MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro

Lyu, Zhong-Shi; Mao, Zhizhong; Wang, Honglian; Yin, Fei; Chen, Tielin; Wan, Qianya; Wang, Ming; Wang, Nian; Xiao, Jiangming; Wei, Hongyuan; Li, Xun; Liu, Yi; Zhou, Qin

doi:10.1016/j.bbrc.2013.09.059

Cited by 20 publications

(27 citation statements)

References 27 publications

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“…Then, the MM cells and UB form nephrons by two cellular processes: MET and tubule genesis [6]. These reports indicate that MM cells are the original cells of nephron generation and inductively interact with UB in kidney development [7,8]. In addition, self-renewal (proliferation) and consumption of MM cells determine the formation and complement of nephrons [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…These reports indicate that MM cells are the original cells of nephron generation and inductively interact with UB in kidney development [7,8]. In addition, self-renewal (proliferation) and consumption of MM cells determine the formation and complement of nephrons [8,9]. Consequently, the proliferation, apoptosis and migration of MM cells become especially important in the study of kidney development.…”

Section: Introductionmentioning

confidence: 99%

“…Six2 , a MET-marker, maintains cap mesenchyme multipotent nephron progenitor cells at an undifferentiated state, promotes MM cell proliferation and restrains cell apoptosis during kidney development [8,9,16]. Deficiency of Six2 depletes cap mesenchyme progenitors, ectopic differentiation, and severe kidney hypoplasia and dysplasia [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Zeb1 Is a Potential Regulator of Six2 in the Proliferation, Apoptosis and Migration of Metanephric Mesenchyme Cells

Zhao

Zhou

et al. 2016

IJMS

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Nephron progenitor cells surround around the ureteric bud tips (UB) and inductively interact with the UB to originate nephrons, the basic units of renal function. This process is determined by the internal balance between self-renewal and consumption of the nephron progenitor cells, which is depending on the complicated regulation networks. It has been reported that Zeb1 regulates the proliferation of mesenchymal cells in mouse embryos. However, the role of Zeb1 in nephrons generation is not clear, especially in metanephric mesenchyme (MM). Here, we detected cell proliferation, apoptosis and migration in MM cells by EdU assay, flow cytometry assay and wound healing assay, respectively. Meanwhile, Western and RT-PCR were used to measure the expression level of Zeb1 and Six2 in MM cells and developing kidney. Besides, the dual-luciferase assay was conducted to study the molecular relationship between Zeb1 and Six2. We found that knock-down of Zeb1 decreased cell proliferation, migration and promoted cell apoptosis in MM cells and Zeb1 overexpression leaded to the opposite data. Western-blot and RT-PCR results showed that knock-down of Zeb1 decreased the expression of Six2 in MM cells and Zeb1 overexpression contributed to the opposite results. Similarly, Zeb1 promoted Six2 promoter reporter activity in luciferase assays. However, double knock-down of Zeb1 and Six2 did not enhance the apoptosis of MM cells compared with control cells. Nevertheless, double silence of Zeb1 and Six2 repressed cell proliferation. In addition, we also found that Zeb1 and Six2 had an identical pattern in distinct developing phases of embryonic kidney. These results indicated that there may exist a complicated regulation network between Six2 and Zeb1. Together, we demonstrate Zeb1 promotes proliferation and apoptosis and inhibits the migration of MM cells, in association with Six2.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Zeb1 Is a Potential Regulator of Six2 in the Proliferation, Apoptosis and Migration of Metanephric Mesenchyme Cells

Zhao

Zhou

et al. 2016

IJMS

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“…And dual-luciferase reporter assays were performed in HEK293T. 19 As shown in Figure 2B, ectopic expression of miR-101 inhibited the luciferase activity. Importantly, the suppression was diminished when miR-101 binding site in 3 ¶UTR of Fos was mutated, which indicated that miR-101 suppressed the expression of luciferase †MicroRNA with mirSVR score Gj0.5.…”

Section: Mir-101 Directly Targets the 3 ¶Utr Of Fos And Posttranscripmentioning

confidence: 99%

Atl

Liang

Liu

Zeng

et al. 2014

Int J Gynecol Cancer

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“…Further analysis of metanephros revealed a central role of SIX2 in Electronic supplementary material The online version of this article (doi:10.1007/s13277-015-3456-5) contains supplementary material, which is available to authorized users. maintaining renal progenitor cell pluripotency in kidney developmental processes [13][14][15][16]. Mutation or abnormal expression of the SIX2 gene may result in renal dysplasia or renal cysts [17][18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Assessment of promoter methylation and expression of SIX2 as a diagnostic and prognostic biomarker in Wilms’ tumor

Song

Yue

et al. 2015

Tumor Biol.

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This study was designed to evaluate the utility of expression and DNA methylation patterns of the sine oculis homeobox homolog 2 (SIX2) gene in early diagnosis and prognosis of Wilms' tumor (WT). Methylation-specific polymerase chain reaction (MSP), real-time quantitative polymerase chain reaction (qRT-PCR), receiver operating characteristic (ROC), and survival curve analyses were utilized to measure the expression and DNA methylation patterns of SIX2 in a cohort of WT tissues, with a view to assessing their diagnostic and prognostic value. Relative expression of SIX2 mRNA was higher, while the promoter methylation level was lower in the WT than control group (P < 0.05) and closely associated with poor survival prognosis of WT children (P < 0.05). Increased expression and decreased methylation of SIX2 were correlated with increasing tumor size, clinical stage, vascular invasion, and unfavorable histological differentiation (P < 0.05). ROC curve analysis showed areas under the curve (AUCs) of 0.579 for methylation and 0.917 for expression in WT venous blood, indicating higher diagnostic yield of preoperative SIX2 expression. The preoperative venous blood SIX2 expression level serves as an underlying biomarker for early diagnosis of WT. SIX2 overexpression and concomitantly decreased promoter methylation are significantly associated with poor survival of WT children.

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MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro

Cited by 20 publications

References 27 publications

Zeb1 Is a Potential Regulator of Six2 in the Proliferation, Apoptosis and Migration of Metanephric Mesenchyme Cells

Zeb1 Is a Potential Regulator of Six2 in the Proliferation, Apoptosis and Migration of Metanephric Mesenchyme Cells

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Assessment of promoter methylation and expression of SIX2 as a diagnostic and prognostic biomarker in Wilms’ tumor

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