Androgen receptor suppresses prostate cancer metastasis but promotes bladder cancer metastasis via differentially altering miRNA525-5p/SLPI-mediated vasculogenic mimicry formation

Zhao, Yang; Chen, Jiaqi; Xie, Hongjun; Liu, Tianjie; Chen, Yule; Ma, Zhenkun; Pei, Xinqi; Yang, Wenjie; Li, Lei

doi:10.1016/j.canlet.2019.12.018

Cited by 26 publications

(14 citation statements)

References 56 publications

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“…On the other hand, Sanguedolce et al, 2020 did find significant relevance for a correlation between the lack of androgen receptor expression and recurrent disease [116]. Yang et al, 2020 have reported the differential effects of the AR in the promotion of cancer metastasis in bladder cancer, while suppressing prostate cancer metastasis [117]. Yasui et al, 2019 also found that a high AR mRNA-expressing group tended to have a longer recurrence-free survival, and Katleba et al, 2021 found a low molecular weight variant of the androgen receptor in most bladder cancer malignancies, missing the ligand binding domain [67,118].…”

Section: Bladder Cancer Therapiesmentioning

confidence: 99%

The Role of Androgens and Androgen Receptor in Human Bladder Cancer

et al. 2021

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Bladder cancer (urothelial carcinoma) is one of the most frequently diagnosed neoplasms, with an estimated half a million new cases and 200,000 deaths per year worldwide. This pathology mainly affects men. Men have a higher risk (4:1) of developing bladder cancer than women. Cigarette smoking and exposure to chemicals such as aromatic amines, and aniline dyes have been established as risk factors for bladder cancer and may contribute to the sex disparity. Male internal genitalia, including the urothelium and prostate, are derived from urothelial sinus endoderm; both tissues express the androgen receptor (AR). Several investigations have shown evidence that the AR plays an important role in the initiation and development of different types of cancer including bladder cancer. In this article, we summarize the available data that help to explain the role of the AR in the development and progression of bladder cancer, as well as the therapies used for its treatment.

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Section: Bladder Cancer Therapiesmentioning

confidence: 99%

The Role of Androgens and Androgen Receptor in Human Bladder Cancer

et al. 2021

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“…MiRNAs are non-coding RNAs that contain 20–30 nucleotides. MiR-525-5p, a member of the miRNA families, was recently reported to play roles in regulating cell proliferation, invasion, migration, epithelial-mesenchymal transition (EMT) and metastasis in several tumors, including glioma, cervical cancer, ovarian cancer, prostate cancer and colorectal cancer ( 18 , 19 , 37 – 41 ). These findings indicate that miR525-5p may play an important role in tumor progression.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Yang et al. found that androgen receptor can alter the metastasis of prostate and bladder cancer through changing the expression of the vasculogenic mimicry biomarker SLPI by miR-525-5p; therefore, targeting the androgen receptor–miR-525-5p-SLPI axis may be a strategy to suppress prostate cancer metastasis ( 19 ). However, the roles of lncRNA MDFIC-7 and miRNA-525-5p in chordoma progression have not been reported.…”

Section: Introductionmentioning

confidence: 99%

“…Zhang et al demonstrated that miR-525-5p plays a role in mediating the invasion of trophoblast cells by regulating HOXD10; miR-525-5p overexpression promoted proliferation, invasion and EMT of HTR-8 cells and regulated pre-eclampsia placenta (18). Moreover, Yang et al found that androgen receptor can alter the metastasis of prostate and bladder cancer through changing the expression of the vasculogenic mimicry biomarker SLPI by miR-525-5p; therefore, targeting the androgen receptor-miR-525-5p-SLPI axis may be a strategy to suppress prostate cancer metastasis (19). However, the roles of lncRNA MDFIC-7 and miRNA-525-5p in chordoma progression have not been reported.…”

