MiR-452 promotes an aggressive colorectal cancer phenotype by regulating a Wnt/β-catenin positive feedback loop

Li, Tingting; Jian, Xiangyu; He, Han; Lai, Qiuhua; Li, Xianzheng; Deng, Danling; Liu, Tengfei; Zhu, Jiehong; Jiao, Hong-Li; Ye, Yaping; Wang, Shuyang; Yang, Mei; Zheng, Lin; Zhou, Weijie; Ding, Yan‐Qing

doi:10.1186/s13046-018-0879-z

Cited by 34 publications

(25 citation statements)

References 36 publications

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“…Since T cell factor/lymphatic enhancement factor is an effective transcription factor in the miR-452 promoter, in turn, miR-452 transcription is promoted by Wnt signaling, forming a positive feedback loop. 46 In addition, a negative feedback loop was found between the miRNA and Wnt signaling pathway. miR-145, a tumor suppressor miRNA, can interact with TCF4-β-catenin complex, recruit polycomb repressive complex 2 (PRC2) histone trimethylase, and suppress Wnt signal transduction.…”

Section: Wnt Signaling and Micro-rnasmentioning

confidence: 99%

<p>New Advances in Canonical Wnt/β-Catenin Signaling in Cancer</p>

Wen¹,

Wu²,

Awadasseid³

et al. 2020

CMAR

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Wnt/β-catenin-mediated signaling is a key pathway regulating tissue growth and development, and tumorigenesis, and has received increasing attention in recent years. In addition to participating in healthy tissue and organ development, ectopic activation of the pathway can cause a variety of tumors and other pathologies. The pathway plays a critical role in many processes such as proliferation, differentiation, apoptosis, migration, invasion, epithelial–mesenchymal transition and cancer cell stemness. The importance of the Wnt signal is self-evident. This review describes the underlying mechanism of Wnt signaling pathway and highlights the latest findings on the relationship between Wnt signaling pathway and tumorigenesis. In addition, the potential relationship between miRNAs and Wnt signaling is presented. Furthermore, we discuss the intrinsic link between Wnt signaling and cancer cell stemness, which shed light on the malignant progression of tumor cells. Finally, cancer treatment strategies based on the canonical Wnt signaling pathway are summarized, hoping to help clinical development.

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Section: Wnt Signaling and Micro-rnasmentioning

confidence: 99%

<p>New Advances in Canonical Wnt/β-Catenin Signaling in Cancer</p>

Wen¹,

Wu²,

Awadasseid³

et al. 2020

CMAR

View full text Add to dashboard Cite

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“…qRT-PCR was performed on the Applied Biosystems 7500 Sequence Detection system with IQTM SYBR Green Supermix (Bio-Rad Laboratories, Hercules, CA, USA) and 5 ng of cDNA and 10 pM of each primer. The cycling conditions were set as previously described [20]. The data were normalized to the geometric mean of the housekeeping gene GAPDH or to U6 small nuclear RNA expression and calculated according to the 2 -ΔΔCT method.…”

Section: Rna Extraction and Qrt-pcrmentioning

confidence: 99%

Hsa_circ_001680 affects the proliferation and migration of CRC and mediates its chemoresistance by regulating BMI1 through miR-340

et al. 2020

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Background: Accumulating evidence indicates that circular RNAs (circRNAs) act as microRNA (miRNA) sponges to directly inhibit specific miRNAs and alter their ability to regulate gene expression at the post-transcriptional level; this mechanism is believed to occur in various cancers. However, the expression level, precise function and mechanism of circ_001680 in colorectal carcinoma (CRC) are largely unknown. Methods: qRT-PCR was used to detect the expression of circ_001680 and miR-340 in human CRC tissues and their matched normal tissues. Bioinformatics analyses and dual-fluorescence reporter assays were used to evaluate whether circ_001680 could bind to miR-340. Circ_001680 overexpression and knockdown cell lines were constructed to investigate the proliferation and migration abilities in vivo and in vitro through function-based experiments, including CCK8, plate clone formation, transwell, and wounding healing assays. The relationships among circ_001680, miR-340 and BMI1 were investigated by bioinformatics analyses, dual-fluorescence reporter system, FISH, RIP and RNA pull down assays. Sphere forming assays and flow cytometry analyses were used to assess the effect of circ_001680 on the stemness characteristics of CRC cells. Results: Circ_001680 was more highly expressed in of CRC tissue than in matched adjacent normal tissues from the same patients. Circ_001680 was observed to enhance the proliferation and migration capacity of CRC cells. Furthermore, dual-fluorescence reporter assays confirmed that circ_001680 affects the expression of BMI1 by targeting miR-340. More importantly, we also found that circ_001680 could promote the cancer stem cell (CSC) population in CRC and induce irinotecan therapeutic resistance by regulating the miR-340 target gene BMI1. Conclusions: Our results demonstrated that circ_001680 is a part of a novel strategy to induce chemotherapy resistance in CRC through BMI1 upregulation. Moreover, circ_001680 may be a promising diagnostic and prognostic marker to determine the success of irinotecan-based chemotherapy.

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“…Studies have shown that miR-92a-3p is upregulated in CRC and promotes the migration of CRC by targeting NF2 (Alcantara and Garcia, 2019). MiR-452 activates Wnt/ β-catenin to promote CRC metastasis (Li et al, 2018a). In addition to upregulated miRNAs, downregulated miRNAs such as miR-144 , miR-548c-5p , and miR-198 also play important roles in tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

MiR-506 Targets UHRF1 to Inhibit Colorectal Cancer Proliferation and Invasion via the KISS1/PI3K/NF-κB Signaling Axis

Lin

Chen

Zheng

et al. 2019

Front. Cell Dev. Biol.

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BackgroundThe UHRF1 gene is an epigenetic modification factor that mediates tumor suppressor gene silencing in a variety of cancers. Related studies have reported that UHRF1 can inhibit the expression of the KISS1 gene. However, the regulatory mechanism underlying UHRF1 expression in colorectal cancer (CRC) is still unclear. The aim of this study was to gain a better understanding of the regulation of UHRF1 expression in CRC and to determine whether it regulates the mechanism by which KISS1 promotes CRC metastasis.MethodsIn the present study, the levels of miR-506, UHRF1 and KISS1 expression in CRC tissues and in human CRC cell lines were studied using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation, migration, and invasion assays are used to detect cell proliferation, migration, and invasion. A dual-luciferase reporter system was used to confirm the target gene of miR-506.ResultsThis study found that UHRF1 protein is highly expressed in CRC tissues and negatively correlated with KISS1 protein expression. UHRF1 overexpression activates the PI3K/NF-κB signaling pathway by inhibiting the mRNA expression levels of pathway mediators. Bioinformatics analysis and luciferase reporter gene assays confirmed that miR-506 targets UHRF1.ConclusionThis study identified the regulation of UHRF1 expression in CRC and the mechanism of CRC metastasis. UHRF1 may be a new potential target molecule for future CRC metastasis treatment.

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MiR-452 promotes an aggressive colorectal cancer phenotype by regulating a Wnt/β-catenin positive feedback loop

Cited by 34 publications

References 36 publications

<p>New Advances in Canonical Wnt/β-Catenin Signaling in Cancer</p>

<p>New Advances in Canonical Wnt/β-Catenin Signaling in Cancer</p>

Hsa_circ_001680 affects the proliferation and migration of CRC and mediates its chemoresistance by regulating BMI1 through miR-340

MiR-506 Targets UHRF1 to Inhibit Colorectal Cancer Proliferation and Invasion via the KISS1/PI3K/NF-κB Signaling Axis

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