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Advanced Molecular Research in Tumors
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Advanced Molecular Research in Tumors

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: 31 October 2024 | Viewed by 4810

Special Issue Editor

Dr. Keisaku Sato

E-Mail Website
Guest Editor
Faculty Affairs and Professional Development, Indiana University, VA D2005, GAST, Indianapolis, IN, USA
Interests: hepatology; ductular reaction; liver fibrosis; hepatocellular carcinoma; cholangiocarcinoma

Special Issue Information

Dear Colleagues,

Cancer is one of the most lethal diseases worldwide, resulting in millions of deaths each year. Patients at the advanced stage suffer poor prognosis with limited treatment options; therefore, critical advancements in cancer research are still required, especially for early diagnosis and treatments. Previous studies have made significant progress in the field. Genome-wide association studies and screening have identified susceptible loci and gene mutations and aberrations associated with carcinogenesis and tumor metastasis. Advanced technology has introduced novel approaches in cancer research. Other key areas include the identification of novel biomarkers via bioinformatics or meta-analysis leading to early diagnosis; early diagnosis and prognosis prediction using artificial intelligence; novel therapeutic approach targeting immune checkpoints; patient-derived organoids or xenografts allowing to design personalized treatment options; and drug delivery to tumor cells using nanoparticles or extracellular vesicles.

We are excited to announce the Special Issue “Advanced Molecular Research in Tumors” of the International Journal of Molecular Sciences. Our goal is to introduce readers with novel technologies, methodologies, and approaches in cancer research. This Special Issue focuses on basic science research leading to an understanding of the pathophysiology of, early diagnosis of, and novel treatment options in any type of cancer. We welcome high-quality original research papers and comprehensive reviews from both established experts and emerging researchers in the field.

Dr. Keisaku Sato
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

  • cancer biomarkers
  • cancer progression
  • cancer bioinformatics
  • immunotherapy
  • cancer organoids
  • nanoparticles
  • extracellular vesicles
  • patient-derived xenografts
  • artificial intelligence

Published Papers (4 papers)

