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

Li, Weiling; Jiang, Guojun; Zhou, Jianping; Wang, Hongmin; Gong, Zegang; Zhang, Zheng; Min, Ke; Zhu, Hua; Tan, Yongfei

doi:10.1159/000366351

Cited by 56 publications

(47 citation statements)

References 29 publications

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“…For instance, miR-1290 was significantly upregulated in ESCC tissue samples, and ectopic miR-1290 expression potently promoted ESCC cell growth, migration and invasion in vitro (25). 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).…”

Section: Discussionmentioning

confidence: 98%

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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Section: Discussionmentioning

confidence: 98%

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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“…Transcription factor Snail suppresses E-cadherin effecting cell differentiation, and migratory and invasive properties, inducing cell movement and survival. It is already reported that miR-140 targeting Slug (Snail2) to regulate the invasion in EC [1]. GSK3β binds to and phosphorylates Snail, thereby regulating its function, and together these proteins act as a molecular switch for many signaling pathways [25].…”

Section: Psat1 Induces Cell Invasion In Escc Cell Linesmentioning

confidence: 99%

“…It is the eighth most common cancer globally and the sixth most common cause of cancerrelated death [1][2][3][4]. This type of cancer is about four times more common in men than in women and there are vastly different rates of occurrence between countries with China accounting for about half of all cases [5,6].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Phosphoserine Aminotransferase 1 (PSAT1) Predicts Poor Prognosis and Associates with Tumor Progression in Human Esophageal Squamous Cell Carcinoma

Liu

Jia

Chen

et al. 2016

Cell Physiol Biochem

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Background/Aims: Phosphoserine aminotransferase 1 (PSAT1) is over-expressed in many carcinoma tissues, however little is known regarding its expression and function in esophageal carcinogenesis. This study investigated the expression of PSAT1 in human esophageal squamous cell carcinoma (ESCC) tissues to determine the relationship between PSAT1 expression and clinicopathological factors. Methods: The expression of PSAT1 in 64 surgical resections from esophageal carcinogenesis patients was examined by quantitative RT-PCR and immunohistochemistry and the results were compared with clinicopathological factors. In vitro experiments were performed in ESCC cells overexpressing PSAT1 to measure cell viability and invasion. Tumor formation in vivowas examined by injection of tumor cells into immunocompromised mice subcutaneously. Results: PSAT1 expression was elevated in ESCC tissues compared to normal esophageal tissues. Increased PSAT1 expression was significantly associated with stage of disease, lymph node metastasis, distant metastasis and poor prognosis. In vitro, PSAT1 overexpression promoted ESCC cell proliferation and matrigel invasion. In vivo, injection of mice with ECSS cells overexpressing PSAT1 enhanced tumor formation. Western blot analysis revealed that PSAT1 upregulated the expression and/or activity of GSK3β/Snail. Conclusion: PSAT1 plays a crucial role in the development of ESCC and predicts poor survival. Therefore, PSAT1 may be a promising novel anticancer therapeutic target.

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“…PCR was performed under the following conditions: Denaturation at at 50˚C for 2 min, followed by 40 cycles of 95˚C for 15 sec and 60˚C for 1 min. Protein expression was quantified using the 2 -∆CT method, as previously described (11).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of H19 promotes invasion and induces epithelial-to-mesenchymal transition in esophageal cancer

et al. 2015

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Abstract. Long non-coding RNAs (lncRNAs) have previously been reported to be involved in cancer invasion, proliferation and apoptosis. However, the association between the lncRNA, H19, and esophageal cancer (EC) has remained elusive. In the present study, reverse transcription quantitative-polymerase chain reaction revealed that the expression of H19 was significantly increased and associated with tumor depth and metastasis in 133 EC samples. Furthermore, MTT and Transwell assays revealed that overexpression of H19 in vitro promoted the proliferation and invasion of EC cell lines, whereas knockdown of H19 inhibited the proliferation and invasion of EC cell lines. In addition, it was identified that an upregulation of H19 induced epithelial-to-mesenchymal transition, while the opposite effect was observed following the downregulation of H19. In conclusion, H19 has a significant role in the development of EC and may serve as a potential prognostic marker and therapeutic target for EC. IntroductionEsophageal carcinoma (EC) is the eighth most aggressive and malignant type of cancer, with a high incidence that varies according to geographic location and ethnicity (1). Despite progress in the development of diagnostic and therapeutic options, the survival rates for EC patients remain poor. Therefore, the identification of novel genes involved in the tumorigenesis and development of EC is urgently required.Long non-coding RNAs (lncRNAs) are a class of RNAs that have been reported to be involved in the regulation, invasion, proliferation and apoptosis of multiple tumors (2,3). The association between H19 expression and the progression of various types of cancer has been demonstrated in previous studies. One study found that the overexpression of lncRNA H19 enhanced the carcinogenesis and metastasis of gastric cancer (4). MALAT-1, an abundant lncRNA present in many human cell types, has been suggested to regulate the alternative splicing of a subset of pre-messenger (m)RNAs by modulating serine/arginine splicing factor activity. This factor in turn regulates tissue or cell-type-specific alternative splicing in a phosphorylation-dependent manner (5). However, the role of H19 in EC is yet to be elucidated.The epithelial-to-mesenchymal transition (EMT) has an important role in the invasion of various types of cancer by transforming adherent and polarized epithelial cells into invasive and motile mesenchymal cells (6,7). A number of transcription factors involved in EMTs, including Twist and Snail, increase the expression level of mesenchymal markers, including fibronectin, collagen and Vimentin, and decrease the expression of epithelial markers, including E-cadherin. The breakdown of tight junctions results in the loss of epithelial markers and the acquisition of mesenchymal markers (8-10).In the present study, the expression levels of H19 in EC were investigated, in order to elucidate the role of H19 in EC. Materials and methods Clinical

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

Cited by 56 publications

References 29 publications

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

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

Overexpression of Phosphoserine Aminotransferase 1 (PSAT1) Predicts Poor Prognosis and Associates with Tumor Progression in Human Esophageal Squamous Cell Carcinoma

Upregulation of H19 promotes invasion and induces epithelial-to-mesenchymal transition in esophageal cancer

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