Advances in the Pathology of Prostate Cancer

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 2754

Special Issue Editor

Division of Cancer Research and Training, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA
Interests: cancer chemoprevention and therapy; anti-cancer phytochemicals; combination treatment; mechanistic study; biomarker/target identification
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prostate cancer remains one of the most common malignancies among men worldwide, and its complex pathology necessitates continuous exploration and analysis. Deeper insights into the molecular and cellular underpinnings of this disease will help us discover new diagnostic and prognostic markers and identify and validate chemopreventive/therapeutic targets and biomarkers for the evaluation of chemopreventive/therapeutic responses.  

In this Special Issue, we seek original research articles and reviews on various aspects of prostate cancer’s pathology. The topics of interest include, but are not limited to, the molecular basis of prostate cancer, advancements in diagnostic techniques, emerging biomarkers, histopathological correlations with chemopreventive/therapeutic outcomes, and novel therapeutic strategies.

We encourage submissions from researchers across the globe. Together, let us advance our understanding of prostate cancer pathology to improve patients’ care and outcomes. We look forward to receiving your valuable contributions.

Dr. Piwen Wang
Guest Editor

Manuscript Submission Information

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Keywords

  • prostate cancer
  • molecular pathology
  • biomarker
  • chemoprevention
  • therapy

Published Papers (2 papers)

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Research

13 pages, 3146 KiB  
Article
Prostate Cancer-Specific Lysine 53 Acetylation of Cytochrome c Drives Metabolic Reprogramming and Protects from Apoptosis in Intact Cells
by Paul T. Morse, Junmei Wan, Tasnim Arroum, Mackenzie K. Herroon, Hasini A. Kalpage, Viktoriia Bazylianska, Icksoo Lee, Elisabeth I. Heath, Izabela Podgorski and Maik Hüttemann
Biomolecules 2024, 14(6), 695; https://doi.org/10.3390/biom14060695 - 14 Jun 2024
Viewed by 563
Abstract
Cytochrome c (Cytc) is important for both mitochondrial respiration and apoptosis, both of which are altered in cancer cells that switch to Warburg metabolism and manage to evade apoptosis. We earlier reported that lysine 53 (K53) of Cytc is acetylated [...] Read more.
Cytochrome c (Cytc) is important for both mitochondrial respiration and apoptosis, both of which are altered in cancer cells that switch to Warburg metabolism and manage to evade apoptosis. We earlier reported that lysine 53 (K53) of Cytc is acetylated in prostate cancer. K53 is conserved in mammals that is known to be essential for binding to cytochrome c oxidase and apoptosis protease activating factor-1 (Apaf-1). Here we report the effects of this acetylation on the main functions of cytochrome c by expressing acetylmimetic K53Q in cytochrome c double knockout cells. Other cytochrome c variants analyzed were wild-type, K53R as a control that maintains the positive charge, and K53I, which is present in some non-mammalian species. Intact cells expressing K53Q cytochrome c showed 49% decreased mitochondrial respiration and a concomitant increase in glycolytic activity (Warburg effect). Furthermore, mitochondrial membrane potential was decreased, correlating with notably reduced basal mitochondrial superoxide levels and decreased cell death upon challenge with H2O2 or staurosporine. To test for markers of cancer aggressiveness and invasiveness, cells were grown in 3D spheroid culture. K53Q cytochrome c-expressing cells showed profoundly increased protrusions compared to WT, suggesting increased invasiveness. We propose that K53 acetylation of cytochrome c is an adaptive response that mediates prostate cancer metabolic reprogramming and evasion of apoptosis, which are two hallmarks of cancer, to better promote tumor survival and metastasis. Full article
(This article belongs to the Special Issue Advances in the Pathology of Prostate Cancer)
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14 pages, 3499 KiB  
Article
Enhanced Chemoprevention of Prostate Cancer by Combining Arctigenin with Green Tea and Quercetin in Prostate-Specific Phosphatase and Tensin Homolog Knockout Mice
by Qiongyu Hao, Susanne M. Henning, Clara E. Magyar, Jonathan Said, Jin Zhong, Matthew B. Rettig, Jaydutt V. Vadgama and Piwen Wang
Biomolecules 2024, 14(1), 105; https://doi.org/10.3390/biom14010105 - 14 Jan 2024
Viewed by 1616
Abstract
The low bioavailability of most phytochemicals limits their anticancer effects in humans. The present study was designed to test whether combining arctigenin (Arc), a lignan mainly from the seed of Arctium lappa, with green tea (GT) and quercetin (Q) enhances the chemopreventive [...] Read more.
The low bioavailability of most phytochemicals limits their anticancer effects in humans. The present study was designed to test whether combining arctigenin (Arc), a lignan mainly from the seed of Arctium lappa, with green tea (GT) and quercetin (Q) enhances the chemopreventive effect on prostate cancer. We performed in vitro proliferation studies on different cell lines. We observed a strong synergistic anti-proliferative effect of GT+Q+Arc in exposing androgen-sensitive human prostate cancer LNCaP cells. The pre-malignant WPE1-NA22 cell line was more sensitive to this combination. No cytotoxicity was observed in normal prostate epithelial PrEC cells. For an in vivo study, 3-week-old, prostate-specific PTEN (phosphatase and tensin homolog) knockout mice were treated with GT+Q, Arc, GT+Q+Arc, or the control daily until 16 weeks of age. In vivo imaging using prostate-specific membrane antigen (PSMA) probes demonstrated that the prostate tumorigenesis was significantly inhibited by 40% (GT+Q), 60% (Arc at 30 mg/kg bw), and 90% (GT+Q+Arc) compared to the control. A pathological examination showed that all control mice developed invasive prostate adenocarcinoma. In contrast, the primary lesion in the GT+Q and Arc alone groups was high-grade prostatic intraepithelial neoplasia (PIN), with low-grade PIN in the GT+Q+Arc group. The combined effect of GT+Q+Arc was associated with an increased inhibition of the androgen receptor, the PI3K/Akt pathway, Ki67 expression, and angiogenesis. This study demonstrates that combining Arc with GT and Q was highly effective in prostate cancer chemoprevention. These results warrant clinical trials to confirm the efficacy of this combination in humans. Full article
(This article belongs to the Special Issue Advances in the Pathology of Prostate Cancer)
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