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Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0

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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: closed (31 August 2023) | Viewed by 25298

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Dr. Giulia Russo

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Dipartimento di Farmacia, Università degli Studi di Napoli Federico II, Naples, Italy
Interests: tumorigenesis; cancer therapy; TP53, TGFβ, TNFα signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

According to the World Health Organization, cancer is the most common cause of premature death in developed countries. Conventional cancer treatment involves the therapeutic application of chemotherapeutic agents associated with surgical therapy. However, the clinical outcome of this therapeutic approach can be unsatisfactory, especially in patients with advanced disease. Furthermore, common chemotherapeutic drugs show high levels of toxicity for normal cells, which is often associated with the development of chemoresistance. For these reasons, oncological research has focused on finding innovative therapies that increase the specificity of the treatment and reduce their drawbacks. New therapeutic approaches for cancer treatment, currently under evaluation in many clinical trials worldwide, include but are not limited to molecules targeting the nucleolus, natural antioxidants and phytochemicals in combination with common chemotherapeutic drugs, expression of genes triggering apoptosis, tumor suppressors, targeted silencing mediated by siRNAs, and the nanodelivery of chemotherapeutics.

The combination of new and conventional approaches allows oncologists to select the best and most personalized therapy for cancer treatment.

This Special Issue, led by Dr. Giulia Russo with the assistance of our Topical Advisory Panel Members and the GE’s assistant editor Dr. Annalisa Pecoraro (Department of Pharmacy, University of Naples Federico II, 80131 Napoli, Italy), will document studies on the molecular mechanism underlying tumorigenesis and on innovative strategies for cancer treatment.

Dr. Giulia Russo
Guest Editor

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Keywords

cancer
nucleolus
nucleolar stress
tumorigenesis
cancer therapy

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Published Papers (11 papers)

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Research

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26 pages, 17110 KiB

Open AccessArticle

Dynamic Interplay in Tumor Ecosystems: Communication between Hepatoma Cells and Fibroblasts

by Gábor Petővári, Gábor Tóth, Lilla Turiák, Anna L. Kiss, Krisztina Pálóczi, Anna Sebestyén, Adrián Pesti, András Kiss, Kornélia Baghy, Katalin Dezső, Tibor Füle, Péter Tátrai, Ilona Kovalszky and Andrea Reszegi

Int. J. Mol. Sci. 2023, 24(18), 13996; https://doi.org/10.3390/ijms241813996 - 12 Sep 2023

Cited by 2 | Viewed by 1966

Abstract

Tumors are intricate ecosystems where cancer cells and non-malignant stromal cells, including cancer-associated fibroblasts (CAFs), engage in complex communication. In this study, we investigated the interaction between poorly (HLE) and well-differentiated (HuH7) hepatoma cells and LX2 fibroblasts. We explored various communication channels, including soluble factors, metabolites, extracellular vesicles (EVs), and miRNAs. Co-culture with HLE cells induced LX2 to produce higher levels of laminin β1, type IV collagen, and CD44, with pronounced syndecan-1 shedding. Conversely, in HuH7/LX2 co-culture, fibronectin, thrombospondin-1, type IV collagen, and cell surface syndecan-1 were dominant matrix components. Integrins α6β4 and α6β1 were upregulated in HLE, while α5β1 and αVβ1 were increased in HuH7. HLE-stimulated LX2 produced excess MMP-2 and 9, whereas HuH7-stimulated LX2 produced excess MMP-1. LX2 activated MAPK and Wnt signaling in hepatoma cells, and conversely, hepatoma-derived EVs upregulated MAPK and Wnt in LX2 cells. LX2-derived EVs induced over tenfold upregulation of SPOCK1/testican-1 in hepatoma EV cargo. We also identified liver cancer-specific miRNAs in hepatoma EVs, with potential implications for early diagnosis. In summary, our study reveals tumor type-dependent communication between hepatoma cells and fibroblasts, shedding light on potential implications for tumor progression. However, the clinical relevance of liver cancer-specific miRNAs requires further investigation. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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11 pages, 2372 KiB

