HnRNPK/miR-223/FBXW7 feedback cascade promotes pancreatic cancer cell growth and invasion

He, Deyan; Huang, Cheng; Zhou, Qingxin; Liu, Dawei; Xiong, Longhui; Xiang, Hongxia; Ma, Guangnian; Zhang, Zhiyong

doi:10.18632/oncotarget.15529

Cited by 29 publications

(32 citation statements)

References 28 publications

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“…It is well known that miRNAs can regulate cell proliferation, invasion and metastasis by altering the expression of tumor suppressor genes or the oncogenes, thus contributing to the initiation and development of human tumors. miR-223-3p has been characterized as a oncogene in multiple tumors, such as pancreatic cancer, prostate cancer, ovarian cancer, lung cancer and gastric cancer, by targeting different genes, such as FBXW7, SEPT6, SOX11, EPB41L3 35 – 38 . In our study, we verified the oncogenic role of miR-223-3p in gastric cancer, which is consistent with the results from Ma et al 33 Importantly, we found that the miR-223-3p inhibitor reversed CagA-mediated promotion of cell proliferation and migration.…”

Section: Discussionmentioning

confidence: 99%

NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression

Yang

Liu

et al. 2018

Cell Death Dis

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Infection with Helicobacter pylori (H. pylori) and the resulting gastric inflammation is regarded as the strongest risk factor for gastric carcinogenesis and progression. NF-κB plays an important role in linking H. pylori-mediated inflammation to cancer. However, the underlying mechanisms are poorly understood. In this study, we find that H. pylori infection induces miR-223-3p expression in H. pylori CagA-dependent manner. NF-κB stimulates miR-223-3p expression via directly binding to the promoter of miR-223-3p and is required for H. pylori CagA-mediated upregulation of miR-223-3p. miR-223-3p promotes the proliferation and migration of gastric cancer cells by directly targeting ARID1A and decreasing its expression. Furthermore, miR-223-3p/ARID1A axis is involved in CagA-induced cell proliferation and migration. In the clinical setting, the level of miR-223-3p is upregulated, while ARID1A is downregulated significantly in human gastric cancer tissues compared with the corresponding noncancerous tissues. The expression level of miR-223-3p is significantly higher in H. pylori-positive gastric cancer tissues than that in H. pylori-negative tissues. Moreover, a negative correlation between miR-223-3p and ARID1A expression is found in the gastric cancer tissues. Taken together, our findings suggested NF-κB/miR-223-3p/ARID1A axis may link the process of H. pylori-induced chronic inflammation to gastric cancer, thereby providing a new insight into the mechanism underlying H. pylori-associated gastric diseases.

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Section: Discussionmentioning

confidence: 99%

NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression

Yang

Liu

et al. 2018

Cell Death Dis

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“…miRNA-223 is a haematopoietic cell-specific miRNA, and recent studies have shown that miR-223 is almost exclusively expressed in myeloid cell lineage. 31 miR-223 has a wide range of targeted inhibitory effects, including RHOB, 40 FBXW7, 41 FOXO 42 and other important disease targets. In vitro , NLRP3 has been shown to be inhibited by miR-223 37 and has received widespread attention.…”

Section: Discussionmentioning

confidence: 99%

Ly6G+ neutrophil-derived miR-223 inhibits the NLRP3 inflammasome in mitochondrial DAMP-induced acute lung injury

Feng

Zhang

et al. 2017

Cell Death Dis

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MicroRNA (miRNA) mediates RNA interference to regulate a variety of innate immune processes, but how miRNAs coordinate the mechanisms underlying acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in patients with pulmonary inflammatory injury is still unknown. In this study, we demonstrated that miR-223 limits the number of Ly6G+ neutrophils and inhibits the activity of the NLRP3 inflammasome to alleviate ALI induced by mitochondrial damage-associated molecular patterns (DAMPs) (MTDs). miR-223 expression is increased in the lungs of MTD-induced mice or ARDS patients following trauma/transfusion or following the physiological remission of ALI/ARDS. miR-223−/+ mice exhibited more severe ALI and cytokine dysregulation. Other studies have shown that MTD-induced increases in miR-223 expression are mainly contributed by Ly6G+ neutrophils from the haematopoietic system. miR-223 blocks bone marrow-derived Ly6G+ neutrophil differentiation and inhibits peripheral cytokine release. In addition, MTD-induced miR-223 expression activates a negative feedback pathway that targets the inhibition of NLRP3 expression and IL-1β release; therefore, miR-223 deficiency can lead to the sustained activation of NLRP3-IL-1β. Finally, elimination of peripheral Ly6G+ neutrophils and pharmacological blockade of the miR-223–NLRP3–IL-1β signalling axis could alleviate MTD-induced ALI. In summary, miR-223 is essential for regulating the pathogenesis of DAMP-induced ALI.

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“…In gastric carcinoma, inhibition of miR-25 induces cell apoptosis through up-regulation of FBXW7 and down-regulation of FBXW7 substrates, such as cyclin E and c-Myc [ 129 ]. Additionally, miR-223 is significantly up-regulated in gastric cancer, pancreatic ductal adenocarcinoma, and ESCC [ 130 – 132 ]. ESCC tissues having lower FBXW7 and higher miR-223 expression show poorer overall survival and lower 5-year survival [ 131 ].…”

Section: Clinical Significance Of Fbxw7 Loss Of Function In Human Canmentioning

confidence: 99%

FBXW7: a critical tumor suppressor of human cancers

2018

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The ubiquitin-proteasome system (UPS) is involved in multiple aspects of cellular processes, such as cell cycle progression, cellular differentiation, and survival (Davis RJ et al., Cancer Cell 26:455-64, 2014; Skaar JR et al., Nat Rev Drug Discov 13:889-903, 2014; Nakayama KI and Nakayama K, Nat Rev Cancer 6:369-81, 2006). F-box and WD repeat domain containing 7 (FBXW7), also known as Sel10, hCDC4 or hAgo, is a member of the F-box protein family, which functions as the substrate recognition component of the SCF E3 ubiquitin ligase. FBXW7 is a critical tumor suppressor and one of the most commonly deregulated ubiquitin-proteasome system proteins in human cancer. FBXW7 controls proteasome-mediated degradation of oncoproteins such as cyclin E, c-Myc, Mcl-1, mTOR, Jun, Notch and AURKA. Consistent with the tumor suppressor role of FBXW7, it is located at chromosome 4q32, a genomic region deleted in more than 30% of all human cancers (Spruck CH et al., Cancer Res 62:4535-9, 2002). Genetic profiles of human cancers based on high-throughput sequencing have revealed that FBXW7 is frequently mutated in human cancers. In addition to genetic mutations, other mechanisms involving microRNA, long non-coding RNA, and specific oncogenic signaling pathways can inactivate FBXW7 functions in cancer cells. In the following sections, we will discuss the regulation of FBXW7, its role in oncogenesis, and the clinical implications and prognostic value of loss of function of FBXW7 in human cancers.

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HnRNPK/miR-223/FBXW7 feedback cascade promotes pancreatic cancer cell growth and invasion

Cited by 29 publications

References 28 publications

NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression

NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression

Ly6G+ neutrophil-derived miR-223 inhibits the NLRP3 inflammasome in mitochondrial DAMP-induced acute lung injury

FBXW7: a critical tumor suppressor of human cancers

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