MiRNA-145 suppresses lung adenocarcinoma cell invasion and migration by targeting N-cadherin

Mo, Dongping; Yang, Dan; Xiao, Xianmin; Sun, Ruihong; Huang, Lei; Xu, Jian

doi:10.1007/s10529-017-2290-9

Cited by 39 publications

(26 citation statements)

References 16 publications

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“…The dysregulation of miRNA-145 expression has been reported in different types of cancers. In bladder cancer and lung cancer, miRNA-145 inhibits migration and invasion of tumor cells by directly targeting N-cadherin [12,13]. In the present study, we found that the expression of miRNA-145 was down-regulated in PC tissues comparing to the paired adjacent no cancerous tissues.…”

Section: Discussionsupporting

confidence: 53%

MicroRNA-145 suppresses epithelial to mesenchymal transition in pancreatic cancer cells by inhibiting TGF-β signaling pathway

Chen¹,

Xu²,

Yao³

et al. 2020

J. Cancer

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TGF-β signaling plays a critical role in tumor progression and many approaches have been made to inhibit its functions. MicroRNA is one of the approaches that inhibit TGF-β signaling and can be used as a promising treatment for cancer. This study explored the role of miRNA-145 in pancreatic cancer (PC) development. The expression of miRNA-145 in PC tissues and paired adjacent normal tissues was examined by qRT-PCR. The expression of miRNA-145 in PC cells and the ability of cell migration and invasion were detected both in vivo and in vitro. The results showed that miRNA-145 was down-regulated in PC tissues and PC cells. Increasing the expression of miRNA-145 in PC cells inhibited the TGF-β signaling pathway and epithelial-mesenchymal transition (EMT) process. Scratch assay and transwell assay showed that miRNA-145 inhibited the migration and invasion in PC cells. In vivo experiments confirmed that miRNA-145 mimics delayed the growth of PC xenografts comparing with miRNA-145 inhibitor. Our results suggested that miRNA-145 can inhibit epithelial to mesenchymal transition (EMT) and tumor growth by suppressing TGF-β signaling pathway. Thus, miRNA-145 could be a potential therapeutic for targeting TGF-β signaling in PC treatment.

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Section: Discussionsupporting

confidence: 53%

MicroRNA-145 suppresses epithelial to mesenchymal transition in pancreatic cancer cells by inhibiting TGF-β signaling pathway

Chen¹,

Xu²,

Yao³

et al. 2020

J. Cancer

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“…N-cadherin, which is an adhesion molecule of EMT, was first identified in the nervous system [28]. As reported, depletion of N-cadherin suppressed cell invasion and migration in LUAD [29]. As a biomarker of EMT, Vimentin is an intermediate filament protein that plays a role in cell migration to keep structure and motility [30].…”

Section: Discussionmentioning

confidence: 94%

STRIP2, a member of the striatin‐interacting phosphatase and kinase complex, is implicated in lung adenocarcinoma cell growth and migration