Open AccessArticle

Specific Targeting of STAT3 in B Cells Suppresses Progression of B Cell Lymphoma

by Lipei Wang, Mingqian Zhou, Xiangyu Kong, Shouzhen Wu, Chuanlin Ding, Xiaoling Hu, Haixun Guo and Jun Yan

Int. J. Mol. Sci. 2023, 24(17), 13666; https://doi.org/10.3390/ijms241713666 - 4 Sep 2023

Cited by 1 | Viewed by 1795

Abstract

The signal transducer and activator of transcription 3 (STAT3), which regulates multiple oncogenic processes, has been found to be constitutively activated in lymphoma, suggesting its potential as a therapeutic target. Here, we constructed an anti-CD19-N-(4-carboxycyclohexylmethyl) maleimide N-hydroxysuccinimide ester (SMCC)-protamine (CSP)-STAT3 small interfering RNA (siRNA) conjugate and demonstrated that the CSP-STAT3 siRNA conjugate could specifically bind to normal B cells and A20 lymphoma cells in vitro. It decreased the STAT3 expression in B cell lymphoma cell lines (A20, SU-DHL-2 and OCI-Ly3), resulting in reduced proliferation of lymphoma cells featured with lower S-phase and higher apoptosis. Using an A20 transplantable lymphoma model, we found that the CSP-STAT3 siRNA conjugate significantly inhibited tumor growth and weight. Ki-67, p-STAT3, STAT3, and serum IL-6 levels were all significantly reduced in A20-bearing mice treated with CSP-STAT3 siRNA. These findings indicate that specifically targeting STAT3 siRNA to B cell lymphoma cell lines can significantly decrease STAT3 activity and inhibit tumor progression in vitro and in vivo, suggesting its potential utilization for cancer treatment. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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23 pages, 6361 KiB

Open AccessArticle

Nitric Oxide Prevents Glioblastoma Stem Cells’ Expansion and Induces Temozolomide Sensitization

by Luisa Salvatori, Silvia Malatesta, Barbara Illi, Maria Patrizia Somma, Cinzia Fionda, Helena Stabile, Rosaria Anna Fontanella and Carlo Gaetano

Int. J. Mol. Sci. 2023, 24(14), 11286; https://doi.org/10.3390/ijms241411286 - 10 Jul 2023

Cited by 2 | Viewed by 1558

Abstract

Glioblastoma multiforme (GBM) has high mortality and recurrence rates. Malignancy resilience is ascribed to Glioblastoma Stem Cells (GSCs), which are resistant to Temozolomide (TMZ), the gold standard for GBM post-surgical treatment. However, Nitric Oxide (NO) has demonstrated anti-cancer efficacy in GBM cells, but its potential impact on GSCs remains unexplored. Accordingly, we investigated the effects of NO, both alone and in combination with TMZ, on patient-derived GSCs. Experimentally selected concentrations of diethylenetriamine/NO adduct and TMZ were used through a time course up to 21 days of treatment, to evaluate GSC proliferation and death, functional recovery, and apoptosis. Immunofluorescence and Western blot analyses revealed treatment-induced effects in cell cycle and DNA damage occurrence and repair. Our results showed that NO impairs self-renewal, disrupts cell-cycle progression, and expands the quiescent cells’ population. Consistently, NO triggered a significant but tolerated level of DNA damage, but not apoptosis. Interestingly, NO/TMZ cotreatment further inhibited cell cycle progression, augmented G0 cells, induced cell death, but also enhanced DNA damage repair activity. These findings suggest that, although NO administration does not eliminate GSCs, it stunts their proliferation, and makes cells susceptible to TMZ. The resulting cytostatic effect may potentially allow long-term control over the GSCs’ subpopulation. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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11 pages, 898 KiB

Open AccessArticle

CD276 as a Candidate Target for Immunotherapy in Medullary Thyroid Cancer

by Kinga Hińcza-Nowak, Artur Kowalik, Agnieszka Walczyk, Iwona Pałyga, Danuta Gąsior-Perczak, Agnieszka Płusa, Janusz Kopczyński, Magdalena Chrapek, Stanisław Góźdź and Aldona Kowalska

Int. J. Mol. Sci. 2023, 24(12), 10019; https://doi.org/10.3390/ijms241210019 - 12 Jun 2023

