miR-337 can be a key negative regulator in melanoma

Xiao, Wan'an; Yao, Enyang; Zheng, Wei; Tian, Feng; Tian, Lijie

doi:10.1080/15384047.2017.1323581

Cited by 11 publications

(8 citation statements)

References 31 publications

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“…In this study, it was found that the expression of miR-337 was downregulated in pancreatic cancer tissues and pancreatic cancer cells, which was consistent with another research that miR-337 expression was suppressed in pancreatic cancer tissues [11]. MiR-337 has been reported to exert an inhibitory effect on some tumors such as melanoma and cervical cancer [15,20]. We further investigated the influence of miR-337 on pancreatic cancer cells.…”

Section: Discussionsupporting

confidence: 90%

MiR-337 suppresses pancreatic cancer development via STAT3/Wnt/β-catenin axis

Shi

Han³

et al. 2021

Anti-Cancer Drugs

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MiRNA is an important regulator of tumorigenesis and tumor progression. MiR-337 expression was increased in pancreatic cancer tissues and it was associated with patients' survival. This study aimed to explore the influence and the potential working mechanism of miR-337 on the malignant behaviors of pancreatic cancer cells. MiR-337 expression was detected by qRT-PCR. The expression levels of STAT3, epithelial-mesenchymal transition-related genes and Wnt/β-Catenin pathway genes were evaluated by qRT-PCR and western blot. Cell counting kit -8 and colony formation assays were conducted to examine the proliferation of AsPC-1 and SW1990 cells. Wound healing and transwell assays were performed to determine the migration and invasion of AsPC-1 and SW1990 cells. The predicted target gene of miR-337 was verified by luciferase reporter assay. The expression of miR-337 was decreased and STAT3 expression was increased in pancreatic cancer tissues as well as tumor cells. Overexpression of miR-337 suppressed proliferation, invasion and migration of AsPC-1 and SW1990 cells. MiR-337 targeted 3′UTR of STAT3 and inhibited STAT3 expression. In addition, exogenous STAT3 partially restored the inhibitory role of miR-337 on proliferation, invasion and migration of AsPC-1 and SW1990 cells. Moreover, miR-337 impeded the expression of Wnt/β-catenin pathway-related genes. Through the saving experiment, we found that the inhibitory effect of miR-337 on AsPC-1 and SW1990 cells was abolished by the addition of LiCl. These outcomes expounded that miR-337 inactivated the Wnt/β-catenin pathway to suppress the malignant behaviors of pancreatic cancer cells through targeting STAT3. This study may provide a novel biomarker for diagnosis and a new therapeutic target for pancreatic cancer treatment.

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Section: Discussionsupporting

confidence: 90%

MiR-337 suppresses pancreatic cancer development via STAT3/Wnt/β-catenin axis

Shi

Han³

et al. 2021

Anti-Cancer Drugs

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“…MicroRNAs (miRNAs) are non‐coding short RNAs that regulate gene expression and negatively impact the stability and translation of mRNAs by binding to complementary sequences at 3′ untranslated region (3′UTR) 10 . It was reported that miR‐137 acted as a tumour repressor in malignant melanoma, 11 and miR‐337 was demonstrated to be a vital negative regulator in melanoma 12 . As one of the miRNAs, miR‐495‐3p was involved in the development of melanoma.…”

Section: Introductionmentioning

confidence: 99%

Down‐regulated HDAC3 elevates microRNA‐495‐3p to restrain epithelial‐mesenchymal transition and oncogenicity of melanoma cells via reducing TRAF5

Duan

Hao

2020

J Cellular Molecular Medi

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MicroRNAs (miRNAs) are emerging biomarkers in biological processes and the role of miR‐495‐3p has been identified in melanoma, while the detailed molecular mechanisms remain to be further explored. We aim to explore the effect of histone deacetylase 3 (HDAC3) and miR‐495‐3p on epithelial‐mesenchymal transition (EMT) and oncogenicity of melanoma cells by regulating tumour necrosis factor receptor‐associated factor 5 (TRAF5). Levels of HDAC3, miR‐495‐3p and TRAF5 in melanoma tissues and pigmented nevus tissues were determined, and the predictive roles of HDAC3 and miR‐495‐3p in prognosis of melanoma patients were measured. The melanoma cells were screened and transfected with relative oligonucleotides and plasmids, and the expression of HDAC3, miR‐495‐3p and TRAF5, and phenotypes of melanoma cells were gauged by a series of assays. The relations between HDAC3 and miR‐495‐3p, and between miR‐495‐3p and TRAF5 were confirmed. HDAC3 and TRAF5 were increased while miR‐495‐3p was decreased in melanoma cells and tissues, and the low expression of miR‐495‐3p as well as high expression of HDAC3 indicated a poor prognosis of melanoma patients. Inhibited HDAC3 elevated miR‐495‐3p to suppress EMT and oncogenicity of melanoma cells by reducing TRAF5. HDAC3 particularly bound to miR‐495‐3p and TRAF5 was the target gene of miR‐495‐3p. Our results revealed that down‐regulated HDAC3 elevates miR‐495‐3p to suppress malignant phenotypes of melanoma cells by inhibiting TRAF5, thereby repressing EMT progression of melanoma cells. This study may provide novel targets for melanoma treatment.

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“…STAT3 expression has been related to tumor metastasis and cellular apoptosis in various cancers mediated by miR-337 [7,9,12]. Therefore, we determined the effect of miR-337 expression on STAT3 in CTCL cells.…”

Section: Mir-337 Targeted the 3′-untranslated Region (Utr) Of Stat3mentioning

confidence: 99%

“…Studies have demonstrated the downregulation of miR-337 expression in many cancers [7][8][9][10][11][12]. Notably, miR-337 has been reported to mediate the expression of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) in non-small cell lung cancer, melanoma, and hepatocellular carcinoma cells [7,9,12].…”

Section: Introductionmentioning

confidence: 99%

miR-337 suppresses cutaneous T-cell lymphoma via the STAT3 pathway

Xia

et al. 2019

Cell Cycle

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Cutaneous T-cell lymphoma (CTCL) is associated with the downregulation of miR-337 expression, although the exact underlying mechanism is unknown. In the present work, we investigated the molecular mechanism and function of miR-337 in regulating CTCL cell viability and invasion. We observed that miR-337 expression was downregulated in both CTCL tumors and cell lines. Furthermore, CCK assay, BrdU incorporation assay, and flow cytometry revealed that transfection with the miR-337 mimic resulted in decreased proliferation and increased apoptotic levels in CTCL cells. Results of the Transwell migration assay indicated that the miR-337 mimic decreased CTCL cell invasion in vitro. Both bioinformatics prediction and the dual-luciferase reporter assay revealed that miR-337 targets the 3′-UTR of STAT3 for silencing. Overexpression of STAT3 counteracted the pro-apoptotic influence of miR-337 in CTCL cell lines and restored their invasion properties. The results thus indicate that the miR-337-STAT3 axis inhibits the proliferation of malignant T cells and that miR-337 may serve as a promising therapeutic target for CTCL.

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miR-337 can be a key negative regulator in melanoma

Cited by 11 publications

References 31 publications

MiR-337 suppresses pancreatic cancer development via STAT3/Wnt/β-catenin axis

MiR-337 suppresses pancreatic cancer development via STAT3/Wnt/β-catenin axis

Down‐regulated HDAC3 elevates microRNA‐495‐3p to restrain epithelial‐mesenchymal transition and oncogenicity of melanoma cells via reducing TRAF5

miR-337 suppresses cutaneous T-cell lymphoma via the STAT3 pathway

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