MiR-377 inhibits the proliferation of pancreatic cancer by targeting Pim-3

Chang, Weijie; Liu, Menggang; Xu, Jianhua; Fu, Hangwei; Zhou, Bo; Yuan, Tao; Chen, Ping

doi:10.1007/s13277-016-5295-4

Cited by 40 publications

(33 citation statements)

References 45 publications

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“…3,6 MicroRNAs (miRs) have been found to be promising regulators of gene expression in various biological and pathologic processes of tumors, including carcinogenesis, tumor growth, tumor differentiation, carcinoma metastasis, cancer apoptosis, and epithelial-mesenchymal transition (EMT). 7,8 Evidence has demonstrated that miRs act as either tumor suppressors or oncogenes by interfering in the basepairing with target mRNA and altering various signaling pathways associated with the disease. 9 MiR-300, a member of the miRNA family, localizes in the Dlk1-Dio3 microRNA cluster, region 14q32.31.…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐300 promotes apoptosis and inhibits proliferation, migration, invasion and epithelial‐mesenchymal transition via the Wnt/β‐catenin signaling pathway by targeting CUL4B in pancreatic cancer cells

Zhang

Chen

et al. 2017

J of Cellular Biochemistry

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The study aims to verify the hypothesis that up-regulation of microRNA-300 (miR-300) targeting CUL4B promotes apoptosis and suppresses proliferation, migration, invasion, and epithelialmesenchymal transition (EMT) of pancreatic cancer cells by regulating the Wnt/β-catenin signaling pathway. Pancreatic cancer tissues and adjacent tissues were collected from 110 pancreatic cancer patients. Expression of miR-300, CUL4B, Wnt, β-catenin, E-cadherin, N-cadherin, Snail, GSK-3β, and CyclinD1 were detected using qRT-PCR and Western blot. CFPAC-1, Capan-1, and PANC-1 were classified into blank, negative control (NC), miR-300 mimics, miR-300 inhibitors, siRNA-CUL4B, and miR-300 inhibitors + siRNA-CUL4B groups. The proliferation, migration, invasion abilities, the cell cycle distribution, and apoptosis rates were measured in CCK-8 and Transwell assays. Pancreatic cancer tissues showed increased CUL4B expression but decreased miR-300 expression. When miR-300 was lowly expressed, CUL4B was upregulated which in-turn activated the Wnt/β-catenin pathway to protect the β-catenin expression and thus induce EMT. When miR-300 was highly expressed, CUL4B was downregulated which in-turn inhibited the Wnt/β-catenin pathway to prevent EMT. Weakened cell migration and invasion abilities and enhanced apoptosis were observed in the CUL4B group. The miR-300 inhibitors group exhibited an evident increase in growth rate accompanied the largest tumor volume. Smaller tumor volume and slower growth rate were observed in the miR-300 mimics and siRNA-CUL4B group. Our study concludes that lowly expressed miR-300 may contribute to highly expressed CUL4B activating the Wnt/β-catenin signaling pathway and further stimulating EMT, thus promoting proliferation and migration but suppressing apoptosis of pancreatic cancer cells. K E Y W O R D SCUL4B, epithelial-mesenchymal transition, invasion, microRNA-300, migration, pancreatic cancer, Wnt/β-catenin signaling pathway

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Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐300 promotes apoptosis and inhibits proliferation, migration, invasion and epithelial‐mesenchymal transition via the Wnt/β‐catenin signaling pathway by targeting CUL4B in pancreatic cancer cells

Zhang

Chen

et al. 2017

J of Cellular Biochemistry

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“…Accumulating evidence shows that miRNA are involved in tumorigenesis and metastasis of various human cancers, including HPAC . Furthermore, miRNA have been implicated to function as both tumorigenic or tumor‐suppressing genes .…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence shows that miRNA are involved in tumorigenesis and metastasis of various human cancers, including HPAC. (21)(22)(23) Furthermore, miRNA have been implicated to function as both tumorigenic or tumor-suppressing genes. (11) The overexpression of miR-372 in some cancers (24,25) has been reported to play an oncogenic role.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of ULK1 by microRNA‐372 inhibits the survival of human pancreatic adenocarcinoma cells

