miR-224 targets BTRC and promotes cell migration and invasion in colorectal cancer

Zheng, Qi; Yu, Jane; Li, Chenggang; Li, Jiali; Wang, Jiping; Wang, Shuyang

doi:10.1007/s13205-020-02477-x

Cited by 15 publications

(14 citation statements)

References 25 publications

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“…In this study, we found that miR-224-5p level was signi cantly upregulated in CRC cells, and downregulation of miR-224-5p could induce cell apoptosis and inhibit cell migration and invasion. Consistent with our present results, zheng et al showed that miR-224 overexpression promoted CRC cell proliferation and migration via targeting BTRC [19]. In addition, liang et al showed that downregulation of miR-224 could suppress the proliferation and trigger the apoptosis of adriamycin-resistant CRC cells [36].…”

Section: Discussionsupporting

confidence: 91%

“…Currently, miR-224-5p has been identi ed to be dysregulated in human cancers, including CRC [19,35]. In this study, we found that miR-224-5p level was signi cantly upregulated in CRC cells, and downregulation of miR-224-5p could induce cell apoptosis and inhibit cell migration and invasion.…”

Section: Discussionmentioning

confidence: 68%

“…1D). Zheng et al revealed that miR-224 level was increased in CRC tissues [19]. Meanwhile, in the TCGA dataset, high levels of miR-224-5p in patients with CRC are associated with a shorter overall survival, indicating that increased miR-224-5p levels may predict poor overall survival in patients with CRC (Fig.…”

Section: Identi Cation Of Dems In Crcmentioning

confidence: 97%

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Exosomal miR-224-5p from colorectal cancer cells promotes malignant transformation of human colon normal cells by promoting cell proliferation through downregulation of CMTM4

Yang

Guo-yin

et al. 2021

Preprint

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Background Interactions between malignant cells and neighboring normal cells is important for carcinogenesis. In addition, cancer cell-derived exosomes have been shown to promote the malignant transformation of recipient cells, but the mechanisms remain unclear. Methods The level of miR-224-5p in colorectal cancer (CRC) cell-derived exosomes was determined by RT-qPCR assay. In addition, PKH26 dye-labeled exosomes were used to assess the efficacy of the transfer of exosomes between SW620 and CCD 841 CoN cells. Results In this study, we found that overexpression of miR-224-5p significantly promoted the proliferation, migration and invasion of SW620 cells. In addition, miR-224-5p can be transferred from SW620 cells to CCD 841 CoN cells via exosomes. SW620 cell-derived exosomes overexpressing miR-224-5p markedly promoted proliferation, migration and invasion of CCD 841 CoN cells. Meanwhile, SW620 cell-derived exosomal miR-224-5p notably decreased the expression of CMTM4 in CCD 841 CoN cells. Furthermore, SW620 cell-derived exosomal miR-224-5p significantly inhibited tumor growth in a xenograft model in vivo. Conclusion These findings suggested that SW620 cell-derived exosomal miR-224-5p could promote malignant transformation and tumorigenesis in vitro and in vivo via downregulation of CMTM4, suggesting that miR-224-5p might be a potential target for therapies in CRC.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 68%

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Exosomal miR-224-5p from colorectal cancer cells promotes malignant transformation of human colon normal cells by promoting cell proliferation through downregulation of CMTM4

Yang

Guo-yin

et al. 2021

Preprint

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“… 34 Zhou discovered that miR-193a-3p is upregulated in patients with glioma and promotes the invasion, migration, and EMT of glioma by inhibiting the expression of BTRC protein. 35 …”

Section: Discussionmentioning

confidence: 99%

Establishment of Sunitinib-Resistant Xenograft Model of Renal Cell Carcinoma and the Identification of Drug-Resistant Hub Genes and Pathways

Xie¹,

Shangguan²,

Chen³

et al. 2021

DDDT

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Introduction Sunitinib is the first-line targeted drug for the treatment of advanced renal cell carcinoma (RCC), but its therapeutic potential is limited by premature drug resistance. In an attempt to overcome this limitation, a sunitinib-resistant cell-derived xenograft (CDX) model of clear cell renal cell carcinoma (ccRCC) in vivo was constructed in this study. The molecular mechanism of drug resistance was analyzed using sequencing and bioinformatics tools. Methods First, mice were injected subcutaneously with tumor cells 786-O to create tumors and were simultaneously treated with sunitinib. After three consecutive passages, a drug-resistant xenograft model was obtained. Then, key pathways and genes were identified via second-generation sequencing of the tissue and the examination of differentially expressed genes (DEGs) with bioinformatics tools. Results Analysis of sequencing data revealed that 646 DEGs were upregulated and 465 were downregulated in the drug-resistant tissues when compared with the sensitive tissues. GO showed that the DEGs were significantly enriched in angiogenesis, cell hypoxia response, and apoptosis. KEGG analysis demonstrated that the main pathways were PI3K-Akt, HIF-1, NF-kappa B, and MAPK. Modular analysis of the PPI network indicated that the GO and KEGG analyses of module 1 with the highest ranking were mainly related to ubiquitinase activity. Similarly, the GO and KEGG analyses of the top 10 hub genes were also chiefly linked to ubiquitinase activity. Then, comprehensive expression analysis of the hub genes, and finally, the genes BTRC and TRIM32 were identified, which were consistent in all observations. Conclusion In this study, through the construction of in vitro models and bioinformatics analysis, the important pathways and key genes related to ccRCC sunitinib resistance were discovered. Among them, ubiquitinase may play an important role in drug resistance and may be a potential therapeutic target and biomarker.

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“…As an important member of miRNA, miR-224 is significantly upregulated in colorectal cancer. Overexpression of miR-224 promotes the migration and invasion of colorectal cancer cells [7] . In addition, miR-224 mediates proliferation of human colon cancer cell line (HCT116) by targeting Smad4 [8] .…”

mentioning

confidence: 99%

Study on Effect of Vitexicarpin on the Biological Behavior of Colorectal Cancer Cells by Circ_0000419/MicroRNA-224

Huang¹,

Cao²,

Peng³

et al. 2021

ijps

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miR-224 targets BTRC and promotes cell migration and invasion in colorectal cancer

Cited by 15 publications

References 25 publications

Exosomal miR-224-5p from colorectal cancer cells promotes malignant transformation of human colon normal cells by promoting cell proliferation through downregulation of CMTM4

Exosomal miR-224-5p from colorectal cancer cells promotes malignant transformation of human colon normal cells by promoting cell proliferation through downregulation of CMTM4

Establishment of Sunitinib-Resistant Xenograft Model of Renal Cell Carcinoma and the Identification of Drug-Resistant Hub Genes and Pathways

Study on Effect of Vitexicarpin on the Biological Behavior of Colorectal Cancer Cells by Circ_0000419/MicroRNA-224

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