Section: Introductionmentioning

confidence: 99%

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Long Non-Coding RNA MDFIC-7 Promotes Chordoma Progression Through Modulating the miR-525-5p/ARF6 Axis

et al. 2021

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BackgroundChordoma, an extremely rare malignant tumor, remains difficult to be cured because of its strong local invasiveness and high recurrence rate. Long non-coding RNAs (lncRNAs) have been demonstrated to play multiple roles in various cancers. The purpose of this study was to investigate the modulatory function of lncRNA MDFIC-7 in chordoma and to elucidate its underlying mechanisms.MethodsQuantitative real-time polymerase chain reaction was performed to detect the expression of lncRNA MDFIC-7 in tumor tissues and adjacent nontumorous tissues collected from 15 chordoma patients, as well as in chordoma cell lines. Gene silencing and overexpression experiments were carried out by RNA interference and lentiviral transduction. The effect of lncRNA MDFIC-7 on the proliferation of chordoma cells was evaluated by cell counting kit-8 assay, colony formation assay and xenograft tumor experiments. RNA immunoprecipitation and dual luciferase reporter assays were conducted to evaluate the binding between lncRNA MDFIC-7 and miRNA-525-5p and the interaction between miR-525-5p and the 3′ untranslated region of ADP-ribosylation factor 6 (ARF6) mRNA. The glycolytic capacity and mitochondrial function of chordoma cells were measured by the Seahorse Bioscience XF96 Extracellular Flux Analyzer.ResultsThe expression of lncRNA MDFIC-7 was higher in chordoma tumor tissues than in adjacent non-tumor tissues. Downregulation of lncRNA MDFIC-7 reduced colony formation and cell proliferation in chordoma cells and decreased xenograft tumor growth in a nude mouse model. Moreover, lncRNA MDFIC-7 knockdown attenuated the Warburg effect in chordoma cells and xenograft tumors. LncRNA MDFIC-7 knockdown elevated miR-525-5p levels and decreased ARF6 expressions. Overexpression of ARF6 reversed the inhibitory effect of lncRNA MDFIC-7 knockdown on cell proliferation and the Warburg effect in chordoma cells and xenograft tumors. Mechanistically, lncRNA MDFIC-7, as a molecular sponge of miR-525-5p, negatively regulated miR-525-5p expression and promoted the gene expression of ARF6, a miR-525-5p target.ConclusionOur findings demonstrate that lncRNA MDFIC-7 acts as a molecular sponge to competitively bind to miR-525-5p and promote expression of ARF6. The lncRNA MDFIC-7/miR-525-5p/ARF6 axis regulates chordoma progression and the Warburg effect in chordoma, suggesting that lncRNA MDFIC-7 and miR-525-5p could be promising therapeutic targets for the treatment of chordoma.

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“…The identification of vascular channels lacking ECs was introduced by Maniotis et al, who reported the plasticity of aggressive cancer cells forming de novo vascular networks in highly aggressive uveal melanomas [35]. VM has been described in a plethora of tumors, including carcinomas of the breast [36], ovary [37], bladder [38], lung [39] and prostate [40], as well as sarcomas [41], glioblastomas [42], astrocytomas [43] and melanomas [44]. The functional channels (that are not vessels) are composed of tumor cells with stem cell features, and present characteristic patterns in addition to the erythrocytes inside them.…”

Section: Non-angiogenic Intratumoral Vascularizationmentioning

confidence: 99%

The Metastatic Capacity of Melanoma Reveals Alternative Pathways of Cancer Dissemination

Corsini

Ravelli

Grillo

et al. 2021

IJTM

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For many years the growth of solid tumors has been associated with their vascularization. The new vessels are needed to deliver oxygen and nutrients within the tumor mass. At the same time, these poorly stabilized vessels act as “Trojan horses” and open a way out for cancer cells. More recently, tumors have been identified whose growth appears to be independent of endothelial cell activity. Here we describe the ability of cancer cells to differentiate and reorganize themself in channels similar to blood vessels containing blood flow, overcoming the need for the angiogenic process of tumor vascularization. Together with the new vessels arising both from angiogenic and vasculogenic processes, these vessel-like structures can be exploited by tumor cells as a guide for migration and metastatic dissemination. In addition to classical intravascular dissemination, cancer cells can acquire pericytic features, interact with the endothelial basal lamina and migrate toward vessels or outside of the vessels. As expected, these alternative tumor behaviors assume greater importance if we consider that drugs with anti-angiogenic action directed against endothelial cells or their ligands are currently used in cancer therapy.

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Androgen receptor suppresses prostate cancer metastasis but promotes bladder cancer metastasis via differentially altering miRNA525-5p/SLPI-mediated vasculogenic mimicry formation

Cited by 26 publications

References 56 publications

The Role of Androgens and Androgen Receptor in Human Bladder Cancer

The Role of Androgens and Androgen Receptor in Human Bladder Cancer

Long Non-Coding RNA MDFIC-7 Promotes Chordoma Progression Through Modulating the miR-525-5p/ARF6 Axis

The Metastatic Capacity of Melanoma Reveals Alternative Pathways of Cancer Dissemination

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