miR-22 is down-regulated in gastric cancer, and its overexpression inhibits cell migration and invasion via targeting transcription factor Sp1

Guo, Meimei; Hu, Lihua; Wang, Yongqiang; Chen, Peng; Huang, Jianguo; Lü, Ning; He, Jianghong; Liao, Cheng-Gong

doi:10.1007/s12032-013-0542-7

Cited by 69 publications

(54 citation statements)

References 29 publications

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“…miRs, which regulate the expression of their target genes by base pairing with seed sequences in the 3'-UTR of mRNAs, have been shown to regulate the expression of Sp1 (39,40). In a previous study, miR-22 was reported to be downregulated in GC and inhibited cell proliferation, migration and invasion by targeting Sp1 (41). The results of the present study suggested that miR-429 suppresses GC cell migration and invasion by directly targeting Sp1.…”

Section: Discussionsupporting

confidence: 57%

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

Yang

Liu

et al. 2017

Oncology Letters

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Abstract. microRNAs (miRs) have been reported to have an important role in tumorigenesis and tumor progression. Although miR-429 has been shown to be downregulated in gastric cancer (GC), the function of miR-429 in the metastasis of GC has yet to be investigated. In the present study, GC cells were transfected with miR-429, and reverse transcription-quantitative polymerase chain reaction, cell migration assays, cell invasion assays, western blot analysis and luciferase assays were conducted to investigate the role of miR-429 in GC cells. It was demonstrated that miR-429 expression was markedly increased following transfection of the cells with miR-429. Furthermore, miR-429 was shown to inhibit the migration and invasion of GC cell lines. In addition, this study provided evidence that miR-429 directly targets specificity protein 1 in GC cells. The results of the present study may enhance current knowledge regarding the molecular basis of cancer metastasis and provide a potential therapeutic strategy for GC.

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Section: Discussionsupporting

confidence: 57%

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

Yang

Liu

et al. 2017

Oncology Letters

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“…miR-29b and miR-375 function as tumor suppressors in TSCC through targeting SP1 (39,40). miR-145, miR-133a, miR-133b, miR-22 and miR-335 serve an important role in the biology of gastric cancer by regulating SP1 directly (41)(42)(43). miR-145 was also found to regulate SP1 in ovarian cancer cells sensitized to paclitaxel (44).…”

Section: Discussionmentioning

confidence: 95%

MicroRNA-149 targets specificity protein 1 to suppress human tongue squamous cell carcinoma cell proliferation and motility

Chen

2016

Oncology Letters

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“…Subsequently, ubiquitous miR-22 expression has been identified in a variety of tissues (14). We have identified that miR-22 is downregulated in gastric cancer and its overexpression inhibits cell migration and invasion (15). Lately, several targets of miR-22 have been reported to mediate its tumor-suppressive effect, such as tumor-suppressive PTEN, Max genes, p21 and oncogene c-Myc expression, etc (14)(15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

A Regulatory Loop Involving miR-22, Sp1, and c-Myc Modulates CD147 Expression in Breast Cancer Invasion and Metastasis

et al. 2014

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Breast cancer is the most common cancer in women for which the metastatic process is still poorly understood. CD147 is upregulated in breast cancer and has been associated with tumor progression, but little is known about its regulatory mechanisms. In this study, we demonstrated that CD147 was overexpressed in breast cancer tissues and cell lines, and the high expression correlated with tumor invasion and metastasis. We also found that the transcription factors Sp1 and c-Myc could bind to the CD147 promoter and enhance its expression. The CD147 mRNA has a 748-bp 3 0 -untranslated region (UTR) with many miRNA target sites, suggesting possible regulation by miRNAs. We discovered that miR-22 repressed CD147 expression by directly targeting the CD147 3 0 UTR. We also determined that miR-22 could indirectly participate in CD147 modulation by downregulating Sp1 expression. miR-22 could form an autoregulatory loop with Sp1, which repressed miR-22 transcription by binding to the miR-22 promoter. Together with the c-Myc-mediated inhibition of miR-22 expression, our investigation identified a miR-22/Sp1/c-Myc network that regulates CD147 gene transcription. In addition, miR-22 overexpression suppressed breast cancer cell invasion, metastasis, and proliferation by targeting CD147 in vitro and in vivo. Furthermore, we found that miR-22 was significantly downregulated in breast cancer tissues and that its expression was inversely correlated with the tumor-node-metastasis stage and lymphatic metastasis in patients. Our study provides the first evidence that an miR-22/Sp1/c-Myc network regulates CD147 upregulation in breast cancer and that miR-22 represses breast cancer invasive and metastatic capacities. Cancer Res; 74(14); 3764-78. Ó2014 AACR.

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miR-22 is down-regulated in gastric cancer, and its overexpression inhibits cell migration and invasion via targeting transcription factor Sp1

Cited by 69 publications

References 29 publications

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

MicroRNA-149 targets specificity protein 1 to suppress human tongue squamous cell carcinoma cell proliferation and motility

A Regulatory Loop Involving miR-22, Sp1, and c-Myc Modulates CD147 Expression in Breast Cancer Invasion and Metastasis

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