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Research

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14 pages, 2847 KiB  
Article
The Expression Patterns and Implications of MALAT1, MANCR, PSMA3-AS1 and miR-101 in Esophageal Adenocarcinoma
by Athanasios Syllaios, Maria Gazouli, Michail Vailas, Konstantinos S. Mylonas, Stratigoula Sakellariou, Stavros Sougioultzis, Ioannis Karavokyros, Theodoros Liakakos and Dimitrios Schizas
Int. J. Mol. Sci. 2024, 25(1), 98; https://doi.org/10.3390/ijms25010098 - 20 Dec 2023
Viewed by 1084
Abstract
Esophageal adenocarcinoma (EAC) is a malignant tumor with poorly understood molecular mechanisms. This study endeavors to elucidate how the long non-coding RNAs (lncRNAs) MALAT1, MANCR and PSMA3-AS1, as well as the microRNA miR-101, exhibit specific expression patterns in the pathogenesis [...] Read more.
Esophageal adenocarcinoma (EAC) is a malignant tumor with poorly understood molecular mechanisms. This study endeavors to elucidate how the long non-coding RNAs (lncRNAs) MALAT1, MANCR and PSMA3-AS1, as well as the microRNA miR-101, exhibit specific expression patterns in the pathogenesis and prognosis of EAC. A total of 50 EAC tissue samples (tumors and lymph nodes) and a control group comprising 26 healthy individuals were recruited. The samples underwent quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analyses. The relative expression levels of MALAT1, MANCR, PSMA3-AS1, and miR-101 were ascertained and correlated with various clinicopathological parameters including TNM staging, tumor characteristics (size and grade of the tumor) lymphatic invasion, disease-free (DFS) and overall survival (OS) of EAC patients. Quantitative analyses revealed that MALAT1 and MANCR were significantly upregulated in EAC tumors and positive lymph nodes when compared to control tissues (p < 0.05). Such dysregulations correlated positively with advanced lymphatic metastases and a higher N stage. DFS in the subgroup of patients with negative lymph nodes was higher in the setting of low-MANCR-expression patients compared to patients with high MANCR expression (p = 0.02). Conversely, miR-101 displayed a significant downregulation in EAC tumors and positive lymph nodes (p < 0.05), and correlated negatively with advanced tumor stage, lymphatic invasion and the grade of the tumor (p = 0.006). Also, patients with low miR-101 expression showed a tendency towards inferior overall survival. PSMA3-AS1 did not demonstrate statistically significant alterations (p > 0.05). This study reveals MALAT1, MANCR, and miR-101 as putative molecular markers for prognostic evaluation in EAC and suggests their involvement in EAC progression. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Tumors)
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13 pages, 1973 KiB  
Article
High Filamin a Expression in Adrenocortical Carcinomas Is Associated with a Favourable Tumour Behaviour: A European Multicentric Study
by Rosa Catalano, Barbara Altieri, Anna Angelousi, Maura Arosio, Francesca Bravi, Letizia Canu, Giorgio A. Croci, Mario Detomas, Emanuela Esposito, Emanuele Ferrante, Stefano Ferrero, Carmina T. Fuss, Gregory Kaltsas, Otilia Kimpel, Laura-Sophie Landwehr, Michaela Luconi, Valentina Morelli, Gabriella Nesi, Emma Nozza, Silviu Sbiera, Andreea L. Serban, Cristina L. Ronchi, Giovanna Mantovani and Erika Peverelliadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2023, 24(23), 16573; https://doi.org/10.3390/ijms242316573 - 21 Nov 2023
Viewed by 966
Abstract
The insulin-like growth factor 2 (IGF2) promotes cell growth by overactivating the IGF system in an autocrine loop in adrenocortical carcinomas (ACCs). The cytoskeleton protein filamin A (FLNA) acts as a repressor of IGF2 mitogenic signalling in ACC cells. The aims of this [...] Read more.
The insulin-like growth factor 2 (IGF2) promotes cell growth by overactivating the IGF system in an autocrine loop in adrenocortical carcinomas (ACCs). The cytoskeleton protein filamin A (FLNA) acts as a repressor of IGF2 mitogenic signalling in ACC cells. The aims of this study were to test FLNA expression by immunohistochemistry in 119 ACCs and 26 adrenocortical adenomas (ACAs) and to evaluate its relationship with clinicopathological features and outcome in ACCs. We found that 71.4% of ACCs did not express FLNA, whereas FLNA absence was a rare event in ACAs (15.4%, p < 0.001 vs. ACCs). In addition, the expression of FLNA was associated with a less aggressive tumour behaviour in ACCs. Indeed, the subgroup of ACCs with high FLNA showed a lower ENSAT stage, Weiss score, and S-GRAS score compared to ACCs with low FLNA expression (p < 0.05). Moreover, patients with high FLNA had a longer overall survival than those with low FLNA (p < 0.05). In conclusion, our data suggest that FLNA may represent a “protective” factor in ACCs, and the integration of FLNA immunohistochemical expression in ACC tissues along with other clinical and molecular markers could be helpful to improve diagnostic accuracy and prognosis prediction in ACCs. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Tumors)
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18 pages, 23283 KiB  
Article
BIRC5 Inhibition Is Associated with Pyroptotic Cell Death via Caspase3-GSDME Pathway in Lung Adenocarcinoma Cells
by Qingwei Zhang, Ximing Chen, Yingying Hu, Tong Zhou, Menghan Du, Run Xu, Yongchao Chen, Pingping Tang, Zhouxiu Chen and Jiamin Li
Int. J. Mol. Sci. 2023, 24(19), 14663; https://doi.org/10.3390/ijms241914663 - 28 Sep 2023
Cited by 3 | Viewed by 1257
Abstract
Lung adenocarcinoma (LUAD) is a prevalent type of thoracic cancer with a poor prognosis and high mortality rate. However, the exact pathogenesis of this cancer is still not fully understood. One potential factor that can contribute to the development of lung adenocarcinoma is [...] Read more.
Lung adenocarcinoma (LUAD) is a prevalent type of thoracic cancer with a poor prognosis and high mortality rate. However, the exact pathogenesis of this cancer is still not fully understood. One potential factor that can contribute to the development of lung adenocarcinoma is DNA methylation, which can cause changes in chromosome structure and potentially lead to the formation of tumors. The baculoviral IAP repeat containing the 5 (BIRC5) gene encodes the Survivin protein, which is a multifunctional gene involved in cell proliferation, migration, and invasion of tumor cells. This gene is elevated in various solid tumors, but its specific role and mechanism in lung adenocarcinoma are not well-known. To identify the potential biomarkers associated with lung adenocarcinoma, we screened the methylation-regulated differentially expressed genes (MeDEGs) of LUAD via bioinformatics analysis. Gene ontology (GO) process and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were applied to investigate the biological function and pathway of MeDEGs. A protein–protein interaction (PPI) network was employed to explore the key module and screen hub genes. We screened out eight hub genes whose products are aberrantly expressed, and whose DNA methylation modification level is significantly changed in lung adenocarcinoma. BIRC5 is a bona fide marker which was remarkably up-regulated in tumor tissues. Flow cytometry analysis, lactate dehydrogenase release (LDH) assay and Micro-PET imaging were performed in A549 cells and a mouse xenograft tumor to explore the function of BIRC5 in cell death of lung adenocarcinoma. We found that BIRC5 was up-regulated and related to a high mortality rate in lung adenocarcinoma patients. Mechanically, the knockdown of BIRC5 inhibited the proliferation of A549 cells and induced pyroptosis via caspase3/GSDME signaling. Our findings have unraveled that BIRC5 holds promise as a novel biomarker and therapeutic target for lung adenocarcinoma. Additionally, we have discovered a novel pathway in which BIRC5 inhibition can induce pyroptosis through the caspase3-GSDME pathway in lung adenocarcinoma cells. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Tumors)
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Review

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26 pages, 834 KiB  
Review
MicroRNAs as Potential Biomarkers of Environmental Exposure to Polycyclic Aromatic Hydrocarbons and Their Link with Inflammation and Lung Cancer
by Pablo Letelier, Rolando Saldías, Pía Loren, Ismael Riquelme and Neftalí Guzmán
Int. J. Mol. Sci. 2023, 24(23), 16984; https://doi.org/10.3390/ijms242316984 - 30 Nov 2023
Cited by 3 | Viewed by 1169
Abstract
Exposure to atmospheric air pollution containing volatile organic compounds such as polycyclic aromatic hydrocarbons (PAHs) has been shown to be a risk factor in the induction of lung inflammation and the initiation and progression of lung cancer. MicroRNAs (miRNAs) are small single-stranded non-coding [...] Read more.
Exposure to atmospheric air pollution containing volatile organic compounds such as polycyclic aromatic hydrocarbons (PAHs) has been shown to be a risk factor in the induction of lung inflammation and the initiation and progression of lung cancer. MicroRNAs (miRNAs) are small single-stranded non-coding RNA molecules of ~20–22 nucleotides that regulate different physiological processes, and their altered expression is implicated in various pathophysiological conditions. Recent studies have shown that the regulation of gene expression of miRNAs can be affected in diseases associated with outdoor air pollution, meaning they could also be useful as biomarkers of exposure to environmental pollution. In this article, we review the published evidence on miRNAs in relation to exposure to PAH pollution and discuss the possible mechanisms that may link these compounds with the expression of miRNAs. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Tumors)
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