miR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2

Zhang, Z R; Yang, Nanyan

doi:10.4149/neo_2020_190823n811

Cited by 21 publications

(18 citation statements)

References 27 publications

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“…Low miR-33a-5p level expression was associated with TNM stage and lymph node metastasis in PDAC patients. Consistently, miR-33a-5p was downregulated in colorectal cancer [ 16 ], melanoma [ 26 ] and osteosarcoma [ 14 ]. Decreased miR-33a-5p expression was closely associated with poor prognosis in ESCC [ 15 ].…”

Section: Discussionmentioning

confidence: 93%

Tumor suppressive role of miR-33a-5p in pancreatic ductal adenocarcinoma cells by directly targeting RAP2A

2021

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Background The suppressive effects of miR-33a-5p have been reported in colorectal cancer and lung cancer. However, the functional role of miR-33a-5p in pancreatic ductal adenocarcinoma (PDAC) has not yet been elucidated. Methods The expression of miR-33a-5p was determined using reverse-transcription quantitative PCR (RT-qPCR) in PDAC tissues and cell lines. The association between miR-33a-5p expression and clinical categorical parameters was analyzed by the chi-square test. Cell proliferation was analyzing by Cell Counting Kit -8 (CCK-8) assay. Transwell assay was utilized to assess cell migration and invasion. The interactions between miR-33a-5p and RAP2A were verified by luciferase reporter assay, RT-qPCR, western blot analysis and RNA immunoprecipitation (RIP) assay. Results Here, we observed for the first time that miR-33a-5p expression level was significantly decreased in PDAC tissues and cell lines. There was a significant association between decreased miR-33a-5p expression and TNM stage or lymph node metastasis. Overexpression of miR-33a-5p significantly inhibited SW1990 and PANC-1 cell proliferation, migration and invasion. Knockdown of miR-33a-5p remarkedly promoted cell proliferation, migration and invasion in BxPC-3 and ASPC-1. Mechanistically, RAP2A was confirmed as the target of miR-33a-5p in PDAC cells. Moreover, RAP2A overexpression abolished miR-33a-5p-mediated suppressive effects on SW1990 and PANC-1 cells. Conclusions Taken together, these results suggest that miR-33a-5p exerted tumor suppressive effects on PDAC cells by targeting RAP2A, which might provide a new theoretical basis for the clinical treatment of PDAC.

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Section: Discussionmentioning

confidence: 93%

Tumor suppressive role of miR-33a-5p in pancreatic ductal adenocarcinoma cells by directly targeting RAP2A

2021

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“…As previously reported, the expression of SNAI2 was revealed to share positive association with histopathological grade and survival time of patients with glioma, which was involved with the activation of the PI3K/Akt pathway [ 27 ]. Furthermore, SNAI2-knockdown was also reported to suppress the activation of the PI3K/Akt/mTOR pathway, thereby suppressing the development of melanoma [ 28 ]. Similarly, SLUG could bind to PTEN promoter region to transcriptionally repress PTEN, thereby regulating the PTEN/AKT pathway and thus possibly favoring prostate cancer stem cell progression [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Transcription factor SNAI2 exerts pro-tumorigenic effects on glioma stem cells via PHLPP2-mediated Akt pathway

Peng

Chen

et al. 2022

Cell Death Dis

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The current study aimed to investigate the effects associated with SNAI2 on the proliferation of glioma stem cells (GSCs) to elucidate its underlying molecular mechanism in the development of glioma. The expression of Snail family transcriptional repressor 2 (SNAI2) in glioma tissues was initially predicted via bioinformatics analysis and subsequently confirmed by reverse transcription quantitative polymerase chain reaction (RT-qPCR), which revealed that SNAI2 was highly expressed in glioma tissues as well as GSCs, with an inverse correlation with overall glioma patient survival detected. Loss- and gain- of-function assays were performed to determine the roles of SNAI2 and pleckstrin homology domain and leucine rich repeat protein phosphatase 2 (PHLPP2) on GSC viability, proliferation and apoptosis. Data were obtained indicating that SNAI2 promoted the proliferation of GSCs, while overexpressed PHLPP2 brought about a contrasting trend. As detected by chromatin immunoprecipitation, RT-qPCR and agarose gel electrophoresis, SNAI2 bound to the promoter region of PHLPP2 and repressed the transcription of PHLPP2 while SNAI2 was found to inhibit PHLPP2 resulting in activation of the Akt pathway. Finally, the roles of SNAI2 and PHLPP2 were verified in glioma growth in nude mice xenografted with tumor. Taken together, the key findings of the present study suggest that SNAI2 may promote the proliferation of GSCs through activation of the Akt pathway by downregulating PHLPP2.

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“… 21 MiR-33a-5p represses the metastasis and growth of melanoma cells by modulating the expression of SNAI2. 37 MR-489-3p/SIX1 signaling modulates the glycolytic potential and cell proliferation in melanoma. 38 Moreover, the role of miRNA-145 in the modulation of melanoma has been identified.…”

Section: Discussionmentioning

confidence: 99%

Bergamottin Induces DNA Damage and Inhibits Malignant Progression in Melanoma by Modulating miR-145/Cyclin D1 Axis

Zhao¹,

Liao²

2021

OTT

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Background Melanoma is a prevalent skin cancer with the high rate of metastasis and mortality, affecting the increasing number of people worldwide. Bergamottin (BGM) is a natural furanocoumarin derived from grapefruits and presents the potential anti-cancer activity in several tumor models. However, the role of BGM in the development of melanoma remains unclear. Here, we aimed to explore the effect of BGM on the DNA damage and progression of melanoma. Methods The effect of BGM on the melanoma progression was analyzed by CCK-8 assays, colony formation assays, transwell assays, Annexin V-FITC Apoptosis Detection Kit, cell-cycle analysis, in vivo tumorigenicity analysis. The mechanism investigation was performed using luciferase reporter gene assays, qPCR assays, and Western blot analysis. Results We identified that BGM repressed cell proliferation, migration, and invasion of melanoma cells. BGM induced cell cycle arrest at the G0/G1 phase and enhanced apoptosis of melanoma cells. The DNA damage in the melanoma cells was stimulated by the BGM treatment. Meanwhile, BGM was able to up-regulate the expression of miR-145 and miR-145 targeted Cyclin D1 in the melanoma cells. Furthermore, BGM inhibited the progression of melanoma by targeting miR-145/Cyclin D1 axis in vitro. BGM attenuated the tumor growth of melanoma in vivo. Conclusion Thus, we conclude that BGM induces DNA damage and inhibits tumor progression in melanoma by modulating the miR-145/Cyclin D1 axis. Our finding provides new insights into the mechanism by which BGM modulates the development of melanoma. BGM may be applied as a potential anti-tumor candidate for the clinical treatment of melanoma.

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miR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2

Cited by 21 publications

References 27 publications

Tumor suppressive role of miR-33a-5p in pancreatic ductal adenocarcinoma cells by directly targeting RAP2A

Tumor suppressive role of miR-33a-5p in pancreatic ductal adenocarcinoma cells by directly targeting RAP2A

Transcription factor SNAI2 exerts pro-tumorigenic effects on glioma stem cells via PHLPP2-mediated Akt pathway

Bergamottin Induces DNA Damage and Inhibits Malignant Progression in Melanoma by Modulating miR-145/Cyclin D1 Axis

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