HOXA9, PCDH17, POU4F2, and ONECUT2 as a Urinary Biomarker Combination for the Detection of Bladder Cancer in Chinese Patients with Hematuria

Wu, Yishuo; Jiang, Guangliang; Zhang, Ning; Liu, Shenghua; Lin, Xiaoling; Perschon, Chelsea; Zheng, S. Lilly; Ding, Qiang; Wang, Xiang; Na, Rong; Sun, Jing; Xu, Jianfeng

doi:10.1016/j.euf.2018.09.016

Cited by 36 publications

(18 citation statements)

References 21 publications

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“…21,22 Recent studies showed that PCDH8, PCDH10 and PCDH17 acted as tumor suppressors in a variety of human cancers. [23][24][25][26][27][28][29][30][31][32][33][34] PCDH9 is another member of the PCDH family located in the 13q21.32 of human genome. Previous studies demonstrated that PCDH9 was down-regulated in cancers, such as glioblastoma, hepatocellular carcinoma and gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-200a-3p promoted the malignant behaviors of ovarian cancer cells through regulating PCDH9

Shi¹,

Yang²,

Zhang³

et al. 2019

OTT

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Background: Increasing evidence has revealed that the aberrant expression of microRNAs (miRNAs) plays vital roles in the development and progression of ovarian cancer. MiR-200a-3p was found to act as an oncogene in a variety of cancers, however, the expression and function of miR-200a-3p in ovarian cancer has not been characterized. Materials and methods: The expression of miR-200a-3p in ovarian cancer tissues and cell lines was detected by the RT-qPCR. The influence of miR-200a-3p on the growth of ovarian cancer cells was determined with the Cell Counting Kit-8 assay, colony formation and cell invasion assay. The binding of miR-200a-3p with the 3ʹ-untranslated region (UTR) of PDCH9 was detected by luciferase reporter assay. The expression of PCDH9 was investigated by RT-qPCR and Western blot analysis. Results: miR-200a-3p was up-regulated in ovarian cancer tissues and cell lines. Highly expressed miR-200a-3p was significantly associated with the tumor size, tumor metastasis and TNM stage. Overexpression of miR-200a-3p markedly promoted the proliferation, colony formation and invasion of ovarian cancer cells. Functional study uncovered that miR-200a-3p bound the 3ʹ-untranslated region (UTR) of PCDH9 and decreased the expression of PCDH9 in ovarian cancer cells. The expression of miR-200a-3p in ovarian cancer tissues was significantly negatively correlated with that of PCDH9. Restored PCDH9 inhibited the promoting effect of miR-200a-3p on the proliferation of ovarian cancer cells. Conclusion: Our results suggested the potential oncogenic function of miR-200a-3p via modulating PCDH9 in ovarian cancer.

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Section: Introductionmentioning

confidence: 99%

MiR-200a-3p promoted the malignant behaviors of ovarian cancer cells through regulating PCDH9

Shi¹,

Yang²,

Zhang³

et al. 2019

OTT

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“…ONECUT2 is a transcription factor associated with development, and recent evidence has shown that aberrant expression of ONECUT2 in cancers is relevant in cancer progression. [32][33][34] The expression of ONECUT2 has been found to be upregulated and drives tumor aggressiveness in ovarian cancer, prostate cancer and colorectal cancer. [35][36][37][38] Moreover, it has been found that ONECUT2 was involved in the regulation of cancer stem cell-like features in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

THUMPD3-AS1 Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2

Hu¹,

Chen²,

Li³

et al. 2019

OTT

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Background: Of all malignancies, lung cancer is the leading cause of death, and non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancers. In this study, the long non-coding RNA (lncRNA) THUMPD3-AS1 was observed to be highly expressed in NSCLC and correlated with TNM stages and relapse, suggesting that THUMPD3-AS1 is involved in the regulation of NSCLC. Methods: The aim of this study was to investigate the regulatory function and mechanism of THUMPD3-AS1 in NSCLC cells by cellular function and molecular biology experiments. Results: Overexpression and knockdown analysis revealed that THUMPD3-AS1 promoted tumor progression by increasing cell proliferation and self-renewal of NSCLC cells. Moreover, THUMPD3-AS1 may act as an endogenous sponge of microRNA-543 (miR-543) which can regulate the target gene ONECUT2 in NSCLC cells. Conclusion: Our study indicated that THUMPD3-AS1 regulated NSCLC cell self-renewal by regulating the expression of miR-543 and ONECUT2, and THUMPD3-AS1 can potentially act as a biomarker or therapeutic target in NSCLC.

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“…Hence, aberrant DNA methylation was proposed as a promising biomarker for BC detection, prognosis, and therapeutic target [ 50 , 51 ]. For example, a panel comprising HOXA9 , PCDH17 , POU4F2 , and ONECUT2 methylation detected BC with 90.5% sensitivity and 73.2% specificity in urine samples from Chinese patients presenting hematuria, leading the authors to estimate that about 60% of cystoscopies could be avoided [ 52 ]. Furthermore, a methylation panel composed of GDF15 , TMEFF2 , and VIM discriminated BC patients from healthy controls and prostate or renal cancer patients with a sensitivity of 94% and specificity of 90% in urine sediment samples [ 53 ], whereas the UroMark assay based on 150 CpG loci detected BC in voided urine samples with 98% sensitivity and 97% specificity [ 54 ].…”

Section: Dna Methylationmentioning

confidence: 99%

DNA Methylation as a Therapeutic Target for Bladder Cancer

Nunes

Henrique

Jerónimo

et al. 2020

Cells

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Bladder cancer (BC) is the tenth most frequent cancer worldwide and is associated with high mortality when diagnosed in its most aggressive form, which is not reverted by the current treatment options. Thus, the development of new therapeutic strategies, either alternative or complementary to the current ones, is of major importance. The disruption of normal epigenetic mechanisms, namely, DNA methylation, is a known early event in cancer development. Consequently, DNA methyltransferase (DNMT) inhibitors constitute a promising therapeutic target for the treatment of BC. Although these inhibitors, mainly nucleoside analogues such as 5-azacytidine (5-aza) and decitabine (DAC), cause re-expression of tumor suppressor genes, inhibition of tumor cell growth, and increased apoptosis in BC experimental models and clinical trials, they also show important drawbacks that prevent their use as a valuable option for the treatment of BC. However, their combination with chemotherapy and/or immune-checkpoint inhibitors could aid in their implementation in the clinical practice. Here, we provide a comprehensive review of the studies exploring the effects of DNA methylation inhibition using DNMTs inhibitors in BC, from in vitro and in vivo studies to clinical trials.

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HOXA9, PCDH17, POU4F2, and ONECUT2 as a Urinary Biomarker Combination for the Detection of Bladder Cancer in Chinese Patients with Hematuria

Cited by 36 publications

References 21 publications

<p>MiR-200a-3p promoted the malignant behaviors of ovarian cancer cells through regulating PCDH9</p>

<p>MiR-200a-3p promoted the malignant behaviors of ovarian cancer cells through regulating PCDH9</p>

<p>THUMPD3-AS1 Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2</p>

DNA Methylation as a Therapeutic Target for Bladder Cancer

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