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Upregulation of miRNA?301a?3p promotes tumor progression in gastric cancer by suppressing NKRF and activating NF??B signaling.

ABSTRACT: MicroRNA?301a (miRNA/miR?301a) and nuclear factor (NF)??B signaling play important roles in tumor invasion, migration and progression. However, the role of miRNA?301a?3p in human gastric cancer (GC), and specifically in the activation of NF??B signaling, remains unclear. The aim of the present study was to investigate miRNA?301a?3p expression in GC progression and the molecular mechanisms as regards the regulation of NF??B signaling. Reverse transcription?quantitative polymerase chain reaction (RT?qPCR) was used to detect miRNA?301a?3p expression in GC and paired normal tissues. The association between the expression of miRNA?301a?3p and patient pathological parameters and the prognosis of GC was statistically analyzed using an in situ hybridization (ISH) assay. An MTS assay and a Transwell assay were performed to evaluate the effects of miRNA?301a?3p on the proliferation, invasion and migration of GC cells. RT?qPCR and western blot analysis were used to analyze the association between miRNA?301a?3p and nuclear factor??B repressing factor (NKRF) expression and the corresponding downstream NF??B signaling molecules. A luciferase assay was used to verify the target effect of miRNA?301a?3p and NKRF. It was found that miRNA?301a?3p expression was significantly higher in 30 cases of primary GC compared with matched normal tissues. Additionally, the ISH assay indicated that the high expression of miRNA?301a?3p in GC was associated with tumor invasion depth, lymph node metastasis, lymph node invasion and tumor metastasis stage. Patients whose tumors had a higher miRNA?301a?3p expression level exhibited a poorer prognosis. The in vitro assay indicated that miRNA?301a?3p affected the proliferative and invasive ability of GC cells by targeting the expression of NKRF, which then affected NF??B signaling. Therefore, it was hypothesize that miRNA?301a?3p promotes GC progression and affects the prognosis of patients with GC by targeting NKRF, which in turn, directly influences NF??B activation.

SUBMITTER: Xu X

PROVIDER: S-EPMC7307585 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Upregulation of miRNA‑301a‑3p promotes tumor progression in gastric cancer by suppressing NKRF and activating NF‑κB signaling.

Xu Xiaodong X Xia Yingjie Y Ma Jie J Li Weijun W Niu Nan N Li Xiao X Tao Houquan H Xu Ji J He Xujun X

International journal of oncology 20200526 2

MicroRNA‑301a (miRNA/miR‑301a) and nuclear factor (NF)‑κB signaling play important roles in tumor invasion, migration and progression. However, the role of miRNA‑301a‑3p in human gastric cancer (GC), and specifically in the activation of NF‑κB signaling, remains unclear. The aim of the present study was to investigate miRNA‑301a‑3p expression in GC progression and the molecular mechanisms as regards the regulation of NF‑κB signaling. Reverse transcription‑quantitative polymerase chain reaction ( ...[more]

PMID: 32468020

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Project description:Brain damage following cerebral ischemia-reperfusion (I/R) is a complicated pathophysiological course, in which inflammation and oxidative stress have been suggested to serve an important role. Toll-like receptor 4 (TLR4) has been suggested to be involved in secondary inflammatory process in cerebral ischemia. Nuclear factor erythroid 2-related factor 2 (Nrf2), an important regulator of the antioxidant host defense, maintains the cellular redox homeostasis. Tissue kallikrein (TK) has been proven to elicit a variety of biological effects in ischemic stroke through its anti-inflammatory and anti-oxidant properties. However, the mechanisms underlying its beneficial effects remain poorly defined. The present study examined the hypothesis that TK attenuates ischemic cerebral injury via the TLR4/nuclear factor-κB (NF-κB) and Nrf2 signaling pathways. Using a transient rat middle cerebral artery occlusion (MCAO) model, the effects of immediate and delayed TK treatment subsequent to reperfusion were investigated. The neurological deficits, infarct size, and the expression of TLR4/NF-κB and Nrf2 pathway in ischemic brain tissues were measured at 24 following MCAO. The results indicated that TK immediate treatment significantly improved neurological deficits and reduced the infarct size, accompanied by the inhibition of TLR4 and NF-κB levels, and the activation of Nrf2 pathway. Furthermore, TK delayed treatment also exerted neuroprotection against I/R injury. However, the neuroprotective effect of TK immediate treatment was better compared with that of TK delayed treatment. In conclusion, the results indicated that TK protected the brain against ischemic injury in rats after MCAO through its anti-oxidative and anti-inflammatory effects. Suppression of TLR4/NF-κB and activation of the Nrf2 pathway contributed to the neuroprotective effects induced by TK in cerebral ischemia. Therefore, TK may provide an effective intervention with a wider therapeutic window for ischemic stroke.

Dataset Information

Upregulation of miRNA?301a?3p promotes tumor progression in gastric cancer by suppressing NKRF and activating NF??B signaling.

Publications

Upregulation of miRNA‑301a‑3p promotes tumor progression in gastric cancer by suppressing NKRF and activating NF‑κB signaling.

Similar Datasets

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