RNA-Binding Protein Quaking, a Critical Regulator of Colon Epithelial Differentiation and a Suppressor of Colon Cancer

Yang, Guodong; Fu, Haiyan; Zhang, Jie; Lü, Xin; Yu, Fang; Jin, Liang; Bai, Li‐Yuan; Huang, Bo; Shen, Lan; Feng, Yue; Yao, Libo; Lu, Zifan

doi:10.1053/j.gastro.2009.08.001

Cited by 113 publications

(143 citation statements)

References 39 publications

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“…The present study demonstrated that miR-155 expression is positively correlated with lymph node metastasis in colon cancer, which is consistent with the results of a previous study (6). Furthermore, our study clarified the connection between miR-155 and QKI, which exerts anti-proliferative and differentiative functions in gastric and colon cancer (8,9). In accordance with previous studies (6,8,9,20), our results demonstrated that the low expression of QKI is due to the high expression of miR-155.…”

Section: Discussionsupporting

confidence: 82%

“…5B). E-cadherin, a cell adhesion-related protein (13) whose expression is suppressed in colon cancer cells, and lactase, a differentiation marker of colon cells which is expressed at a low level in colon cancer cells, both play significant roles in the differentiation of colon cancer cells (9,14). Treatment with the miR-155 inhibitor and QKI overexpression vector increased the expression of e-cadherin and lactase, which promoted colon cancer cell differentiation; the results obtained through transfection of miR-155 inhibitor were similar (Fig.…”

Section: Mir-155 Suppresses the Invasion Capabilities Of Sw480 Cells mentioning

confidence: 99%

“…Furthermore, lymph node metastases have long been associated with higher proliferation and invasion abilities. At the same time, a type of RNA-binding protein named quaking (QKI), which suppresses gastric cancer cell proliferation by decreasing β-catenin expression (8), has been detected in colon cancer (9). The phenomenon of high miR-155 expression and low QKI expression in colon cancer prompted us to investigate the correlation between them and further ascertain whether miR-155 affects the differentiation of colon cancer by targeting QKI directly.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-155 promotes the proliferation and invasion abilities of colon cancer cells by targeting quaking

Gao

Huang

et al. 2014

Molecular Medicine Reports

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Abstract. The increasing expression of microRNA-155 (miR-155) and decreasing expression of RNA-binding protein quaking (QKI) in colon cells have been observed previously. In this study, we attempted to establish the correlation between miR-155 and QKI. In addition, we assessed whether the expression of miR-155 and QKI is linked to the proliferation and invasion capabilities of colon cells. Firstly, nineteen tumor samples, divided into two groups according to the presence or absence of lymphatic metastasis, were obtained from colon cancer patients at the First Affiliated Hospital of Wenzhou Medical University, China. The expression level of miR-155 and QKI was measured by quantitative polymerase chain reaction (qPCR). Secondly, the GES-1, SW480 and COLO205 cell lines were cultured and the expression level of QKI and miR-155 was also assessed by qPCR. Thirdly, a luciferase reporter gene assay was performed to detect the association between miR-155 and QKI, and qPCR and western blot analysis were performed to confirm the effects of miR-155 on the expression of QKI at the mRNA and protein level. Subsequently, the SW480 cells were used in the following experiments. Following treatment with miR-155 inhibitor and QKI overexpression vector, western blot analysis, propidium iodide (PI) staining and a cell scratch assay were carried out to assess the effects of miR-155 on the proliferation and invasion potential of colon cancer cells. qPCR findings revealed higher miR-155 expression and lower QKI expression in colon cancer tissues as well as the colon cancer cell lines SW480 and COLO205. The relative luciferase activity of the 3' untranslated region (3'UTR) was decreased by approximately 45% when SW480 cells stimulated by mimic-miR-155 were combined with the wild-type 3'UTR constructs. In addition, when the cells were treated with mimic-miR-155, QKI expression was significantly decreased at the mRNA and protein level. These outcomes revealed that miR-155 decreased the production of QKI by acting on the 3'UTR of the QKI gene. Furthermore, PI staining and the cell scratch assay revealed that miR-155 influenced the cell cycle and invasion abilities of colon cancer cells by directly targeting QKI and decreased the production of QKI by acting on the 3'UTR of the QKI gene. This study has demonstrated the correlation between miR-155 and QKI, in which miR-155 regulates the cell cycle and invasion ability of colon cancer cells via the modulation of QKI expression. Our study provides novel therapeutic strategies for colon cancer therapy.

