Elevated expression of ZNF217 promotes prostate cancer growth by restraining ferroportin-conducted iron egress

Jiang, Xingkang; Zhang, Chang-wen; Qi, Shiyong; Guo, Shuai; Chen, Yue; Du, Eugenie; Zhang, Hongtuan; Wang, Xiaoming; Liu, Ranlu; Qiao, Baomin; Yang, Kuo; Xu, Yong

doi:10.18632/oncotarget.12753

Cited by 19 publications

(17 citation statements)

References 47 publications

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“…Co-expression analysis indicated that circRNAs were closely correlated with certain mRNAs, some of which were reported to play vital roles in PCa, such as ZNF217 and STK4 [28,29]. Conceivably, circRNAs might influence PCa carcinogenesis via these mRNAs.…”

Section: Discussionmentioning

confidence: 94%

Hsa_Circ_0001206 is downregulated and inhibits cell proliferation, migration and invasion in prostate cancer

Song

Zhuo

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Our study is to explore the expression profiles and potential functions of circRNAs in prostate cancer (PCa). A total of 95 circRNAs and 830 mRNAs were screened to be significantly differentially expressed in PCa tissues by microarrays. Co-expression and competitive endogenous RNA (ceRNA) network were constructed to reveal the potential regulatory mechanisms of circRNAs. Three circRNAs, hsa_circ_0001206, hsa_circ_0001633, and hsa_circ_0009061 were validated to be down-regulated in PCa by quantitative real-time PCR (qRT-PCR) and hsa_circ_0001206 as well as hsa_circ_0009061 was significantly associated with clinical features of PCa patients. Meanwhile, Receiver Operating Characteristic (ROC) curves showed their good diagnostic value as biomarkers for PCa. The down-regulation of hsa_circ_001206 was partly because of the regulation of DExH-Box Helicase 9 (DHX9). Moreover, overexpression of hsa_circ_0001206 inhibited PCa cell proliferation, migration, and invasion in vitro and prevented tumor growth in vivo. Dual-luciferase reporter assays showed hsa_circ_0001206 could directly bind to miR-1285-5p. The expression of Smad4, a well-known suppressive gene in PCa, can be increased by overexpression of hsa_circ_0001206 and this effect could be partly reversed by co-transfection of miR-1285-5p mimic. The study revealed expression profiles and potential functions of circRNAs and demonstrated hsa_circ_0001206 played a suppressive role in the pathogenesis of PCa. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 94%

Hsa_Circ_0001206 is downregulated and inhibits cell proliferation, migration and invasion in prostate cancer

Song

Zhuo

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Cells were collected for ChIP by EZ-ChIP kit (Millipore, USA), as described previously [ 42 ]. Primer sequences were listed in Supplementary Table S1 .…”

Section: Methodsmentioning

confidence: 99%

Genetic and epigenetic silencing of mircoRNA-506-3p enhances COTL1 oncogene expression to foster non-small lung cancer progression

et al. 2016

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Although previous studies suggested that microRNA-506-3p (miR-506-3p) was frequently downregulated, and functioned as a tumor suppressor in several cancers, the biological role and intrinsic regulatory mechanisms of miR-506-3p in non-small cell lung cancer (NSCLC) remain elusive. The present study found miR-506-3p expression was downregulated in advanced NSCLC tissues and cell lines. The expression of miR-506-3p in NSCLC was inversely correlated with larger tumor size, advanced TNM stage and lymph node metastasis. In addition, we also found patients with lower expression of miR-506-3p had a poor prognosis than those patients with higher expression of miR-506-3p. Function studies demonstrated that aberrant miR-506-3p expression modulates tumor cell growth, cell mobility, cell migration and invasion in vitro and in vivo. Mechanistic investigations manifested that coactosin-like protein 1 (COTL1) was a direct downstream target of miR-506-3p. Knockdown of COTL1 mimicked the tumor-suppressive effects of miR-506-3p overexpression in A549 cells, whereas COTL1 overexpression enhanced the tumorigenic function in HCC827 cells. Importantly, we also found GATA3 transcriptionally actives miR-506-3p expression, and the long non-coding RNA urothelial carcinoma-associated 1 (UCA1) exerts oncogenic function in NSCLC by competitively ‘sponging’ miRNA-506. Together, our combined results elucidated genetic and epigenetic silencing of miR-506-3p enhances COTL1 oncogene expression to foster NSCLC progression.

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“…Similarly, FPN dowregulation has also been observed in PCa ( 41 – 44 ). By stimulating FPN activity we can curb the growth and proliferation of PCa ( 41 – 45 ). This occurs due to cellular iron deprivation caused by increased activity of FPN.…”

Section: Iron Export In Pca Cellsmentioning

confidence: 99%

Iron Metabolism in Prostate Cancer; From Basic Science to New Therapeutic Strategies

Vela

2018

Front. Oncol.

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An increasing amount of research has recently strengthened the case for the existence of iron dysmetabolism in prostate cancer. It is characterized with a wide array of differential expression of iron-related proteins compared to normal cells. These proteins control iron entry, cellular iron distribution but also iron exit from prostate cells. Iron dysmetabolism is not an exclusive feature of prostate cancer cells, but it is observed in other cells of the tumor microenvironment. Disrupting the machinery that secures iron for prostate cancer cells can retard tumor growth and its invasive potential. This review unveils the current understanding of the ways that prostate cancer cells secure iron in the tumor milieu and how can we exploit this knowledge for therapeutic purposes.

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Elevated expression of ZNF217 promotes prostate cancer growth by restraining ferroportin-conducted iron egress

Cited by 19 publications

References 47 publications

Hsa_Circ_0001206 is downregulated and inhibits cell proliferation, migration and invasion in prostate cancer

Hsa_Circ_0001206 is downregulated and inhibits cell proliferation, migration and invasion in prostate cancer

Genetic and epigenetic silencing of mircoRNA-506-3p enhances COTL1 oncogene expression to foster non-small lung cancer progression

Iron Metabolism in Prostate Cancer; From Basic Science to New Therapeutic Strategies

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