Cited by 4 | Viewed by 1555

Abstract

Medullary thyroid cancer (MTC) is a rare malignancy, and the treatment of metastatic MTC is challenging. In previous work, immune profiling (RNA-Seq) of MTC identified CD276 as a potential target for immunotherapy. CD276 expression was 3-fold higher in MTC cells than in normal tissues. Paraffin blocks from patients with MTC were analyzed by immunohistochemistry to confirm the results of RNA-Seq. Serial sections were incubated with anti-CD276 antibody, and scored according to staining intensity and the percentage of immunoreactive cells. The results showed that CD276 expression was higher in MTC tissues than in controls. A lower percentage of immunoreactive cells correlated with the absence of lateral node metastasis, lower levels of calcitonin after surgery, no additional treatments, and remission. There were statistically significant associations of intensity of immunostaining and percentage of CD276 immunoreactive cells with clinical factors and the course of the disease. These results suggest that targeting this immune checkpoint molecule CD276 could be a promising strategy for the treatment of MTC. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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17 pages, 4406 KiB

Open AccessArticle

Necroptosis Induced by Delta-Tocotrienol Overcomes Docetaxel Chemoresistance in Prostate Cancer Cells

by Marina Montagnani Marelli, Giangiacomo Beretta and Roberta Manuela Moretti

Int. J. Mol. Sci. 2023, 24(5), 4923; https://doi.org/10.3390/ijms24054923 - 3 Mar 2023

Cited by 4 | Viewed by 2190

Abstract

Prostate cancer (PCa) represents the fifth cause of cancer death in men. Currently, chemotherapeutic agents for the treatment of cancers, including PCa, mainly inhibit tumor growth by apoptosis induction. However, defects in apoptotic cellular responses frequently lead to drug resistance, which is the main cause of chemotherapy failure. For this reason, trigger non-apoptotic cell death might represent an alternative approach to prevent drug resistance in cancer. Several agents, including natural compounds, have been shown to induce necroptosis in human cancer cells. In this study we evaluated the involvement of necroptosis in anticancer activity of delta-tocotrienol (δ-TT) in PCa cells (DU145 and PC3). Combination therapy is one tool used to overcome therapeutic resistance and drug toxicity. Evaluating the combined effect of δ-TT and docetaxel (DTX), we found that δ-TT potentiates DTX cytotoxicity in DU145 cells. Moreover, δ-TT induces cell death in DU145 cells that have developed DTX resistance (DU-DXR) activating necroptosis. Taken together, obtained data indicate the ability of δ-TT to induce necroptosis in both DU145, PC3 and DU-DXR cell lines. Furthermore, the ability of δ-TT to induce necroptotic cell death may represent a promising therapeutical approach to overcome DTX chemoresistance in PCa. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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13 pages, 3433 KiB

Open AccessCommunication

Another Brick to Confirm the Efficacy of Rigosertib as Anticancer Agent

by Alessio Malacrida, Marie Deschamps-Wright, Roberta Rigolio, Guido Cavaletti and Mariarosaria Miloso

Int. J. Mol. Sci. 2023, 24(2), 1721; https://doi.org/10.3390/ijms24021721 - 15 Jan 2023

Cited by 4 | Viewed by 2081

Abstract

Rigosertib is a small molecule in preclinical development that, due to its characteristics as a dual PLK1 and PI3K inhibitor, is particularly effective in counteracting the advance of different types of tumors. In this work, we evaluated the efficacy of Rigosertib and the expression of p53 in five different human tumor cell lines in vitro, A549 (lung adenocarcinoma), MCF-7 and MDA-MB231 (breast cancer cells), RPMI 8226 (multiple myeloma), and U87-MG (glioblastoma). We demonstrated that in all cell lines, the effect was dose- and time-dependent, but A549 cells were the most sensible to the treatment while higher concentrations were required for the most resistant cell line U87-MG. Moreover, the highest and lowest p53 levels have been observed, respectively, in A459 and U87-MG cells. The alterations in the cell cycle and in cell-cycle-related proteins were observed in A549 at lower concentrations than U87-MG. In conclusion, with this article we have demonstrated that Rigosertib has different efficacy depending on the cell line considered and that it could be a potential antineoplastic agent against lung cancer in humans. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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18 pages, 3376 KiB