et al. 2020

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Lung adenocarcinoma (LUAD) accounts for ~40% of lung cancer cases, and the 5‐year relative survival rate is no more than 1%. Dysregulation of components of striatin‐interacting phosphatase and kinase (STRIPAK) complexes is associated with various diseases, including cancer. Striatin‐interacting protein 2 (STRIP2), also called Fam40b, has been reported to regulate tumor cell growth and migration. Here, we investigated the role of STRIP2 in LUAD growth, migration and the underlying mechanisms. Analysis of data from The Cancer Genome Atlas database revealed that STRIP2 is highly expressed and predicted poor outcomes in patients with LUAD. Moreover, quantitative RT‐PCR (qRT‐PCR) analysis revealed that the mRNA expression of STRIP2 is greater in all tested LUAD cells than in a normal lung cell line. To investigate the function of STRIP2, we overexpressed STRIP2 in SPC‐A1 cells and depleted STRIP2 in Calu‐3 cells. Cell proliferation was evaluated by Cell Counting Kit‐8 and colony‐forming assays, and Transwell assay was employed to test cell invasion and migration. Our results indicate that STRIP2 depletion suppressed cell proliferation, invasion and migration in Calu‐3 cells, and overexpression of STRIP2 had the opposite effects in SPC‐A1 cells. Moreover, we discovered that STRIP2 depletion reduced the protein levels of p‐Akt and phosphorylated‐mammalian target of rapamycin (p‐mTOR) in Calu‐3 cells, whereas STRIP2 overexpression increased levels of these proteins in SPC‐A1 cells. Furthermore, we found that silencing of STRIP2 clearly enhanced protein levels of E‐cadherin and reduced levels of N‐cadherin, Vimentin and matrix metalloproteinase‐9 in Calu‐3 cells, whereas overexpression of STRIP2 had the opposite effect in SPC‐A1 cells. Our data indicate that STRIP2 promotes the proliferation and motility of LUAD cells, and this may be mediated through the regulation of the Akt/mTOR pathway and epithelial–mesenchymal transition. These results may facilitate the development of therapeutic strategies to treat LUAD.

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“…Epithelial-mesenchymal transition (EMT) is an important mechanism leading to invasion and metastasis of various cancers (4)(5)(6). Cells undergoing EMT lose the epithelial features and acquire some mesenchymal features, which is associated with the upregulation of N-cadherin and downregulation of E-cadherin (6).…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA CCAT2 promotes epithelial-mesenchymal transition involving Wnt/β-catenin pathway in epithelial ovarian carcinoma cells

et al. 2017

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Abstract. Long non-coding RNA colon cancer-associated transcript 2 (CCAT2) is dysregulated in a variety of types of human cancer. However, the role of CCAT2 in epithelial ovarian carcinoma (EOC) remains largely unknown. The aim of this study is to investigate the effect of CCAT2 on epithelial-mesenchymal transition (EMT) and related molecular mechanisms in epithelial ovarian cancer cells. In the current paper, we found that CCAT2 was significantly upregulated in EOC SKOV3, A2780 and HO8910 cell lines compared with the normal ovarian epithelial HUM-CELL-0088 cell line. Functional assays demonstrated that the knockdown of CCAT2 inhibited migration and invasion of EOC cells in vitro. Moreover, our results showed that silencing CCAT2 inhibited EMT by the upregulation of epithelial cadherin and downregulation of neural cadherin, zinc finger protein SNAI and Twist-related protein 1 in SKOV3 and A2780 cell lines. But, that was reversed by the treatment with lithium chloride (LiCl), by which the canonical Wnt/β-catenin pathway could be activated. In addition, we further investigated the role of CCAT2 in the modulation of Wnt/β-catenin signaling pathway. Our results revealed that knockdown of CCAT2 inhibited the expression of β-catenin and the activity of T-cell factor/lymphoid enhancer factor, acting as a key transcription factor of Wnt signaling pathway. Collectively, these results indicate that CCAT2 may promote EMT, at least partly through Wnt/β-catenin signaling pathway in EOC cells. Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer.

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MiRNA-145 suppresses lung adenocarcinoma cell invasion and migration by targeting N-cadherin

Abstract: MiR-145 could inhibit invasion and migration of lung adenocarcinoma cell lines by directly targeting N-cadherin.

Cited by 39 publications

References 16 publications

MicroRNA-145 suppresses epithelial to mesenchymal transition in pancreatic cancer cells by inhibiting TGF-β signaling pathway

MicroRNA-145 suppresses epithelial to mesenchymal transition in pancreatic cancer cells by inhibiting TGF-β signaling pathway

STRIP2, a member of the striatin‐interacting phosphatase and kinase complex, is implicated in lung adenocarcinoma cell growth and migration

Long non-coding RNA CCAT2 promotes epithelial-mesenchymal transition involving Wnt/β-catenin pathway in epithelial ovarian carcinoma cells

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