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Section: Discussionsupporting

confidence: 82%

Section: Mir-155 Suppresses the Invasion Capabilities Of Sw480 Cells mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA-155 promotes the proliferation and invasion abilities of colon cancer cells by targeting quaking

Gao

Huang

et al. 2014

Molecular Medicine Reports

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“…To investigate the functional implications of these methylation events, the abundance of p27 kip1 was monitored in Sk-Hep1 and SK-Hep1ϩ cells. It is known that QKI-5 binds to and stabilizes p27 kip1 RNA, leading to the accumulation of the corresponding protein, which induces cell cycle arrest (54). We found increased levels of p27 kip1 in SK-Hep1ϩ cells, in parallel to methylation of QKI-5, suggesting that methylation might increase QKI-5 activity as no change on its steady-state levels were detected (Fig.…”

Section: Mta Increases the Proliferation Rate Of Sk-hep1mentioning

confidence: 47%

Methylthioadenosine (MTA) Regulates Liver Cells Proteome and Methylproteome: Implications in Liver Biology and Disease

Bigaud

Corrales

2016

Molecular & Cellular Proteomics

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“…The decreased expression of QKI has been implicated in the pathogenesis of many types of human disease, including a number of types of cancer (8,13). Yang et al (14) reported that the levels of QKI5/6 were significantly reduced or absent in colorectal cancer (CRC) cells. It has also been observed that the downregulation of QKI in colon cancers may be partially due to the hypermethylation of the QKI promoter region.…”

Section: Introductionmentioning

confidence: 99%

MiR-574-5p mediates the cell cycle and apoptosis in thyroid cancer cells via Wnt/β-catenin signaling by repressing the expression of Quaking proteins

Zhang

Xiao

et al. 2018

Oncol Lett

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Abstract. Thyroid cancer is the most frequently occurring type of endocrine tumor, with a rapidly increasing incidence rate. MicroRNA (miR)-574-5p is a candidate oncogene in various types of cancer. The present study identified that miR-574-5p affected the cell cycle distribution and apoptosis of BCPAP and FTC133 thyroid cancer cells via β-catenin/Wnt signaling by targeting Quaking proteins (QKIs). An MTT assay demonstrated that the knockdown of miR-574-5p suppressed the proliferation of the thyroid cancer cells. Fluorescence-activated cell sorting analysis demonstrated that the inhibition of miR-574-5p induced the G 1 /S phase arrest and apoptosis of the cells. Reverse transcription-quantitative polymerase chain reaction and western blot analyses revealed that the knockdown of miR-574-5p significantly upregulated the mRNA and protein expression levels of QKIs. Furthermore, western blot analysis identified that the knockdown of miR-574-5p also repressed the Wnt/β-catenin pathway via downregulating the expression of β-catenin, cyclin D1 and survivin, and upregulating the phosphorylation of β-catenin. The further depletion of QKIs in combination with the knockdown of miR-574-5p not only increased the expression of β-catenin, cyclin D1 and survivin, but also rescued the apoptosis of thyroid cancer cells induced by the miR-574-5p knockdown. In conclusion, these findings indicated that the aberrant upregulation of miR-574-5p may be oncogenic, through regulating the Wnt/β-catenin pathway by targeting QKIs.

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RNA-Binding Protein Quaking, a Critical Regulator of Colon Epithelial Differentiation and a Suppressor of Colon Cancer

Cited by 113 publications

References 39 publications

MicroRNA-155 promotes the proliferation and invasion abilities of colon cancer cells by targeting quaking

MicroRNA-155 promotes the proliferation and invasion abilities of colon cancer cells by targeting quaking

Methylthioadenosine (MTA) Regulates Liver Cells Proteome and Methylproteome: Implications in Liver Biology and Disease

MiR-574-5p mediates the cell cycle and apoptosis in thyroid cancer cells via Wnt/β-catenin signaling by repressing the expression of Quaking proteins

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