Cell Biology in Kidney Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 4935

Special Issue Editors


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Guest Editor
Division of Medical Oncology, Cardinal Massaia Hospital, Department of Oncology, University of Turin, Corso Dante Alighieri 202, 14100 Asti, Italy
Interests: kidney; urothelial
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Guest Editor
Division of Medical Oncology, Department of Oncology, University of Turin, San Luigi Hospital, Regione Gonzole 10, 10040 Orbassano, Italy
Interests: kidney; urothelial

Special Issue Information

Dear Colleagues,

In the last fifteen years, a better understanding of the molecular mechanisms underlying neoplastic development and progression have led to a radical change in the therapy landscape of advanced renal cell carcinoma.

Renal cell carcinoma is a heterogeneous disease with several genetic and molecular alterations. Angiogenesis is a key player in the pathogenesis of this disease. In particular, the role of the mutations in the Von Hippel-Lindau tumor-suppressor gene, leading to an overexpression of the hypoxia-induced factors, is clearly defined.

The understanding of this biological landscape led to the development of therapies targeting VEGF and mTOR pathways. Three classes of targeted therapies with antiangiogenetic activity have received approval for advanced disease treatment: several tyrosine kinase inhibitors; a monoclonal antibody interfering with VEGF; and two mTOR inhibitors. These drugs have demonstrated impressive results in terms of objective response and progression-free survival.

Very recently, a deep improvement of the interplay between angiogenetic factors and immune cells led to a new revolution in the treatment landscape of this carcinoma. Combinations of immune-checkpoint inhibitors and immune-checkpoint inhibitors plus tyrosine kinase inhibitors have been shown to improve overall survival compared to tyrosine kinase inhibitor monotherapy, shifting the systemic treatment of this tumor from the "targeted therapy era" to the "golden age".

However, many questions remain to be explored. This Special Issue focuses on predictive biomarkers of response to available therapeutic agents, how to overcome the mechanisms of resistance, and the best therapy sequencing in daily clinical practice.

We look forward to your contributions.

Dr. Marcello Tucci
Dr. Consuelo Buttigliero
Guest Editors

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Published Papers (2 papers)

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Research

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18 pages, 10548 KiB  
Article
Cuproptosis-Related MiR-21-5p/FDX1 Axis in Clear Cell Renal Cell Carcinoma and Its Potential Impact on Tumor Microenvironment
by Mingyue Xie, Bo Cheng, Shuang Yu, Yajie He, Yu Cao, Tiejun Zhou, Kun Han, Rongyang Dai and Ronghao Wang
Cells 2023, 12(1), 173; https://doi.org/10.3390/cells12010173 - 31 Dec 2022
Cited by 14 | Viewed by 2670
Abstract
As a newly identified type of programmed cell death, cuproptosis may have an impact on cancer development, including clear cell renal cell carcinoma (ccRCC). Herein, we first noticed that the expression levels of cuproptosis regulators exhibited a tight correlation with the clinicopathological characteristics [...] Read more.
As a newly identified type of programmed cell death, cuproptosis may have an impact on cancer development, including clear cell renal cell carcinoma (ccRCC). Herein, we first noticed that the expression levels of cuproptosis regulators exhibited a tight correlation with the clinicopathological characteristics of ccRCC. The cuproptosis-sensitive sub-type (CSS), classified via consensus clustering analysis, harbored a higher overall survival rate compared to the cuproptosis-resistant sub-type (CRS), which may have resulted from the differential infiltration of immune cells. FDX1, the cuproptosis master regulator, was experimentally determined as a tumor suppressor in ccRCC cells by suppressing the cell growth and cell invasion of ACHN and OSRC-2 cells in a cuproptosis-dependent and -independent manner. The results from IHC staining also demonstrated that FDX1 expression was negatively correlated with ccRCC tumor initiation and progression. Furthermore, we identified the miR-21-5p/FDX1 axis in ccRCC and experimentally verified that miR-21-5p directly binds the 3′-UTR of FDX1 to mediate its degradation. Consequently, a miR-21-5p inhibitor suppressed the cell growth and cell invasion of ACHN and OSRC-2 cells, which could be compensated by FDX1 knockdown, reinforcing the functional linkage between miR-21-5p and FDX1 in ccRCC. Finally, we evaluated the ccRCC tumor microenvironment under the miR-21-5p/FDX1 axis and noted that this axis was strongly associated with the infiltration of immune cells such as CD4+ T cells, Treg cells, and macrophages, suggesting that this signaling axis may alter microenvironmental components to drive ccRCC progression. Overall, this study constructed the miR-21-5p/FDX1 axis in ccRCC and analyzed its potential impact on the tumor microenvironment, providing valuable insights to improve current ccRCC management. Full article
(This article belongs to the Special Issue Cell Biology in Kidney Cancer)
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Review

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19 pages, 338 KiB  
Review
Personalizing Care for Critically Ill Adults Using Omics: A Concise Review of Potential Clinical Applications
by Kay Choong See
Cells 2023, 12(4), 541; https://doi.org/10.3390/cells12040541 - 08 Feb 2023
Cited by 2 | Viewed by 1798
Abstract
Current guidelines for critically ill patients use broad recommendations to promote uniform protocols for the management of conditions such as acute kidney injury, acute respiratory distress syndrome, and sepsis. Although these guidelines have enabled the substantial improvement of care, mortality for critical illness [...] Read more.
Current guidelines for critically ill patients use broad recommendations to promote uniform protocols for the management of conditions such as acute kidney injury, acute respiratory distress syndrome, and sepsis. Although these guidelines have enabled the substantial improvement of care, mortality for critical illness remains high. Further outcome improvement may require personalizing care for critically ill patients, which involves tailoring management strategies for different patients. However, the current understanding of disease heterogeneity is limited. For critically ill patients, genomics, transcriptomics, proteomics, and metabolomics have illuminated such heterogeneity and unveiled novel biomarkers, giving clinicians new means of diagnosis, prognosis, and monitoring. With further engineering and economic development, omics would then be more accessible and affordable for frontline clinicians. As the knowledge of pathophysiological pathways mature, targeted treatments can then be developed, validated, replicated, and translated into clinical practice. Full article
(This article belongs to the Special Issue Cell Biology in Kidney Cancer)
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