Chen

Zhang

et al. 2017

Cancer Science

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Dysregulation of microRNA (miRNA) expression in various cancers and their role in cancer progression is well documented. The purpose of this study was to investigate the biological role of miR‐372 in human pancreatic adenocarcinoma (HPAC). We collected 20 pairs of HPAC tissues and adjacent non‐cancerous tissues to detect miR‐372 expression levels. We transfected BXPC‐3 and PANC‐1 cells with miR‐372 inhibitor/mimics to study their effect on cell proliferation, apoptosis, invasion, migration and autophagy. In addition, miR‐372 mimics and a tumor protein UNC51‐like kinase 1 (ULK1) siRNA were co‐transfected into BXPC‐3 and PANC‐1 cells to explore the mechanism of miR‐372 and ULK1 on HPAC tumorigenesis. We found that the expression of miR‐372 was markedly downregulated in HPAC cells compared to adjacent normal tissues. Furthermore, functional assays showed that miR‐372 inhibited cell proliferation, invasion, migration and autophagy in BXPC‐3 and PANC‐1 cells. An inverse correlation between miR‐372 expression and ULK1 expression was observed in HPAC tissues. Downregulation of ULK1 inhibited the overexpression effects of miR‐372, and upregulation of ULK1 reversed the effects of overexpressed miR‐372. Finally, we found that silencing ULK1 or inhibiting autophagy partly rescued the effects of miR‐372 knockdown in HPAC cells, which may explain the influence of miR‐372/ULK1 in HPAC development. Taken together, these results revealed a significant role of the miR‐372/ULK1 axis in suppressing HPAC cell proliferation, migration, invasion and autophagy.

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“…Two miRNAs (miR-374a-3p, miR-340-5p) have yet to be associated with pancreatic cancer but involved in other types of cancer [20,21]. Furthermore, of the top 10 miRNAs down-regulated in spheroids, five miRNAs (miR-486-3p, miR-134-5p, miR-320a, miR-127-3p, and miR-377-3p) have been reported previously to be related to pancreatic cancer, and three of them were found playing an important role in drug resistance (miR320a) [22], cell proliferation (miR-377-3p) [23], or as a tumor suppressor (miR-127-3p) [24],while the other two miRNAs had no further study yet. Four miRNAs, miR-370-3p, miR-185-5p, miR-193a-5p and miR-378a-3p were all associated with chemoresistance and involved in other types of cancer [25][26][27][28].…”

Section: Panc-1 Spheroid Cells Have Higher Tumorigenic Potential In Vivomentioning

confidence: 97%

Transcriptome Profiling of Panc-1 Spheroid Cells with Pancreatic Cancer Stem Cells Properties Cultured by a Novel 3D Semi-Solid System

Yang¹,

Zhang²,

Tang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Pancreatic cancer remains one of the deadliest human malignancies, the lethality of which may be attributed to the presence of pancreatic cancer stem cells (PCSCs), a small subpopulation of cells existing within pancreatic tumor with high carcinogenesis. Therefore, it is crucial to establish an efficient enrichment and culture system of PCSCs and identify the key genes involved in the regulation of PCSCs. The three-dimensional (3D) liquid suspension mammosphere culture system has been established for enrichment and culture of PCSCs in vitro as the cell spheres are likely to originate from individual cell clone, but it has been challenged because the cell spheroids could be a result of cell aggregation. Methods: We optimized the existing culture system by adding methylcellulose to create a 3D semi-solid system which prevented the non-specific aggregation. Then we identified the CSC properties of Panc-1 spheroid cells cultured by this system by detecting the genes associated with stemness and by evaluation of the tumorigenicity in vitro and in vivo through invasion, migration and xenograft experiments methods. Subsequently, we performed high-throughput sequencing (HTS) of the Panc-1 spheroid cells. Results: We confirmed the PCSCs properties and high malignancy of the Panc-1 spheroid cells enriched by our novel 3D semi-solid system both in vitro and in vivo. Hundreds of mRNA, microRNA (miRNA) and dozens of long non-coding RNA (LncRNA) were identified to be differentially regulated in PCSCs-like Panc-1 spheroid cells compared with their parental cells by HTS. Conclusions: Our results demonstrate an efficient enrichment and culture system for Panc-1 spheroid cells with the PCSCs properties. The differentially expressed genes and their targets identified by the HTS of the Panc-1 spheroid cells can serve as new potential biomarkers for pancreatic cancer diagnosis and targeted therapy.

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MiR-377 inhibits the proliferation of pancreatic cancer by targeting Pim-3

Cited by 40 publications

References 45 publications

Retracted: MicroRNA‐300 promotes apoptosis and inhibits proliferation, migration, invasion and epithelial‐mesenchymal transition via the Wnt/β‐catenin signaling pathway by targeting CUL4B in pancreatic cancer cells

Retracted: MicroRNA‐300 promotes apoptosis and inhibits proliferation, migration, invasion and epithelial‐mesenchymal transition via the Wnt/β‐catenin signaling pathway by targeting CUL4B in pancreatic cancer cells

Downregulation of ULK1 by microRNA‐372 inhibits the survival of human pancreatic adenocarcinoma cells

Transcriptome Profiling of Panc-1 Spheroid Cells with Pancreatic Cancer Stem Cells Properties Cultured by a Novel 3D Semi-Solid System

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