miR‐625 down‐regulation promotes proliferation and invasion in esophageal cancer by targeting Sox2

Wang, Zhiqiang; Qiao, Qiao; Chen, Min; Li, Xian‐Hua; Wang, Zhenjun; Liu, Chuanxin; Xie, Zongtao

doi:10.1016/j.febslet.2014.01.035

Cited by 54 publications

(48 citation statements)

References 30 publications

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“…Furthermore, similar conclusions were obtained by Zhao et al, who showed that miR-126 suppresses proliferation and promotes apoptosis in hepatocellular carcinoma cells that overexpress SOX2 [27]. Additionally, Wang et al found that miR-625 was one of the upstream regulators of SOX2, and miR-625 down-regulation could promote proliferation and invasion in esophageal cancer by activating SOX2 [28]. However, whether SOX2 is a target of miR-101 that regulates cell proliferation, migration and invasion of BC cells still remains to be explored.…”

Section: Introductionsupporting

confidence: 64%

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

Wang

Zeng

et al. 2017

Cell Physiol Biochem

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Background: Increasing evidence has demonstrated that microRNAs play a critical role in breast cancer (BC) progression. microRNA-101 (miR-101) has been considered a tumor suppressive miRNA in different cancer types. This study aimed to investigate miR-101 expression in BC tissues and to investigate its roles in BC progression that are mediated by Sex-determining region Y-box 2 (SOX2), a critical oncogene in various cancers. Methods: qRT-PCR and immunohistochemistry were performed to detect miR-101 and SOX2 expression in BC tissues and paired normal tissues or BC cell lines. MTT, transwell migration, wound healing, colony formation, flow cytometric and xenograft assays were performed to determine the influence of miR-101 and SOX2 on the malignant behaviors of BC cells in vitro and in vivo. Results: miR-101 was significantly downregulated in BC tissues and cell lines. miR-101 overexpression inhibited the malignant behaviors of BC cells, both in vitro and in vivo. miR-101 downregulation had the converse effect. A miR-101 binding site was identified by luciferase reporter assay in the 3’UTR of SOX2. SOX2 was upregulated in BC tissues and cell lines, and its upregulation was associated with lymph node metastasis, pathological grade and TNM classification. SOX2 knockdown mimicked the effects of miR-101 overexpression on the malignant behaviors of BC cells, while SOX2 overexpression mitigated the miR-101-induced inhibition of these effects. Conclusions: Our study revealed that miR-101 plays a critical role in suppressing tumor progression by directly targeting SOX2.

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Section: Introductionsupporting

confidence: 64%

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

Wang

Zeng

et al. 2017

Cell Physiol Biochem

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“…miR-140 expression was decreased in the EC tissues and regulated the cell invasion of EC via controlling Slug expression (30). It has also been shown that miR-625 expression is lower in EC tissues than in the corresponding adjacent tissues and may regulate the proliferation and invasion of EC cells by targeting Sox2 (31). miR-103/107 expression has been associated with poor survival rates for ESCC patients (32).…”

Section: Discussionmentioning

confidence: 99%

miR-1291 targets mucin 1 inhibiting cell proliferation and invasion to promote cell apoptosis in esophageal squamous cell carcinoma

et al. 2015

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Abstract. MicroRNAs (miRNAs) are well known as important regulators in various cancer development. In the present study, we focused on the expression and biological function of miR-1291 in esophageal squamous cell carcinoma (ESCC). Compared with adjacent non-tumorous tissue samples, qRT-PCR data showed significant downregulation of miR-1291 in 54 ESCC tissue samples (P<0.05), which was also significantly associated with lymph node metastases and clinical stage (P<0.05). Cell Counting Kit-8 (CCK-8), colony formation, Transwell and flow cytometric apoptosis assays were performed to detect the effect of miR-1291 upregulation, and the results showed inhibition of the proliferation, invasion and promotion of apoptosis in EC9706 and EC-1 cells. Using bioinformatic analyses, we found that mucin 1 (MUC1) was a potential target for miR-1291. Luciferase assays were performed to reveal that miR-1291 inhibited MUC1 expression by targeting the seed region of MUC1 3'-untranslated region (3'UTR). We also found that the expression of MUC1 lacking in 3'UTR abrogated the anti-invasion and pro-apoptosis function of miR-1291. Our results demonstrated the importance of miR-1291 in targeting MUC1 for the regulation of esophagus cancer growth, invasion and apoptosis, and may be helpful for developing new targets for early diagnosis or new therapeutic targets for ESCC.

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“…MiR-16 induced the suppression of cell apoptosis while promote proliferation in esophageal squamous cell carcinoma [21]. miR-625 down-regulation promotes proliferation and invasion in esophageal cancer by targeting Sox2 [22]. Here, we sought to provide evidence for downexpression of miR-140 targeting of Slug to promote the invasion in EC.…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Jiang

Zhou

et al. 2014

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) are reported to regulate cell invasion and functions by interfering with the translation of target mRNAs, but the role of miRNAs in esophageal cancer (EC) remains unclear. Methods: RT-PCR and Western blot were used to detect the expression of miRNAs and candidate genes in EC samples (n=89). miR-140 mimics and inhibitor were tansfected in human TE-1 and Eca-109 cells. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter assay. The markers of EMT were detected by using Western blot. Results: miR-140 expression was decreased in the EC tissues compared with the corresponding adjacent tumor tissues. Low expression of miR-140 promotes cell invasion by using transwell assay, while the effect of miR-140 high expression is reverse. Slug, a target gene of miR-140, was examined by luciferase assay and Western blot. Conclusions: miR-140 may regulate the cell invasion of EC via controlling Slug expression.

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miR‐625 down‐regulation promotes proliferation and invasion in esophageal cancer by targeting Sox2

Cited by 54 publications

References 30 publications

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

miR-1291 targets mucin 1 inhibiting cell proliferation and invasion to promote cell apoptosis in esophageal squamous cell carcinoma

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

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