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Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 7979

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Special Issue Editors

Dr. Silvia Di Agostino

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IRCCS Regina Elena National Cancer Institute, Roma, Italy
Interests: genomic instability; cell cycle checkpoints; dna repair; transcriptional regulation; molecular oncology; head and neck; p53 family; mutant p53; hippo pathway
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Dr. Vittoria Rago

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Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Arcavacata di Rende, 87036 Cosenza, Italy
Interests: male reproduction; testicular cancer; prostate cancer
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Dr. Anna Perri

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Department of Experimental and Clinical Medicine, University “Magna Graecia” Catanzaro, 88100 Catanzaro, Italy
Interests: molecular biology; signal transduction; p75NTR-signaling; apoptosis; autophagy; EMT; renal and peritoneal fibrosis; inflammation; biological activity of natural compounds in cancer and chronic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit a manuscript to the Special Issue “Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments”. Most types of urogenital cancer present with non-specific symptoms and the arrival of the diagnosis is often late.

Despite progress in the most innovative tumor therapies, the appearance of chemoresistance and metastasis represents a common cause of death in patients suffering from urological neoplasms. Therefore, it is necessary to develop new early diagnosis approaches and therapies that can improve treatment outcomes. For this purpose, it seems important to implement an understanding of the molecular mechanisms that occur in urological tumors and the research on molecular biomarkers capable of predicting tumor behavior and the risk of disease recurrence and chemoresistance.

The main aim of this Special Issue is to publish original research articles and reviews relating to urological neoplasms.

We look forward to receiving your contributions.

The aspects to address are as follows:

Molecular mechanisms involved in the carcinogenesis of urogenital tumors;
New treatment and diagnosis approaches for urogenital tumors;
Identification of specific molecular targets for urogenital tumors;
New knowledge on etiological factors (viruses, nutrition, and environmental contaminants).

Dr. Silvia Di Agostino
Dr. Vittoria Rago
Dr. Anna Perri
Guest Editors

Manuscript Submission Information

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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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

prostate cancer
bladder cancer
renal cell carcinoma
testicular cancer
ovarian cancer
endometrial cancer
carcinogenesis
biomarkers
early diagnosis
upper urinary tract tumors
diagnosis
treatment
environmental factors
diet

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Published Papers (10 papers)

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Research

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19 pages, 7484 KiB

Open AccessArticle

Comprehensive Integrated Analysis Reveals the Spatiotemporal Microevolution of Cancer Cells in Patients with Bone-Metastatic Prostate Cancer

by Yinghua Feng, Xiuli Zhang, Guangpeng Wang, Feiya Yang, Ruifang Li, Lu Yin, Dong Chen, Wenkuan Wang, Mingshuai Wang, Zhiyuan Hu, Yuan Sh and Nianzeng Xing

Biomedicines 2025, 13(4), 909; https://doi.org/10.3390/biomedicines13040909 - 9 Apr 2025

Viewed by 83

Abstract

Background/Objectives: Bone metastasis is a frequent and life-threatening event in advanced cancers, affecting up to 70–85% of prostate cancer patients. Understanding the cellular and molecular mechanisms underlying bone metastasis is essential for developing targeted therapies. This study aimed to systematically characterize the heterogeneity and microenvironmental adaptation of prostate cancer bone metastases using single-cell transcriptomics. Methods: We integrated the largest single-cell transcriptome dataset to date, encompassing 124 samples from primary prostate tumors, various bone metastatic sites, and non-malignant tissues (e.g., benign prostatic hyperplasia, normal bone marrow). After quality control, 602,497 high-quality single-cell transcriptomes were analyzed. We employed unsupervised clustering, gene expression profiling, mutation analysis, and metabolic pathway reconstruction to characterize cancer cell subtypes and tumor microenvironmental remodeling. Results: Cancer epithelial cells dominated the tumor microenvironment but exhibited pronounced heterogeneity, posing challenges for conventional clustering methods. By integrating genetic and metabolic features, we revealed key evolutionary trajectories of epithelial cancer cells during metastasis. Notably, we identified a novel epithelial subpopulation, NEndoCs, characterized by unique differentiation patterns and distinct spatial distribution across metastatic niches. We also observed significant metabolic reprogramming and recurrent mutations linked to prostate-to-bone microenvironmental transitions. Conclusions: This study comprehensively elucidates the mutation patterns, metabolic reprogramming, and microenvironment adaptation mechanisms of bone metastasis in prostate cancer, providing key molecular targets and clinical strategies for the precise treatment of bone metastatic prostate cancer. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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18 pages, 6195 KiB

