Neoplasms of the Prostate

Bostwick, David G.; Liu, Cheng

doi:10.1016/b978-0-323-54941-7.00009-8

Cited by 7 publications

(7 citation statements)

References 1,496 publications

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“…Existing treatments such as traditional androgen deprivation therapy (ADT) could only delay the progression of prostate cancer at an early stage. Despite initial high response rates, cancer management with ADT is of limited duration, eventually the patients will progress to Castration-resistant prostate cancer (CRPC) [ 3 ]. There is an urgent need for a novel treatment to delay the progression of prostate cancer to CRPC.…”

Section: Introductionmentioning

confidence: 99%

CKAP2L, a crucial target of miR-326, promotes prostate cancer progression

Yan

Wang

et al. 2022

BMC Cancer

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Background The overexpression of aberrant cell cycle signaling pathway associated protein has been implicated in multiple malignancies and the identification of all-important one among is the crux of the precise targeted therapy. CKAP2L (Cytoskeleton Associated Protein 2 Like) plays a newish role in cancer progression through activation of the process of cell cycle and mitosis. In this study, we aim to delineate the prominent dysregulated expression of CKAP2L and comprehensively reveal its deregulation in prostate cancer. Method CKAP2L expression was examined in the normal and tumor tissues of prostate cancer patients with RT-QPCR and Western blot. IHC showed the different expression in normal prostate tissue, tissue of BPH, low Gleason Score and high Gleason Score prostate cancer patients. Transwell, colony formation, MTT and flow cytometry were performed to detected the changes in cellular function in vitro. The xenograft model was conducted for the changes in vivo. Dual luciferase and RIP proved the binding relation between CKAP2L and miR-326. Results In multiple datasets, CKAP2L was found upregulated and positively associated with Gleason grade and poor clinical outcomes of patients. shRNA mediated silence of CKAP2L suppressed cell proliferation, impaired monolayer formation, inhibited cell invasion. CKAP2L was confirmed to be the direct target of miR-326, which had a carcinostatic effect by binding the 3’untranslated regions (3’UTRs) of CKAP2L mRNA. The deletion of CKAP2L resulted in reduced expression of genes involved in the mitotic cell cycle such as multiple cyclin-dependent kinases and cyclins, but also several genes encoding proteins involved in chromosome segregation and spindle assembly. Conclusion Taken together, CKAP2L plays a carcinogenic role in prostate cancer by regulates the expression of cycle-associated proteins.

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Section: Introductionmentioning

confidence: 99%

CKAP2L, a crucial target of miR-326, promotes prostate cancer progression

Yan

Wang

et al. 2022

BMC Cancer

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“…Increased mtDNAcn in HGPIN. HGPIN is the likely precursor to most human prostate cancers (55,56), yet mtDNAcn levels have not been studied in these lesions. We sought to compare neoplastic epithelial cells in HGPIN to matched benign normal-appearing epithelium.…”

Section: Resultsmentioning

confidence: 99%

MYC-driven increases in mitochondrial DNA copy number occur early and persist throughout prostatic cancer progression

Chen,

Zheng,

Hicks

et al. 2023

JCI Insight

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Increased mitochondrial function may render some cancers vulnerable to mitochondrial inhibitors. Since mitochondrial function is regulated partly by mitochondrial DNA copy number (mtDNAcn), accurate measurements of mtDNAcn could help reveal which cancers are driven by increased mitochondrial function and may be candidates for mitochondrial inhibition. However, prior studies have employed bulk macrodissections that fail to account for cell type–specific or tumor cell heterogeneity in mtDNAcn. These studies have often produced unclear results, particularly in prostate cancer. Herein, we developed a multiplex in situ method to spatially quantify cell type–specific mtDNAcn. We show that mtDNAcn is increased in luminal cells of high-grade prostatic intraepithelial neoplasia (HGPIN), is increased in prostatic adenocarcinomas (PCa), and is further elevated in metastatic castration-resistant prostate cancer. Increased PCa mtDNAcn was validated by 2 orthogonal methods and is accompanied by increases in mtRNAs and enzymatic activity. Mechanistically, MYC inhibition in prostate cancer cells decreases mtDNA replication and expression of several mtDNA replication genes, and MYC activation in the mouse prostate leads to increased mtDNA levels in the neoplastic prostate cells. Our in situ approach also revealed elevated mtDNAcn in precancerous lesions of the pancreas and colon/rectum, demonstrating generalization across cancer types using clinical tissue samples.

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“…(2) Existing treatments such as traditional androgen deprivation therapy (ADT) could only delay the progression of prostate cancer at an early stage. Despite initial high response rates, cancer management with ADT is of limited duration, eventually the patients will progress to Castration resistant prostate cancer (CRPC) (3). There is an urgent need for a novel treatment to delay the progression of prostate cancer to CRPC.…”

Section: Introductionmentioning

confidence: 99%

CKAP2L, a Crucial Target of miR-326, Promotes Prostate Cancer Progression

Yan

Wang

et al. 2021

Preprint

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BackgroundThe overexpression of aberrant cell cycle signaling pathway associated protein has been implicated in multiple malignancies and the identification of all-important one among is the crux of the precise targeted therapy. CKAP2L (Cytoskeleton Associated Protein 2 Like) plays a newish role in cancer progression through activation of the process of cell cycle and mitosis. In this study, we aim to delineate the prominent dysregulated expression of CKAP2L and comprehensively reveal its deregulation in prostate cancer.MethodWe experimentally manipulated CKAP2L gene expression in vitro and in vivo and monitored its effects on cancer-related gene expression, cell migration, proliferation.ResultsIn multiple datasets, CKAP2L was found upregulated and positively associated with Gleason grade and poor clinical outcomes of patients. shRNA mediated silence of CKAP2L suppressed cell proliferation, impaired monolayer formation, inhibited cell invasion. CKAP2L was confirmed to be the direct target of miR-326, which had a carcinostatic effect by binding the 3’untranslated regions (3’UTRs) of CKAP2L mRNA. The deletion of CKAP2L resulted in reduced expression of genes involved in the mitotic cell cycle such as multiple cyclin-dependent kinases and cyclins, but also several genes encoding proteins involved in chromosome segregation and spindle assembly. ConclusionTaken together, miR-326 plays a carcinostatic role in prostate cancer by reducing the expression of CKAP2L .

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Neoplasms of the Prostate

Cited by 7 publications

References 1,496 publications

CKAP2L, a crucial target of miR-326, promotes prostate cancer progression

CKAP2L, a crucial target of miR-326, promotes prostate cancer progression

MYC-driven increases in mitochondrial DNA copy number occur early and persist throughout prostatic cancer progression

CKAP2L, a Crucial Target of miR-326, Promotes Prostate Cancer Progression

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