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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (1 February 2021) | Viewed by 12094

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Prof. Dr. Jack A. Schalken

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Research Director Urology, Dept. of Urology, University Hospital Nijmegen, Box 9101, NL-6500 HB Nijmegen, The Netherlands
Interests: molecular and cellbiology of oncological diseases; cadherine mediated interactions and signal transductions; molecular diagnostics; urogenital oncology; veterinary oncology
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Special Issue Information

Dear Colleagues,

Molecular technology platforms have exponentially developed to a status where individual patient-acquired pathologies can be profiled at various levels. Where does the technology meet unmet clinical needs?

In this Special Issue, we invite you to submit manuscripts that illustrate the clinical utility and impact of molecular research into clinical urological practice. We invite both oncological, as well as non-oncological papers. Topics to be considered include, but are not limited to, precision medicine in GU oncology, new molecular therapeutical targets, biomarkers for non-oncological bladder disease, and advances in molecular tissue engineering.

Prof. Dr. Jack A. Schalken
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.

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Keywords

Precision medicine in GU oncology
New molecular therapeutical targets
Biomarkers for non-oncological bladder disease
Advances in molecular tissue engineering

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Published Papers (4 papers)

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19 pages, 3943 KiB

Open AccessArticle

NLRP3 Inflammasome: A New Pharmacological Target for Reducing Testicular Damage Associated with Varicocele

by Pietro Antonuccio, Antonio Girolamo Micali, Carmelo Romeo, Jose Freni, Giovanna Vermiglio, Domenico Puzzolo, Francesco Squadrito, Natasha Irrera, Herbert R. Marini, Rosa Alba Rana, Giovanni Pallio and Letteria Minutoli

Int. J. Mol. Sci. 2021, 22(3), 1319; https://doi.org/10.3390/ijms22031319 - 28 Jan 2021

Cited by 28 | Viewed by 3138

Abstract

Many bioactive natural compounds are being increasingly used for therapeutics and nutraceutical applications to counteract male infertility, particularly varicocele. The roles of selenium and Polydeoxyribonucleotide (PDRN) were investigated in an experimental model of varicocele, with particular regard to the role of NLRP3 inflammasome. Male rats underwent sham operation and were daily administered with vehicle, seleno-L-methionine (Se), PDRN, and with the association Se-PDRN. Another group of rats were operated for varicocele. After twenty-eight days, sham and varicocele rats were sacrificed and both testes were weighted and analyzed. All the other rats were challenged for one month with the same compounds. In varicocele animals, lower testosterone levels, testes weight, NLRP3 inflammasome, IL-1β and caspase-1 increased gene expression were demonstrated. TUNEL assay showed an increased number of apoptotic cells. Structural and ultrastructural damage to testes was also shown. PDRN alone significantly improved all considered parameters more than Se. The Se-PDRN association significantly improved all morphological parameters, significantly increased testosterone levels, and reduced NLRP3 inflammasome, caspase-1 and IL-1β expression and TUNEL-positive cell numbers. Our results suggest that NLRP3 inflammasome can be considered an interesting target in varicocele and that Se-PDRN may be a new medical approach in support to surgery. Full article

(This article belongs to the Special Issue Molecular Research on Urology 2.0)

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14 pages, 4329 KiB

Open AccessArticle

Many Different LINE-1 Retroelements Are Activated in Bladder Cancer

by Patcharawalai Whongsiri, Wolfgang Goering, Tobias Lautwein, Christiane Hader, Günter Niegisch, Karl Köhrer, Michèle J. Hoffmann and Wolfgang A. Schulz

Int. J. Mol. Sci. 2020, 21(24), 9433; https://doi.org/10.3390/ijms21249433 - 11 Dec 2020

Cited by 7 | Viewed by 2556

Abstract

Human genomes contain about 100,000 LINE-1 (L1) retroelements, of which more than 100 are intact. L1s are normally tightly controlled by epigenetic mechanisms, which often fail in cancer. In bladder urothelial carcinoma (UC), particularly, L1s become DNA-hypomethylated, expressed and contribute to genomic instability and tumor growth. It is, however, unknown which individual L1s are activated. Following RNA-immunoprecipitation with a L1-specific antibody, third generation nanopore sequencing detected transcripts of 90 individual elements in the VM-Cub-1 UC line with high overall L1 expression. In total, 10 L1s accounted for >60% of the reads. Analysis of five specific L1s by RT-qPCR revealed generally increased expression in UC tissues and cell lines over normal controls, but variable expression among tumor cell lines from bladder, prostate and testicular cancer. Chromatin immunoprecipitation demonstrated active histone marks at L1 sequences with increased expression in VM-Cub-1, but not in a different UC cell line with low L1 expression. We conclude that many L1 elements are epigenetically activated in bladder cancer in a varied pattern. Our findings indicate that expression of individual L1s is highly heterogeneous between and among cancer types. Full article

(This article belongs to the Special Issue Molecular Research on Urology 2.0)

