
(This article belongs to the Special Issue Novel Therapeutic Targets in Cancers: 3rd Edition)
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7 pages, 1002 KiB  
Brief Report
Ethnicity-Based Variations in Focal Adhesion Kinase Signaling in Glioblastoma Gene Expression: A Study of the Puerto Rican Hispanic Population
by Tyrel Porter, Miguel Mayol del Valle and Lilia Kucheryavykh
Int. J. Mol. Sci. 2024, 25(9), 4947; https://doi.org/10.3390/ijms25094947 - 1 May 2024
Viewed by 1059
Abstract
Glioblastoma (GBM), an aggressive form of brain cancer, has a higher incidence in non-Hispanics when compared to the US Hispanic population. Using data from RT-PCR analysis of 21 GBM tissue from Hispanic patients in Puerto Rico, we identified significant correlations in the gene [...] Read more.
Glioblastoma (GBM), an aggressive form of brain cancer, has a higher incidence in non-Hispanics when compared to the US Hispanic population. Using data from RT-PCR analysis of 21 GBM tissue from Hispanic patients in Puerto Rico, we identified significant correlations in the gene expression of focal adhesion kinase and proline-rich tyrosine kinase (PTK2 and PTK2B) with NGFR (nerve growth factor receptor), PDGFRB (platelet-derived growth factor receptor B), EGFR (epithelial growth factor receptor), and CXCR1 (C-X-C motif chemokine receptor 1). This study further explores these correlations found in gene expression while accounting for sex and ethnicity. Statistically significant (p < 0.05) correlations with an r value > ±0.7 were subsequently contrasted with mRNA expression data acquired from cBioPortal for 323 GBM specimens. Significant correlations in Puerto Rican male patients were found between PTK2 and PTK2B, NGFR, PDGFRB, EGFR, and CXCR1, which did not arise in non-Hispanic male patient data. The data for Puerto Rican female patients showed correlations in PTK2 with PTK2B, NGFR, PDGFRB, and EGFR, all of which did not appear in the data for non-Hispanic female patients. The data acquired from cBioPortal for non-Puerto Rican Hispanic patients supported the correlations found in the Puerto Rican population for both sexes. Our findings reveal distinct correlations in gene expression patterns, particularly involving PTK2, PTK2B, NGFR, PDGFRB, and EGFR among Puerto Rican Hispanic patients when compared to non-Hispanic counterparts. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets in Cancers: 3rd Edition)
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