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Cancers
Special Issues
Urology Cancers: Drug Resistance and Signaling Mechanism
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Urology Cancers: Drug Resistance and Signaling Mechanism

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 15 December 2024 | Viewed by 2711

Special Issue Editors

Dr. Eswar Shankar

E-Mail Website
Guest Editor
Research Assistant Professor, Medical Oncology Division, Department of Internal Medicine, Wexner Medical Center, Ohio State University，420 W 12th Ave, Columbus, OH 43210, USA
Interests: drug resistance; oncogene; tumor suppressors; apoptosis; epigenetic changes; DNA methylations; combination treatment; angiogenesis
Dr. Ashish Tyagi

E-Mail Website
Guest Editor
Research Assistant Professor, Texas A&M University, College Station, TX, USA
Interests: carcinogenesis; chemotherapy; chemo-resistance; biomarker discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Urologic cancers comprise kidney, bladder, testicular, prostate, and penial cancers. In most cancer types, chemotherapy along with radiotherapy and surgery has become the accepted modality for cure. Patients that progress to the metastatic stage of urologic cancers are at high risk of relapse and death due to the development of resistance to existing therapies. Cancer cells adapt different mechanisms to resist treatment, including alteration in drug transport and metabolism, mutation, and amplification of drug targets, as well as genetic and/or epigenetic reprogramming, leading to impaired apoptosis. Tumor heterogeneity, wherein small subpopulations of cells may acquire resistance under selective drug pressure, can result in multidrug resistance, leading to failure of prevalent treatment modality.

This issue sets a forum for scientists working in urologic cancers to share their findings on mechanisms leading to drug resistance at the cellular and molecular level. The research may have both in vitro and in vivo approaches along with bioinformatic as well as computational analysis. The overall goal of the issue is to address drug resistance due to changes including but not limited to drug inactivation, mutations, and abrogation of the tumor suppressor function of target genes, epigenetic modifications, etc. The issue focuses on findings that outline efforts to overcome drug resistance using the latest technologies, techniques, and models. The issue also invites reviews with detailed updates in this arena.

Dr. Eswar Shankar
Dr. Ashish Tyagi
Guest Editors

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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • drug resistance
  • tumor mutation
  • metastasis
  • epigenetic modification
  • urologic cancer
  • drug inactivation

Published Papers (2 papers)

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Research

12 pages, 3018 KiB  
Article
Anti-Proliferative Effects of Lidocaine as an Autophagy Inducer in Bladder Cancer via Intravesical Instillation: In Vitro and Xenograft Mouse Model Experiments
by Young Chul Yoo, Na-Young Kim, Seokyung Shin, Yunil Yang, Ji Hae Jun, Ju Eun Oh and Myoung Hwa Kim
Cancers 2024, 16(7), 1267; https://doi.org/10.3390/cancers16071267 - 24 Mar 2024
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Abstract
Lidocaine exerts potential anti-tumor effects on various cancer cell lines, and its intravesical instillation is considered safer than intravenous administration for bladder cancer. However, the mechanisms underlying its anti-tumor effects have not been fully elucidated. Here, we aimed to elucidate the anti-tumor molecular [...] Read more.
Lidocaine exerts potential anti-tumor effects on various cancer cell lines, and its intravesical instillation is considered safer than intravenous administration for bladder cancer. However, the mechanisms underlying its anti-tumor effects have not been fully elucidated. Here, we aimed to elucidate the anti-tumor molecular mechanisms of lidocaine in bladder cancer cells and a xenograft model to substantiate the efficacy of its intravesical administration. We investigated the anti-proliferative and autophagyinducing activities of lidocaine in Nara Bladder Tumor No. 2 (NBT-II) rat bladder carcinoma cells using cell viability, flow cytometry, a wound healing assay, and western blotting. We also established a xenograft mouse model of bladder cancer, and cancer growth was examined using in vivo bioluminescence imaging. Lidocaine decreased cell viability, induced G0/G1 phase cell cycle arrest, and inhibited cell migration partially via glycogen synthase kinase (GSK) 3β phosphorylation. Moreover, a combination of lidocaine and SB216763 (a GSK3β inhibitor) suppressed autophagy-related protein expression. Bafilomycin-A1 with lidocaine significantly enhanced microtubule-associated protein 1A/1B-light chain (LC3B) expression; however, it decreased LC3B expression in combination with 3-methyladenine compared to lidocaine alone. In the xenograft mouse model, the bladder cancer volume was reduced by lidocaine. Overall, lidocaine exerts anti-proliferative effects on bladder cancer via an autophagy-inducing mechanism. Full article
(This article belongs to the Special Issue Urology Cancers: Drug Resistance and Signaling Mechanism)
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25 pages, 6742 KiB  
Article
Genome-Wide Screening Identifies Gene AKR1C1 Critical for Resistance to Pirarubicin in Bladder Cancer
by Zhenyu Nie, Yuanhui Gao, Mei Chen, Yanling Peng, Na Guo, Hui Cao, Denggao Huang, Xin Gao and Shufang Zhang
Cancers 2023, 15(9), 2487; https://doi.org/10.3390/cancers15092487 - 26 Apr 2023
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Abstract
Non-muscle-invasive bladder cancer (NMIBC) is a common tumor of the urinary system. Given its high rates of recurrence, progression, and drug resistance, NMIBC seriously affects the quality of life and limits the survival time of patients. Pirarubicin (THP) is a bladder infusion chemotherapy [...] Read more.
Non-muscle-invasive bladder cancer (NMIBC) is a common tumor of the urinary system. Given its high rates of recurrence, progression, and drug resistance, NMIBC seriously affects the quality of life and limits the survival time of patients. Pirarubicin (THP) is a bladder infusion chemotherapy drug recommended by the guidelines for NMIBC. Although the widespread use of THP reduces the recurrence rate of NMIBC, 10–50% of patients still suffer from tumor recurrence, which is closely related to tumor resistance to chemotherapy drugs. This study was performed to screen the critical genes causing THP resistance in bladder cancer cell lines by using the CRISPR/dCas9-SAM system. Thus, AKR1C1 was screened. Results showed that the high expression of AKR1C1 could enhance the drug resistance of bladder cancer to THP both in vivo and in vitro. This gene could reduce the levels of 4-hydroxynonenal and reactive oxygen species (ROS) and resist THP-induced apoptosis. However, AKR1C1 did not affect the proliferation, invasion, or migration of the bladder cancer cells. Aspirin, which is an AKR1C1 inhibitor, could help reduce the drug resistance caused by AKR1C1. After receiving THP treatment, the bladder cancer cell lines could upregulate the expression of the AKR1C1 gene through the ROS/KEAP1/NRF2 pathway, leading to resistance to THP treatment. Using tempol, which is an inhibitor of ROS, could prevent the upregulation of AKR1C1 expression. Full article
(This article belongs to the Special Issue Urology Cancers: Drug Resistance and Signaling Mechanism)
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