Open AccessArticle

First Report of FARSA in the Regulation of Cell Cycle and Survival in Mantle Cell Lymphoma Cells via PI3K-AKT and FOXO1-RAG1 Axes

by Min Feng, Kun Yang, Jia Wang, Guilan Li and Han Zhang

Int. J. Mol. Sci. 2023, 24(2), 1608; https://doi.org/10.3390/ijms24021608 - 13 Jan 2023

Cited by 3 | Viewed by 2107

Abstract

Cancer-associated factors have been largely identified in the understanding of tumorigenesis and progression. However, aminoacyl-transfer RNA (tRNA) synthetases (aaRSs) have so far been neglected in cancer research due to their canonical activities in protein translation and synthesis. FARSA, the alpha subunit of the phenylalanyl-tRNA synthetase is elevated across many cancer types, but its function in mantle cell lymphoma (MCL) remains undetermined. Herein, we found the lowest levels of FARSA in patients with MCL compared with other subtypes of lymphomas, and the same lower levels of FARSA were observed in chemoresistant MCL cell lines. Unexpectedly, despite the essential catalytic roles of FARSA, knockdown of FARSA in MCL cells did not lead to cell death but resulted in accelerated cell proliferation and cell cycle, whereas overexpression of FARSA induced remarkable cell-cycle arrest and overwhelming apoptosis. Further RNA sequencing (RNA-seq) analysis and validation experiments confirmed a strong connection between FARSA and cell cycle in MCL cells. Importantly, FARSA leads to the alteration of cell cycle and survival via both PI3K-AKT and FOXO1-RAG1 axes, highlighting a FARSA-mediated regulatory network in MCL cells. Our findings, for the first time, reveal the noncanonical roles of FARSA in MCL cells, and provide novel insights into understanding the pathogenesis and progression of B-cell malignancies. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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15 pages, 2662 KiB

Open AccessArticle

PARP Inhibitor Inhibits the Vasculogenic Mimicry through a NF-κB-PTX3 Axis Signaling in Breast Cancer Cells

by Justine Chivot, Nathalie Ferrand, Aude Fert, Patrick Van Dreden, Romain Morichon and Michèle Sabbah

Int. J. Mol. Sci. 2022, 23(24), 16171; https://doi.org/10.3390/ijms232416171 - 18 Dec 2022

Cited by 3 | Viewed by 2404

Abstract

Poly (ADP-ribose) polymerase inhibitors (PARPi) are targeted therapies that inhibit PARP proteins which are involved in a variety of cell functions. PARPi may act as modulators of angiogenesis; however, the relationship between PARPi and the vasculogenic mimicry (VM) in breast cancer remains unclear. To determine whether PARPi regulate the vascular channel formation, we assessed whether the treatment with olaparib, talazoparib and veliparib inhibits the vascular channel formation by breast cancer cell lines. Here, we found that PARPi act as potent inhibitors of the VM formation in triple negative breast cancer cells, independently of the BRCA status. Mechanistically, we find that PARPi trigger and inhibit the NF-κB signaling, leading to the inhibition of the VM. We further show that PARPi decrease the expression of the angiogenic factor PTX3. Moreover, PTX3 rescued the PARPi-inhibited VM inhibition. In conclusion, our results indicate that PARPi, by targeting the VM, may provide a new therapeutic approach for triple negative breast cancer. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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Review

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21 pages, 7363 KiB

Open AccessReview

ADP-Ribosylation Factor 6 Pathway Acts as a Key Executor of Mesenchymal Tumor Plasticity

by Ari Hashimoto and Shigeru Hashimoto

Int. J. Mol. Sci. 2023, 24(19), 14934; https://doi.org/10.3390/ijms241914934 - 5 Oct 2023