Open AccessArticle

Engineered Expression of Hepatocyte Growth Factor Activator Inhibitor-1 (HAI-1) Reduces the Growth of Bladder Cancer Cells

by Yuichi Katayama, Takahiro Akioka, Shoichi Kimura, Masato Fujii, Takahiro Nagai, Takumi Kiwaki, Makiko Kawaguchi, Tsuyoshi Fukushima, Yuichiro Sato, Shoichiro Mukai, Toshiyuki Kamoto and Atsuro Sawada

Biomedicines 2025, 13(4), 871; https://doi.org/10.3390/biomedicines13040871 - 3 Apr 2025

Viewed by 138

Abstract

Background: The function of hepatocyte growth factor activator inhibitor (HAI)-1 and HAI-2 in bladder cancer has not been well evaluated. In a previous study, we reported upregulated MET phosphorylation and decreased expression of HAI-1 in bladder cancer as poor prognostic factors. In this study, we analyzed the therapeutic effect of HAI-1 and HAI-2 on bladder cancer cells through the inhibition of MET phosphorylation. Methods: We established stable HAI-1 and HAI-2 overexpression KU-1 cell lines (HAI-1 OE and HAI-2 OE) and HAIs knockdown T24 cell lines (HAI-1 KD and HAI-2 KD). These cell lines were used for cell proliferation, migration, and invasion assay. Next, the cell lines were injected with human fibroblasts subcutaneously in mice, and inhibition of growth was evaluated. Result: Significant inhibition in cancer cell proliferation, motility, and invasiveness was observed in HAI-1 OE and HAI-2 OE compared with the mock in the presence of HGF zymogen, whereas significant upregulation in cancer cell proliferation, motility, and invasiveness was observed in HAI-1 KD and HAI-2 KD cells. In vivo analysis showed significant inhibition of cancer cell growth in HAI-1 OE. Although a tendency toward the inhibition of growth was observed in HAI-2 OE, statistical significance was not achieved. Phosphorylation of MET in cancer tissues was downregulated in both cell lines. Conclusions: HAI-1 may have the therapeutic potential to reduce the growth of bladder cancer through the inhibition of MET phosphorylation. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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11 pages, 1122 KiB

Open AccessArticle

Biomarker-Based Nomogram to Predict Neoadjuvant Chemotherapy Response in Muscle-Invasive Bladder Cancer

by Meritxell Pérez, Juan José Lozano, Mercedes Ingelmo-Torres, Montserrat Domenech, Caterina Fernández Ramón, J. Alfred Witjes, Antoine G. van der Heijden, Maria José Requena, Antonio Coy, Ricard Calderon, Begoña Mellado, Antonio Alcaraz, Antoni Vilaseca and Maria J. Ribal

Biomedicines 2025, 13(3), 740; https://doi.org/10.3390/biomedicines13030740 - 18 Mar 2025

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Abstract

Background/Objectives: The aim of this study was to identify response prediction and prognostic biomarkers in muscle-invasive bladder cancer (MIBC) patients undergoing neoadjuvant chemotherapy (NAC). Methods: A retrospective multicentre study including 191 patients with MIBC who received NAC previous to radical cystectomy (RC) between 1996 and 2013. Gene expression patterns were analysed in 34 samples from transurethral resection of the bladder (TURB) using Illumina microarrays. The expression levels of 45 selected differentially expressed genes between responders and non-responders to NAC were validated by quantitative PCR in an independent cohort of 157 patients. Regression analysis was used to identify predictors of downstaging and relapse. A nomogram for predicting downstaging and relapse—including clinicopathological and gene expression variables—was developed. Results: The expression levels of 1352 transcripts differed between responders and non-responders to NAC. A nomogram based on the most predictive clinical variables (age, Tis (in situ), gender, history of NMIBC, and lymphadenopathy) and genes selected following the Akaike information criterion (AIC) (CBTB16, CHMP6, DDX54, CASP8, LOR, and PLEC) was then created. In addition, a three-gene expression prognostic model to predict tumour relapse was generated. This model was able to discriminate between two groups of patients with a significantly different probability of tumour relapse (HR: 2.11; CI: 1.16–3.83, p = 0.01). Conclusions: Our nomogram based on gene expression and clinical data is a useful tool to predict downstaging and tumour relapse after NAC in MIBC patients. Further validation is warranted. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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10 pages, 1061 KiB