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13 pages, 1776 KiB

Open AccessArticle

Role of Nuclear Claudin-4 in Renal Cell Carcinoma

by Takuya Owari, Takamitsu Sasaki, Kiyomu Fujii, Rina Fujiwara-Tani, Shingo Kishi, Shiori Mori, Takuya Mori, Kei Goto, Isao Kawahara, Yasushi Nakai, Makito Miyake, Yi Luo, Nobumichi Tanaka, Masuo Kondoh, Kiyohide Fujimoto and Hiroki Kuniyasu

Int. J. Mol. Sci. 2020, 21(21), 8340; https://doi.org/10.3390/ijms21218340 - 6 Nov 2020

Cited by 16 | Viewed by 2748

Abstract

Claudin-4 (CLDN4) is a tight junction protein to maintain the cancer microenvironment. We recently reported the role of the CLDN4 not forming tight junction in the induction of epithelial-mesenchymal transition (EMT). Herein, we investigated the role of CLDN4 in renal cell carcinoma (RCC), focusing on CLDN4. CLDN4 expression in 202 RCCs was examined by immunostaining. CLDN4 phosphorylation and subcellular localization were examined using high metastatic human RCC SN12L1 and low metastatic SN12C cell lines. In 202 RCC cases, the CLDN4 expression decreased in the cell membrane and had no correlation with clinicopathological factors. However, CLDN4 was localized in the nucleus in 5 cases (2%), all of which were pT3. Contrastingly, only 6 of 198 nuclear CLDN4-negative cases were pT3. CLDN4 was found in the nuclear fraction of a highly metastatic human RCC cell line, SN12L1, but not in the low metastatic SN12C cells. In SN12L1 cells, phosphorylation of tyrosine and serine residues was observed in cytoplasmic CLDN4, but not in membranous CLDN4. In contrast, phosphorylation of serine residues was observed in nuclear CLDN4. In SN12L1 cells, CLDN4 tyrosine phosphorylation by EphA2/Ephrin A1 resulted in the release of CLDN4 from tight junction and cytoplasmic translocation. Furthermore, protein kinase C (PKC)-ε phosphorylated the CLDN4 serine residue, resulting in nuclear import. Contrarily, in SN12C cells that showed decreased expression of EphA2/Ephrin A1 and PKCε, the activation of EphA2/EphrinA1 and PKCε induced cytoplasmic and nuclear translocation of CLDN4, respectively. Furthermore, the nuclear translocation of CLDN4 promoted the nuclear translocation of Yes-associated protein (YAP) bound to CLDN4, which induced the EMT phenotype. These findings suggest that the release of CLDN4 by impaired tight junction might be a mechanism underlying the malignant properties of RCC. These findings suggest that the release of CLDN4 by impaired tight junction might be one of the mechanisms of malignant properties of RCC. Full article

(This article belongs to the Special Issue Molecular Research on Urology 2.0)

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10 pages, 3114 KiB

Open AccessCase Report

Germline Whole-Gene Deletion of FH Diagnosed from Tumor Profiling

by Arisa Ueki, Kokichi Sugano, Kumiko Misu, Eriko Aimono, Kohei Nakamura, Shigeki Tanishima, Nobuyuki Tanaka, Shuji Mikami, Akira Hirasawa, Miho Ando, Teruhiko Yoshida, Mototsugu Oya, Hiroshi Nishihara and Kenjiro Kosaki

Int. J. Mol. Sci. 2021, 22(15), 7962; https://doi.org/10.3390/ijms22157962 - 26 Jul 2021

Cited by 4 | Viewed by 2979

Abstract

Hereditary leiomyomatosis and renal cell carcinoma (HL (RCC)) entails cutaneous and uterine leiomyomatosis with aggressive type 2 papillary RCC-like histology. HLRCC is caused by pathogenic variants in the FH gene, which encodes fumarate hydratase (FH). Here, we describe an episode of young-onset RCC caused by a genomic FH deletion that was diagnosed via clinical sequencing. A 35-year-old woman was diagnosed with RCC and multiple metastases: histopathological analyses supported a diagnosis of FH-deficient RCC. Although the patient had neither skin tumors nor a family history of HLRCC, an aggressive clinical course at her age and pathological diagnosis of FH-deficient RCC suggested a germline FH variant. After counseling, the patient provided written informed consent for germline genetic testing. She was simultaneously subjected to paired tumor profiling tests targeting the exome to identify a therapeutic target. Although conventional germline sequencing did not detect FH variants, exome sequencing revealed a heterozygous germline FH deletion. As such, paired tumor profiling, not conventional sequencing, was required to identify this genetic deletion. RCC caused by a germline FH deletion has hitherto not been described in Japan, and the FH deletion detected in this patient was presumed to be of maternal European origin. Although the genotype-phenotype correlation in HLRCC-related tumors is unclear, the patient’s family was advised to undergo genetic counseling to consider additional RCC screening. Full article

(This article belongs to the Special Issue Molecular Research on Urology 2.0)

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