Cited by 1 | Viewed by 2169

Abstract

Despite the “big data” on cancer from recent breakthroughs in high-throughput technology and the development of new therapeutic modalities, it remains unclear as to how intra-tumor heterogeneity and phenotypic plasticity created by various somatic abnormalities and epigenetic and metabolic adaptations orchestrate therapy resistance, immune evasiveness, and metastatic ability. Tumors are formed by various cells, including immune cells, cancer-associated fibroblasts, and endothelial cells, and their tumor microenvironment (TME) plays a crucial role in malignant tumor progression and responses to therapy. ADP-ribosylation factor 6 (ARF6) and AMAP1 are often overexpressed in cancers, which statistically correlates with poor outcomes. The ARF6-AMAP1 pathway promotes the intracellular dynamics and cell-surface expression of various proteins. This pathway is also a major target for KRAS/TP53 mutations to cooperatively promote malignancy in pancreatic ductal adenocarcinoma (PDAC), and is closely associated with immune evasion. Additionally, this pathway is important in angiogenesis, acidosis, and fibrosis associated with tumor malignancy in the TME, and its inhibition in PDAC cells results in therapeutic synergy with an anti-PD-1 antibody in vivo. Thus, the ARF6-based pathway affects the TME and the intrinsic function of tumors, leading to malignancy. Here, we discuss the potential mechanisms of this ARF6-based pathway in tumorigenesis, and novel therapeutic strategies. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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20 pages, 1885 KiB

Open AccessReview

Bacterial Therapy of Cancer: A Way to the Dustbin of History or to the Medicine of the Future?

by Larisa N. Ikryannikova, Neonila V. Gorokhovets, Darya A. Belykh, Leonid K. Kurbatov and Andrey A. Zamyatnin, Jr.

Int. J. Mol. Sci. 2023, 24(11), 9726; https://doi.org/10.3390/ijms24119726 - 3 Jun 2023

Cited by 2 | Viewed by 2624

Abstract

Bacteria are the constant companions of the human body throughout its life and even after its death. The history of a human disease such as cancer and the history of microorganisms, particularly bacteria, are believed to closely intertwined. This review was conceived to highlight the attempts of scientists from ancient times to the present day to discover the relationship between bacteria and the emergence or development of tumors in the human body. Challenges and achievements of 21st century science in forcing bacteria to serve for cancer treatment are considered. The future possibilities of bacterial cancer therapy, including the creation of bacterial microrobots, or “bacteriobots”, are also discussed. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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25 pages, 1634 KiB

Open AccessReview

Targeting DNA Methylation in Leukemia, Myelodysplastic Syndrome, and Lymphoma: A Potential Diagnostic, Prognostic, and Therapeutic Tool

by Lenka Kalinkova, Aneta Sevcikova, Viola Stevurkova, Ivana Fridrichova and Sona Ciernikova

Int. J. Mol. Sci. 2023, 24(1), 633; https://doi.org/10.3390/ijms24010633 - 30 Dec 2022

Cited by 7 | Viewed by 3461

Abstract

DNA methylation represents a crucial mechanism of epigenetic regulation in hematologic malignancies. The methylation process is controlled by specific DNA methyl transferases and other regulators, which are often affected by genetic alterations. Global hypomethylation and hypermethylation of tumor suppressor genes are associated with hematologic cancer development and progression. Several epi-drugs have been successfully implicated in the treatment of hematologic malignancies, including the hypomethylating agents (HMAs) decitabine and azacytidine. However, combinations with other treatment modalities and the discovery of new molecules are still the subject of research to increase sensitivity to anti-cancer therapies and improve patient outcomes. In this review, we summarized the main functions of DNA methylation regulators and genetic events leading to changes in methylation landscapes. We provide current knowledge about target genes with aberrant methylation levels in leukemias, myelodysplastic syndromes, and malignant lymphomas. Moreover, we provide an overview of the clinical trials, focused mainly on the combined therapy of HMAs with other treatments and its impact on adverse events, treatment efficacy, and survival rates among hematologic cancer patients. In the era of precision medicine, a transition from genes to their regulation opens up the possibility of an epigenetic-based approach as a diagnostic, prognostic, and therapeutic tool. Full article

(This article belongs to the Special Issue Novel Molecular Mechanisms Underlying Tumorigenesis and Innovative Therapeutic Approaches for Cancer-Fighting 2.0)

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