Open AccessArticle

Low GCNT2/I-Branching Glycan Expression Is Associated with Bladder Cancer Aggressiveness

by Yuki Tobisawa, Keita Nakane, Takuya Koie, Tomoki Taniguchi, Masayuki Tomioka, Risa Tomioka-Inagawa, Kota Kawase, Makoto Kawase and Koji Iinuma

Biomedicines 2025, 13(3), 682; https://doi.org/10.3390/biomedicines13030682 - 10 Mar 2025

Viewed by 406

Abstract

Background/Objectives: Abnormal glycan formation on the cancer cell surface plays a crucial role in regulating tumor functions in bladder cancer. In this study, we investigated the roles of glucosaminyl (N-acetyl) transferase 2 (GCNT2) in bladder cancer progression and immune evasion. GCNT2 synthesizes I-branched polylactosamine chains on cell surface glycoproteins. Understanding its functions will provide insights into tumor–immune interactions, facilitating the development of effective immunotherapeutic strategies. Methods: GCNT2 expression levels in bladder cancer cell lines and patient tumor samples were analyzed via quantitative polymerase chain reaction and immunohistochemistry. GCNT2 functions were assessed via overexpression and knockdown experiments. Its effect on natural killer (NK) cell-mediated cytotoxicity was evaluated via in vitro assay. Cytotoxic granule release from NK cells was measured via enzyme-linked immunosorbent assay. Results: GCNT2 expression was inversely correlated with bladder cancer aggressiveness in both cell lines and patient samples. Low GCNT2 levels were associated with advanced tumor stage and grade, suggesting the tumor-suppressive roles of GCNT2. Notably, GCNT2 overexpression enhanced the susceptibility of bladder cancer cells to NK cell-mediated killing, whereas its knockdown promoted immune evasion. GCNT2-overexpressing cells strongly induced the release of cytotoxic granules from NK cells, indicating enhanced immune recognition. Conclusions: Our findings suggest that aggressive bladder tumors evade NK cell immunity by decreasing the GCNT2 levels and that I-antigen glycans synthesized by GCNT2 are crucial for NK cell recognition by tumor cells. Our findings provide insights into the tumor–immune interactions in bladder cancer and GCNT2 and its associated pathways as potential targets for novel immunotherapeutic strategies. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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23 pages, 4635 KiB

Open AccessArticle

Spontaneous Necrosis of a High-Risk Bladder Tumor Under Immunotherapy for Concurrent Malignant Melanoma: Role of BRAF Mutations and PD-L1 Expression

by Cristian Condoiu, Mihael Musta, Alin Adrian Cumpanas, Razvan Bardan, Vlad Dema, Flavia Zara, Cristian Silviu Suciu, Cristina-Stefania Dumitru, Andreea Ciucurita, Raluca Dumache, Hossam Ismail and Dorin Novacescu

Biomedicines 2025, 13(2), 377; https://doi.org/10.3390/biomedicines13020377 - 5 Feb 2025

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Abstract

Background: Bladder cancer (BC) is a heterogeneous malignancy, and predicting response to immune checkpoint inhibitors (ICIs) remains a challenge. Herein, we investigate a high-risk bladder tumor, which developed during anti-BRAF/MEK therapy for a concurrent advanced BRAF-V600E-positive malignant melanoma (MM) and subsequently underwent complete spontaneous necrosis following Nivolumab immunotherapy, only to recur thereafter while still under the same treatment. This unique scenario provided an opportunity to investigate the roles of BRAF gene mutations in BC pathogenesis, respectively, of PD-L1 expression in immunotherapy response prediction. Methods: We retrospectively analyzed BC specimens obtained via transurethral resection at two critical time-points: prior to the complete spontaneous necrosis under Nivolumab (prenecrosis) and after tumor recurrence postnecrosis (postnecrosis). The BRAF gene mutation status was evaluated using quantitative polymerase chain reaction (qPCR). PD-L1 expression was assessed by immunohistochemistry (IHC), quantified using the combined positive score (CPS), and a cutoff of ≥10 for positivity. Results: Neither pre- nor postnecrosis BC samples harbored BRAF gene mutations. Prenecrosis PD-L1 expression (CPS = 5) indicated a minimal likelihood of response to immunotherapy. However, complete spontaneous necrosis occurred under Nivolumab, followed by recurrence with further reduced PD-L1 expression (CPS = 1). Conclusions: The complete BC regression challenges the conventional role of PD-L1 as a sole predictive biomarker for immunotherapy. This study also highlights the potential role of BRAF/MEK inhibitors in BC oncogenesis and underscores the need for alternative biomarkers, such as tumor mutation burden (TMB) and circulating tumor DNA (ctDNA), to guide treatment selection in BC better. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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14 pages, 2299 KiB

