MicroRNA-153-3p suppress cell proliferation and invasion by targeting SNAI1 in melanoma

Zeng, Hai; Shen, Yan; Wu, Su

doi:10.1016/j.bbrc.2017.04.032

Cited by 51 publications

(41 citation statements)

References 21 publications

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“…Recently, abundant studies have already reported the importance of miRNAs in an increasing number of cancers [5,6]. In melanoma, some miRNAs have been found abnormally expressed, such as miR-153-3p [7], miR-211 [8], miR-196a [9], miR-30b, and miR-30d [10]. They have been revealed as oncogenes or tumor suppressor genes in melanoma.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

Xiong

Liu

Qiu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Melanoma is one of the most aggressive malignant tumors, with increasing incidence, poor prognosis, and lack of any effective targeted therapies. Abnormal expression of miR-29a has been found in several types of cancers, including melanoma. In this study, experiments were performed to investigate the role of miR-29a in melanoma, and the molecular mechanism by which miR-29a represses melanoma. Methods: miR-29 and Bmi1 expression was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability, apoptosis, migration and invasion were respectively determined by Cell Counting Kit-8 assay, Propidium iodide (PI) fluorescein isothiocynate (FITC)-Annexin V staining assay, wound healing assay and transwell assay. Luciferase reporter assay was performed to determine a target gene of miR-29a. Western blot was used to analyze protein expression of apoptosis-related proteins, Bmi1, Wnt/β-catenin and Nuclear factor-κB (NF-κB) pathway target genes. Results: miR-29a was down-regulated in all tested melanoma cell lines. Up-regulation of miR-29a effectively inhibited cell viability, migration, and invasion, but promoted apoptosis in A375 cells. Bmi1 was a direct target gene of miR-29a. Transfection with miR-29a mimic decreased cell migration and invasion and Bmi1 expression in Malme-3M cells, SK-MEL-2, SK-MEL-5, and M14 cell lines. Moreover, miR-29a might suppress growth, migration and invasion of A375 cells by negatively regulating Bmi1. In addition, our results demonstrated that transfection with miR-29a mimic effectively blocked Wnt/β-catenin and NF-κB pathways via down-regulating Bmi1. Conclusion: miR-29a could be functioned as a potential tumor suppressor through direct regulation of Bmi1 in melanoma cells.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

Xiong

Liu

Qiu

et al. 2018

Cell Physiol Biochem

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“…MicroRNAs (miRNAs) are endogenous, small non‐coding RNAs that play an essential role in the regulation of gene expression and tumor progression; in addition, these have been linked to chemotherapy resistance . Many studies have suggested that miR‐153 is a tumor suppressor miRNA . miR‐153‐3p has been reported to suppress the proliferation and invasion of melanoma cells by targeting SNAI1 .…”

Section: Discussionmentioning

confidence: 99%

“…21 Many studies have suggested that miR-153 is a tumor suppressor miRNA. [22][23][24][25] miR-153-3p has been reported to suppress the proliferation and invasion of melanoma cells by targeting SNAI1. 24 MiR-153 was shown to downregulate Snail expression by directly targeting the 3-untranslated region of SNAI1.…”

Section: Discussionmentioning

confidence: 99%

“…[22][23][24][25] miR-153-3p has been reported to suppress the proliferation and invasion of melanoma cells by targeting SNAI1. 24 MiR-153 was shown to downregulate Snail expression by directly targeting the 3-untranslated region of SNAI1. miR-153-3p inhibited proliferation, migration, and invasion of acute lymphoblastic leukemia cells by suppressing inhibitor of growth protein 2 expression.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐153‐3p regulates cell proliferation and cisplatin resistance via Nrf‐2 in esophageal squamous cell carcinoma

et al. 2020

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Background Our recent studies have indicated that miR‐153‐3p is downregulated in the esophageal squamous cell carcinoma (ESCC) cell lines and tissues. Upregulation of miR‐153‐3p was found to inhibit migration and invasion of ESCC cells. However, whether miR‐153‐3p regulates the cisplatin sensitivity in ESCC cells remains unclear. In this study, we explored whether and how miR‐153‐3p regulates the proliferation and confers cisplatin resistance in ESCC by targeting the Nrf‐2 protein. Methods Eca109 cell line was transfected with microRNA‐153‐3p mimics or Nrf‐2siRNA and cell proliferation and cisplatin resistance were studied. A dual‐luciferase reporter assay was performed on Eca109 cells cotransfected with the wild‐type/mutant 3′UTR sequences of Nrf‐2 and control or microRNA‐153‐3p mimics. We determined the correlation between microRNA‐153‐3p and Nrf‐2 expression in human ESCC samples and explored the effect of Nrf‐2 in the overall survival rate of ESCC patients. Results MiR‐153‐3p significantly suppressed cell proliferation and increased the sensitivity of Eca‐109 cells to cisplatin. MiR‐153‐3p showed a negative correlation with Nrf‐2 in human esophageal carcinoma tissues. MiR‐153‐3p suppressed the expression of Nrf‐2 via binding to its 3′‐UTR region. Furthermore, inhibition of Nrf‐2 also decreased cell proliferation and increased the sensitivity of Eca109 cells to cisplatin. High expression of Nrf‐2 in human ESCC samples was associated with poor overall survival of ESCC patients. Conclusion MiR‐153‐3p inhibits cell proliferation and confers cisplatin resistance by downregulating Nrf‐2 expression in Eca‐109 cells. Thus, miR‐153‐3p/Nrf‐2 may play an important role in conferring cisplatin resistance in ESCC. Nrf‐2 appears to be a promising therapeutic target for ESCC.

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“…Another example of miRNA that is described as a direct regulator of SNAIL expression in plenty tumor types is miR-153. The downregulation of SNAIL by miR-153 suppresses human laryngeal squamous cell carcinoma migration and invasion [75], melanoma cells proliferation and invasion [76], esophageal squamous cell carcinoma progression [77], and gastric cancer metastasis [78]; regulates EMT in hepatocellular carcinoma [79]; and diminishes pancreatic ductal adenocarcinoma migration and invasion with miR-153 serving as a prognostic marker [80].…”

Section: Micrornas Directly Targeting Snailmentioning

confidence: 99%

Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

Skrzypek

Majka

2020

Cancers

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SNAIL (SNAI1) is a zinc finger transcription factor that binds to E-box sequences and regulates the expression of genes. It usually acts as a gene repressor, but it may also activate the expression of genes. SNAIL plays a key role in the regulation of epithelial to mesenchymal transition, which is the main mechanism responsible for the progression and metastasis of epithelial tumors. Nevertheless, it also regulates different processes that are responsible for tumor growth, such as the activity of cancer stem cells, the control of cell metabolism, and the regulation of differentiation. Different proteins and microRNAs may regulate the SNAIL level, and SNAIL may be an important regulator of microRNA expression as well. The interplay among SNAIL, microRNAs, long non-coding RNAs, and circular RNAs is a key event in the regulation of tumor growth and metastasis. This review for the first time discusses different types of regulation between SNAIL and non-coding RNAs with a focus on feedback loops and the role of competitive RNA. Understanding these mechanisms may help develop novel therapeutic strategies against cancer based on microRNAs.

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MicroRNA-153-3p suppress cell proliferation and invasion by targeting SNAI1 in melanoma

Cited by 51 publications

References 21 publications

MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

MicroRNA‐153‐3p regulates cell proliferation and cisplatin resistance via Nrf‐2 in esophageal squamous cell carcinoma

Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

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