Hypermethylated in cancer 1 (HIC1) suppresses bladder cancer progression by targeting yes‐associated protein (YAP) pathway

Zhou, Xiaoguang; Zhang, Peng; Han, Hu; Lei, Hongen; Zhang, Xiaodong

doi:10.1002/jcb.27938

Cited by 7 publications

(5 citation statements)

References 43 publications

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“…Hic1 is often found to be epigenetically silenced in various types of human cancers (Wales et al, 1995;Chen et al, 2003); hence, it is considered to be a key player in cancer progression and proliferation (Zheng et al, 2012). Consistent with a recent study demonstrating that the downregulation of Hic1 promoted cell proliferation, whereas overexpression of Hic1 inhibited cell proliferation (Zhou et al, 2019), Hic1 deletion in smooth muscle cells in our study resulted in their increased proliferation, leading to the development of enlarged seminiferous tubules that were surrounded by a larger number of PMCs. In rodents, proliferation of PMCs and Sertoli cells ceases at ∼2 weeks of age, concomitantly with secretion of luminal fluid and entry into meiosis (Setchell, 1970;Orth, 1982;Rato et al, 2010).…”

Section: Discussionsupporting

confidence: 79%

Development and function of smooth muscle cells is modulated by Hic1 in mouse testis

et al. 2020

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In mammalian testis, contractile peritubular myoid cells (PMCs) regulate the transport of sperm and luminal fluid, while secreting growth factors and extracellular matrix proteins to support the spermatogonial stem cell niche. However, little is known about the role of testicular smooth muscle cells during postnatal testicular development. Here we report age-dependent expression of hypermethylated in cancer 1 (Hic1; also known as ZBTB29) in testicular smooth muscle cells, including PMCs and vascular smooth muscle cells, in the mouse. Postnatal deletion of Hic1 in smooth muscle cells led to their increased proliferation and resulted in dilatation of seminiferous tubules, with increased numbers of PMCs. These seminiferous tubules contained fewer Sertoli cells and more spermatogonia, and fibronectin was not detected in their basement membrane. The expression levels of genes encoding smooth muscle contractile proteins, Acta2 and Cnn1, were downregulated in the smooth muscle cells lacking Hic1, and the seminiferous tubules appeared to have reduced contractility. These data imply a role for Hic1 in determining the size of seminiferous tubules by regulating postnatal smooth muscle cell proliferation, subsequently affecting spermatogenesis in adulthood.

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Section: Discussionsupporting

confidence: 79%

Development and function of smooth muscle cells is modulated by Hic1 in mouse testis

et al. 2020

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“…Although Negraes et al Aberrant DNA Methylation in Bladder Cancer Siddiqui, Yaqinuddin have previously reported the hypermethylation of SFN gene in BC, 16 but due to its indistinct hypermethylation pattern in both cancerous and control group, it was not considered favorable for biomarker for BC detection. Similarly, silencing of HIC1 gene due to methylation of their promoter regions has been reported in multiple human cancer types including BC 17 but no significant results were reported in BC to date. In contrast, our study has revealed significant DNA hypermethylation of both SFN and HIC1 genes making them promising biomarkers for BC patients in Saudi Arabia.…”

Section: Resultsmentioning

confidence: 97%

Aberrant DNA Methylation in Bladder Cancer among Saudi Arabia Population

Siddiqui

Yaqinuddin

2021

Journal of Health and Allied Sciences NU

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Tumor biomarkers developed based on the aberrant deoxyribonucleic acid (DNA) methylation patterns in bladder cancer (BC) hold great promise due to their stability, specificity, and known associations with the disease. No study has investigated DNA methylation patterns in BC patients from Saudi population. We analyzed DNA methylation levels of 48 tumor suppressor genes loci in 24 bladder tissues (19 BC and 5 control samples) using Human Tumour Suppressor Genes EpiTect Methyl II Complete PCR Array (Qiagen, Hilden, Germany). We identified significant difference in DNA hypermethylation levels at E2F1, ERBB2, HIC1, OPCML, SFN, SFRP1, SFRP2, SPARC, and TERT gene loci between controls and cancerous samples. SCGB3A1 was differentially methylated in nonmuscle invasive versus muscle invasive BC samples. Results suggest that these aberrant DNA methylation patterns in BC are disease and population specific and can be developed as distinct DNA methylation-based biomarkers for BC detection.

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“…2 D), and its well-known tumor suppressor gene plays a critical role in various cancers [ 19 ]. One study has been shown, that HIC1 inhibits cell growth and migration via regulating YAP pathway in BC [ 20 ], thus we chose HIC1 for the further study. To replicate this finding, we used quantitative RT-PCR (qRT-PCR) and Western blotting to determine the expression levels of HIC1 in ZBTB7A knockdown cells.…”

Section: Resultsmentioning

confidence: 99%

“…In bladder cancer, the promoter of HIC1 existed methylation statuses and the expression of HIC1 was downregulated in BC [ 19 , 33 , 34 ]. HIC1 was reported to inhibit cancer progression via targeting the Yap pathway in BC [ 20 ]. Similarly, our data showed that HIC1 expression was decreased in BC tissues and knockdown of HIC1 promoted cell growth and migration.…”

Section: Discussionmentioning

confidence: 99%

ZBTB7A, a miR-144-3p targeted gene, accelerates bladder cancer progression via downregulating HIC1 expression

Liu

Chou

et al. 2022

Cancer Cell Int

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Background Zinc finger and BTB domain-containing 7A (ZBTB7A) is a member of the POK family of transcription factors that plays an oncogenic or tumor-suppressive role in different cancers depending on the type and genetic context of cancer. However, the function and molecular mechanism of ZBTB7A in bladder cancer (BC) remain elusive. Methods The role of ZBTB7A in bladder cancer was detected by colony formation, transwell, and tumor formation assays. The expression levels of ZBTB7A, HIC1, and miR-144-3p were analyzed by qRT-PCR and Western blot. Bioinformatics analysis and a dual-luciferase reporter assay were used to assess the effect of ZBTB7A on the promoter activity of HIC1. Results The present study revealed that knockdown of ZBTB7A suppressed BC cell growth and migration, as indicated by an approximately 50% reduction in the number of colonies and an approximately 70% reduction in the number of migrated cells. Loss of ZBTB7A inhibited tumor growth in vivo, resulting in a 75% decrease in tumor volume and an 80% decrease in tumor weight. Further mechanistic studies revealed that ZBTB7A bound to the hypermethylated in cancer 1 (HIC1) promoter and downregulated HIC1 expression, accelerating the malignant behavior of BC. Increased expression of ZBTB7A in BC tissues was negatively corrected with the expression of HIC1. Moreover, ZBTB7A was a target of miR-144-3p, which decreased ZBTB7A expression in BC. Conclusion Our data demonstrate that ZBTB7A, a targeted gene of miR-144-3p, promoted tumorigenesis of BC through downregulating HIC1 expression.

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Hypermethylated in cancer 1 (HIC1) suppresses bladder cancer progression by targeting yes‐associated protein (YAP) pathway

Cited by 7 publications

References 43 publications

Development and function of smooth muscle cells is modulated by Hic1 in mouse testis

Development and function of smooth muscle cells is modulated by Hic1 in mouse testis

Aberrant DNA Methylation in Bladder Cancer among Saudi Arabia Population

ZBTB7A, a miR-144-3p targeted gene, accelerates bladder cancer progression via downregulating HIC1 expression

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