Open AccessArticle

Comparison of BCG Tokyo172 Strain Induction Therapy Between Low Dose and Standard Dose for Non-Muscle Invasive Bladder Cancer: Intravesical Instillation of BCG Tokyo172 Strain

by Hideyuki Isobe, Fumitaka Shimizu, Takeshi Ieda, So Nakamura, Naoko Takazawa, Hanna Suetsugu, Kazunori Kajino, Shu Hirai, Hisashi Hirano, Katsuhito Yuzawa and Shigeo Horie

Biomedicines 2025, 13(1), 174; https://doi.org/10.3390/biomedicines13010174 - 13 Jan 2025

Viewed by 876

Abstract

Objectives: The aim of this study was to identify factors that predict recurrence by comparing low-dose and standard-dose Bacillus Calmette-Guérin (BCG) induction therapy in patients with non-muscle invasive bladder cancer (NMIBC). Methods: A total of 273 consecutive NMIBC patients who received low-dose (40 mg) or standard-dose (80 mg) BCG intravesical instillation therapy between January 2004 and December 2023 were analyzed. Recurrence-free survival (RFS) rates were assessed using the Kaplan–Meier method with the log-rank test. Univariate and multivariate Cox proportional hazards regression analyses were used to identify independent predictors of recurrence based on the Club Urológico Español de Tratamiento Oncológico (CUETO) criteria. Results: The log-rank test showed that older age, low BCG dose, number of tumors, and a history of recurrence increased the risk of recurrence significantly. Regarding older patients, recurrence rates were similar between the two dose groups. However, younger patients had significantly lower recurrence rates with standard-dose BCG compared to low-dose BCG. Multiple Cox regression analysis confirmed that older age, low-dose BCG, greater than three tumors, and a history of recurrence were significant predictors of recurrence. Conclusions: In this study, we found that low-dose BCG induction therapy was associated with higher relapse rates compared with standard doses, especially in younger patients. Age-related differences in the immune response to BCG may influence these relapse patterns. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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16 pages, 3274 KiB

Open AccessArticle

Evaluation of BRIP-1 (FANCJ) and FANCI Protein Expression in Ovarian Cancer Tissue

by Mateusz Kozłowski, Dominika Borzyszkowska, Anna Golara, Damian Durys, Katarzyna Piotrowska, Agnieszka Kempińska-Podhorodecka and Aneta Cymbaluk-Płoska

Biomedicines 2024, 12(12), 2652; https://doi.org/10.3390/biomedicines12122652 - 21 Nov 2024

Viewed by 803

Abstract

Background: Ovarian cancer is one of the most common cancers in women. Markers associated with ovarian cancer are still being sought. The aim of this study was to evaluate the expression of BRIP-1 (FANCJ) and FANCI proteins in ovarian cancer tissue and to assess these expressions in differentiating the described clinical features. Methods: The study enrolled 68 patients with ovarian cancer. The cohort was divided into a HGSOC (high-grade serous ovarian cancer) group and a non-HGSOC group, which represented ovarian cancer other than HGSOC. Immunohistochemical evaluation of FANCI and BRIP-1 (FANCJ) protein expression in ovarian cancer tissue samples was performed. All statistical analyses were performed using StatView software (Carry, NC, USA). Results: The FANCI protein mostly showed moderate positive and strong positive expression, while BRIP-1 protein mostly showed no expression or positive expression. Patients with lower expression of FANCI and BRIP-1 showed differences in the clinical stage of HGSOC, which was not observed in patients with higher expression of these proteins. In addition, patients with lower BRIP-1 expression showed differences in menopausal status, which was not observed in patients with higher expression of this protein. Conclusions: This study shows that FANCI protein is a marker associated with lower FIGO stage and histologically high-grade cancer in a group of all ovarian cancers and in non-HGSOC. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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11 pages, 509 KiB

Open AccessArticle

Blood and Serum Se and Zn Levels and 10-Year Survival of Patients after a Diagnosis of Kidney Cancer

by Elżbieta Złowocka-Perłowska, Piotr Baszuk, Wojciech Marciniak, Róża Derkacz, Aleksandra Tołoczko-Grabarek, Marcin Słojewski, Artur Lemiński, Michał Soczawa, Milena Matuszczak, Adam Kiljańczyk, Rodney J. Scott and Jan Lubiński

Biomedicines 2024, 12(8), 1775; https://doi.org/10.3390/biomedicines12081775 - 6 Aug 2024

