Long non‐coding
            RNA
            Malat1 promotes neurite outgrowth through activation of
            ERK
            /
            MAPK
            signalling pathway in N2a cells

The regulatory effect of luteolin on the progression of Alzheimer’s disease (AD) remains unclear from the perspective of apoptosis. The present study aimed to investigate the protective effects of luteolin against Aβ25-35-induced cell apoptosis in pheochromocytoma (PC-12) cells. Aβ25-35 was used to induce an in vitro model of AD. Estradiol was used as a positive control. The PC-12 cells were incubated with luteolin alone or in combination with fulvestrant or U0126. The results showed that luteolin treatment significantly prevents Aβ25-35-induced decrease in cell viability and inhibits Aβ25-35-induced cell apoptosis. After the addition of fulvestrant and U0126, the apoptosis rate of PC-12 cells increased significantly. In addition, luteolin treatment significantly upregulated the expression of Bcl-2 and downregulated the expression of Bax and caspase-3, whereas fulvestrant and U0126 partially reversed the effects of luteolin. Moreover, luteolin treatment upregulated the expression of ERβ and p-ERK1/2, whereas fulvestrant blocked the expression of p-ERK1/2. The study showed that luteolin could activate the ER/ERK/MAPK signalling pathway to protect PC-12 cells against Aβ25-35-induced cell apoptosis via selectively acting on ERβ. Thus, luteolin may be considered as a potential novel therapeutic strategy for AD.

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Role of ERK/MAPK signalling pathway in anti-inflammatory effects of Ecklonia cava in activated human mast cell line-1 cells

Asian Pacific Journal of Tropical Medicine ◽

10.1016/s1995-7645(14)60120-6 ◽

2014 ◽

Vol 7 (9) ◽

pp. 703-708 ◽

Cited By ~ 13

Author(s):

Hye Kyung Kim

Keyword(s):

Mast Cell ◽

Cell Line ◽

Signalling Pathway ◽

Ecklonia Cava ◽

Human Mast Cell ◽

Mapk Signalling Pathway ◽

Erk Mapk ◽

Mapk Signalling ◽

Mast Cell Line

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Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway

BMC Cancer ◽

10.1186/s12885-019-6335-4 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 5

Author(s):

Bo Liu ◽

Hongyan Zhao ◽

Lili Zhang ◽

Xuefeng Shi

Keyword(s):

Signalling Pathway ◽

Migration And Invasion ◽

Transfected Cells ◽

Non Coding Rna ◽

Mapk Signalling ◽

U2os Cells ◽

Umr 106 ◽

Long Non Coding Rna ◽

E Cadherin

Abstract Background Osteosarcoma (OS) is a malignancy of the bone that has no clearly identified prognostic factors for diagnosis. In this study, we evaluated the regulatory role of long non-coding RNA (lncRNA) ANCR on the migration and invasion of OS cells as well as the possible mechanism involving the p38MAPK signalling pathway. Methods ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR. It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection. The proliferation of transfected cells was determined using the CCK-8 and the EdU assays. The migration and invasion of transfected cells were determined by the Transwell assay. The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by Western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells. Results ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCR-induced inhibition of cell migration and invasion. Conclusions Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.

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