miRNA423-5p regulates cell proliferation and invasion by targeting trefoil factor 1 in gastric cancer cells

Liu, Jingjing; Wang, Xu; Yang, Xiao-Ning; Liu, Yunpeng; Shi, Ying; Ren, Jianlin; Guleng, Bayasi

doi:10.1016/j.canlet.2014.01.024

Cited by 79 publications

(63 citation statements)

References 30 publications

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“…Stiuso et al 25 showed that miR-423-5p promotes autophagy in hepatocarcinoma cells, and miR-423-5p was also found to regulate cell proliferation and invasion in gastric cancer cells. 26 In gliomas, miR-423-5p is reportedly overexpressed in Chinese primary glioblastomas 27 and contributes to the malignant phenotype as well as TMZ chemoresistance. 11 However, the expression and function of miR-423-5p in GSCs have remained unknown.…”

Section: Discussionmentioning

confidence: 99%

Retracted - miR-423-5p knockdown enhances the sensitivity of glioma stem cells to apigenin through the mitochondrial pathway

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Retracted - miR-423-5p knockdown enhances the sensitivity of glioma stem cells to apigenin through the mitochondrial pathway

et al. 2017

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“…22,23 Several studies have reported that miR-423-5p functions as a biomarker and has important roles in many types of cancers. [24][25][26] However, there is no research to date that refers to the role of miR-423-5p in glioma tissues. In this study, we report that miR-423-5p is overexpressed in GBMs and is a novel tumor promoter in GBM.…”

Section: Discussionmentioning

confidence: 99%

miR-423-5p contributes to a malignant phenotype and temozolomide chemoresistance in glioblastomas

Zeng

et al. 2016

Neuro-Oncology

111

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Background Gliomas are based on a genetic abnormality and present with a dismal prognosis. MicroRNAs (miRNAs) are considered to be important mediators of gene expression in glioma tissues. Methods Real-time PCR was used to analyze the expression of microRNA-423-5p (miR-423-5p) in human glioma samples and normal brain tissue. Apoptosis, cell cycle, proliferation, immunostaining, transwell, in vitro 2D and 3D migration, and chemosensitivity assays were performed to assess the phenotypic changes in glioma cells overexpressing miRNA-423-5p. Western blotting was used to determine the expression of inhibitor of growth 4 (ING-4)in glioma tissues, and a luciferase reporter assay was conducted to confirm whether ING-4 is a direct target of miR-423-5p. Western blotting was used to identify the potential signaling pathways that are affected in glioma cell growth by miR-423-5p. Xenograft tumors were examined in vivo for the carcinogenic effects of miR-423-5p in glioma tissues. Results We first reported that miR-423-5p expression was increased in gliomas and was a potential tumor promoter via targeting ING-4. The overexpression of miR-423-5p resulted in upregulation of important signaling molecules such as p-AKT and p-ERK1/2. In clinical samples, miR-423-5p was dysregulated, and a corresponding alteration in ING-4 expression was observed (P = .0207). Furthermore, the overexpression of miR-423-5p strengthened glioma cell proliferation, angiogenesis, and invasion. Finally, miR-423-5p overexpression also strengthened GBM neurosphere formation and rendered glioma cells resistant to temozolomide (TMZ). Conclusion This study establishes that miR-423-5p functions as an oncogene in glioma tissues by suppressing ING-4 and suggests that it has therapeutic potential for glioma.

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“…Lu et al [39] demonstrated that serum miR-423-5p was upregulated in the stage I-II colorectal cancer patients compared with the control. Liu et al demonstrated that miR-423-5p increased cell proliferation and invasion through regulating trefoil factor 1 (TFF1) in gastric cancer cells [40]. However, the expression and effect of miR-423-5p are still unknown in osteosarcoma.…”

Section: Discussionmentioning

confidence: 99%

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

Wang¹,

Peng²,

Gong³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidences suggest that dysregulated expression of miRNAs contributes to the progression of various tumors. However, the underlying function of miR-423-5p in osteosarcoma remains unexplored. Methods: The expression of miR-423-5p and STMN1 were determined in osteosarcoma samples and cell lines via quantitative real-time PCR. Colony formation and Cell Counting Kit-8 (CCK-8) assays were performed to measure cell proliferation ability and transwell analysis was used to detect cell invasion, and dual luciferase reporter assay was perform to analysis the interaction between the miR-423-5p and STMN1. Results: The expression levels of miR-423-5p and STMN1 in the osteosarcoma tissues and cell lines were measured by qRT-PCR. Cell viability was determined using the clone formation and CCK-8 assays. A dual-luciferase reporter and Western blot were performed to stdudy the target gene of miR-423-5p. Here, we showed that miR-423-5p expression was downregulated in osteosarcoma tissues and cell lines. However, the expression of stathmin1 (STMN1) was downregulated in osteosarcoma tissues and cell lines. Moreover, STMN1 expression level was negatively correlated with the miR-423-5p expression in the osteosarcoma tissues. We identified STMN1 was a direct target gene of miR-423-5p in osteosarcoma cell. Overexpression of miR-423-5p inhibited osteosarcoma cell proliferation, colony formation and invasion. Furthermore, we demonstrated that STMN1 was involved in miR-423-5p-mediated cell behavior such as cell proliferation, colony formation and invasion in the osteosarcoma cell. Conclusion: Our present study indicated that miR-423-5p acted as a tumor suppressor gene in osteosarcoma partly through inhibiting STMN1 expression.

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miRNA423-5p regulates cell proliferation and invasion by targeting trefoil factor 1 in gastric cancer cells

Cited by 79 publications

References 30 publications

Retracted - miR-423-5p knockdown enhances the sensitivity of glioma stem cells to apigenin through the mitochondrial pathway

Retracted - miR-423-5p knockdown enhances the sensitivity of glioma stem cells to apigenin through the mitochondrial pathway

miR-423-5p contributes to a malignant phenotype and temozolomide chemoresistance in glioblastomas

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

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