Cited by 2 | Viewed by 1284

Abstract

The aim of the project was to evaluate the association between selenium (Se) and zinc (Zn) levels in blood and serum and kidney cancer mortality. In a prospective group of 284 consecutive, unselected patients with kidney cancer, we evaluated their 10-year survival rate in relation to the levels of Se and Zn in their blood and serum. Micronutrient levels were measured using an inductively coupled plasma mass spectrometer. Patients were divided into quartiles based on the distribution of Se and Zn levels arranged in increasing order. The following variables were taken into account in the multivariable models: age at diagnosis, gender, smoking, type of surgery and histopathological examination results. We observed a statistically significant association of all-cause mortality when subgroups with low blood selenium levels were compared to patients with high selenium levels (HR = 7.74; p < 0.001). We found, in addition, that this correlation was much stronger when only men were assessed (HR = 11.6; p < 0.001). We did not find a statistically significant association for zinc alone. When we combined selenium and zinc levels (SeQI-ZnQI vs. SeQIV-ZnQIV), we observed the hazard ratio for kidney cancer death to be 12.4; p = 0.016. For patients in the highest quartile of blood zinc/selenium ratio, compared to those in the lowest, the HR was 2.53; p = 0.008. Our study suggests that selenium levels, combined selenium and zinc levels (SeQI-ZnQI vs. SeQIV-ZnQIV) and zinc-to-selenium ratio (Zn/Se) are attractive targets for clinical trials aimed at improving the survival of kidney cancer patients. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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Review

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14 pages, 1098 KiB

Open AccessReview

The Role of STEAP1 in Prostate Cancer: Implications for Diagnosis and Therapeutic Strategies

by Lingling Zhang, Xinyi Ren, Ran An, Hongchen Song, Yaqi Tian, Xuan Wei, Mingjun Shi and Zhenchang Wang

Biomedicines 2025, 13(4), 794; https://doi.org/10.3390/biomedicines13040794 - 26 Mar 2025

Viewed by 232

Abstract

Prostate cancer (PCa) is one of the most common malignancies and the second leading cause of cancer-related death in men worldwide. The six-transmembrane epithelial antigen of the prostate 1 (STEAP1) is exceptionally overexpressed in PCa, maintaining high expression even in the castration-resistant prostate cancer (CRPC) stage, making it a promising target for diagnosis and treatment. STEAP1-positive extracellular vesicles and STEAP1-PET imaging are optimistic approaches for the non-invasive detection of different stages of PCa. STEAP1-targeted therapy includes an antibody–drug conjugate (ADC), chimeric antigen receptor T cell (CAR-T), T-cell engager (TCE), and vaccines, which demonstrate valuable therapeutic prospects. This review presents the structure and pathophysiological function of STEAP1, synthesizes cutting-edge advances in STEAP1-targeted molecular imaging and clinical applications, and critically analyzes their translational potential to overcome the limitations of current PCa diagnosis and treatment. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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21 pages, 869 KiB

Open AccessReview

Recent Advancements in Research on DNA Methylation and Testicular Germ Cell Tumors: Unveiling the Intricate Relationship

by Alina-Teodora Nicu, Ileana Paula Ionel, Ileana Stoica, Liliana Burlibasa and Viorel Jinga

Biomedicines 2024, 12(5), 1041; https://doi.org/10.3390/biomedicines12051041 - 8 May 2024

Cited by 2 | Viewed by 1967

Abstract

Testicular germ cell tumors (TGCTs) are the most common type of testicular cancer, with a particularly high incidence in the 15–45-year age category. Although highly treatable, resistance to therapy sometimes occurs, with devastating consequences for the patients. Additionally, the young age at diagnosis and the treatment itself pose a great threat to patients’ fertility. Despite extensive research concerning genetic and environmental risk factors, little is known about TGCT etiology. However, epigenetics has recently come into the spotlight as a major factor in TGCT initiation, progression, and even resistance to treatment. As such, recent studies have been focusing on epigenetic mechanisms, which have revealed their potential in the development of novel, non-invasive biomarkers. As the most studied epigenetic mechanism, DNA methylation was the first revelation in this particular field, and it continues to be a main target of investigations as research into its association with TGCT has contributed to a better understanding of this type of cancer and constantly reveals novel aspects that can be exploited through clinical applications. In addition to biomarker development, DNA methylation holds potential for developing novel treatments based on DNA methyltransferase inhibitors (DNMTis) and may even be of interest for fertility management in cancer survivors. This manuscript is structured as a literature review, which comprehensively explores the pivotal role of DNA methylation in the pathogenesis, progression, and treatment resistance of TGCTs. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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