Signaling pathway of MAPK/ERK in cell proliferation, differentiation, migration, senescence and apoptosis

Sun, Yu; Liu, Wenzhou; Liu, Tao; Xu, Feng; Yang, Nuo; Zhou, Hua-Fu

doi:10.3109/10799893.2015.1030412

Cited by 1,423 publications

(991 citation statements)

References 71 publications

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“…Components within the MAPK, ERK and JNK signaling pathways, including insulin, glucocorticoid, hyperbaric oxygen and fibroblast growth factor-6, have been identified as major promoters of osteoblast proliferation in a number of studies (41)(42)(43). Song et al (44) demonstrated that icariin, a flavonoid glucoside isolated from P. corylifolia, promoted MC3T3-E1 osteoblast proliferation by inducing the activation of ERK and JNK, but exerted no effect on the activity of p38 kinase.…”

Section: Discussionmentioning

confidence: 99%

Psoralen stimulates osteoblast proliferation through the activation of nuclear factor-κB-mitogen-activated protein kinase signaling

Feimeng

Huang³

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Osteoporosis is a systemic skeletal disease that leads to increased bone fragility and susceptibility to fracture. Approximately 50% of postmenopausal women develop osteoporosis as a result of postmenopausal estrogen deficiency. To reduce fractures related to osteoporosis in women, previous studies have focused on therapeutic strategies that aim to increase bone formation or decrease bone resorption. However, pharmacological agents that aim to improve bone fracture susceptibility exhibit side effects. Current studies are investigating natural alternatives that possess the benefits of selective estrogen receptor modulators (SERMs) without the adverse effects. Recent studies have indicated that phytoestrogen may be an ideal natural SERM for the treatment of osteoporosis. In Chinese herbal medicine, psoralen, as the predominant substance of Psoralea corylifolia, is considered to be a phytoestrogen and is used as a remedy for osteoporosis. A number of studies have demonstrated the efficacy of psoralen in bone formation. However, the pathways and underlying molecular mechanisms that participate in psoralen-induced osteoblast formation are not well understood. In the present study, hFOB1.19 cells were treated with psoralen at different concentrations (0, 5, 10, 15 and 20 µM) for 0, 24, 36, 48 and 72 h, respectively. Reverse transcription-quantitative polymerase chain reaction and western blot assays were performed to detect glucose transporter 3 (GLUT3) expression. A cell counting kit-8 assay was used to analyze cell proliferation. In addition the effects of mitogen activated protein kinase inhibitors on extracellular signal-regulated kinase (ERK), phosphorylated (p)-ERK, p38, p-p38, c-Jun N-terminal kinase (JNK) and p-JNK expressions and cell proliferation were measured, as was the effect of nuclear factor (NF)-κB inhibitor on P65 and GLUT3 expressions and cell proliferation. The results indicated that psoralen stimulates hFOB1.19 cell proliferation in a dose-dependent manner (P<0.05). Phospho-ERK, p38 and JNK were markedly increased by psoralen compared with the control group (P<0.05), and the specific inhibitors of ERK (SCH772984), p38 (SB203580) and JNK (SP600125) reversed the stimulatory effects of psoralen on signal marker phosphorylation (P<0.05). The rate of psoralen-induced cell proliferation was significantly suppressed by inhibitors of ERK, JNK and p38 compared with psoralen treatment alone (P<0.05). In addition, psoralen stimulated osteoblast proliferation via the NF-κB signaling pathway. Therefore, the present findings suggest that psoralen may be a potential natural alternative to SERMs in the treatment of osteoporosis and fractures.

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Section: Discussionmentioning

confidence: 99%

Psoralen stimulates osteoblast proliferation through the activation of nuclear factor-κB-mitogen-activated protein kinase signaling

Feimeng

Huang³

et al. 2017

Experimental and Therapeutic Medicine

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“…MAPK signaling pathway is reported to be associated with the cell proliferation, differentiation, migration, senescence, and apoptosis, including ERK1/2 and JNK. 28 For example, it has been reported that curcumin suppresses proliferation and migration and induces apoptosis on human placental choriocarcinoma cells via ERK1/2 and stress-activated protein kinase (SAPK)/JNK MAPK signaling pathways. 29 Vitexin suppresses autophagy to induce apoptosis in hepatocellular carcinoma via activation of the JNK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

The role of epithelial cell adhesion molecule N-glycosylation on apoptosis in breast cancer cells

Zhang

Gao

et al. 2017

Tumour Biol.

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Glycosylation of cell surface proteins plays an important role in the regulation of apoptosis. It has been demonstrated that knockdown of epithelial cell adhesion molecule promoted apoptosis, inhibited cell proliferation, and caused cell-cycle arrest. In this study, we investigated whether and how N-glycosylation of epithelial cell adhesion molecule influenced the apoptosis in breast cancer cells. We applied the N-glycosylation mutation epithelial cell adhesion molecule plasmid to express deglycosylation of epithelial cell adhesion molecule and then to study its function. Our results showed that deglycosylation of epithelial cell adhesion molecule promoted apoptosis and inhibited cell proliferation. Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. These findings are important for a better understanding of epithelial cell adhesion molecule apoptosis regulation and suggest epithelial cell adhesion molecule as a potential target for the treatment of breast cancer.

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“…Activation of the MAPK signaling pathway is known to cause the transformation of normal cells to tumor phenotype (6). Thus, inhibition of this pathway may enable restoration of the tumor cells to the untransformed phenotype in vitro, thereby inhibiting the growth of the tumor in the body (50,51).…”

Section: Regulation Of the Mapk Signaling Pathway For Targeted Oral Cmentioning

confidence: 99%

“…Multiple signaling pathways may function in oncogenesis and in the growth of oral malignancies (4,5). Among these is the mitogen activated protein kinase (MAPK) signaling pathway, which regulates the expression of a large number of proteins involved in the control of cell proliferation, differentiation and apoptosis (6,7), and remains a focus of investigation for therapeutic targeting, along with the development of appropriate inhibitors (8). These inhibitors have been demonstrated to be effective for the treatment of oral cancer and other malignancies, including human colon cancer, breast cancer and lung cancer (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

et al. 2017

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Abstract. The mitogen-activated protein kinase (MAPK) signaling pathway is associated with tumor cell proliferation, differentiation, apoptosis, angiogenesis, invasion and metastasis. The present review assesses the involvement of the MAPK signaling pathway in oral cancer progression and invasion based on analysis of individual sub-pathways and their mechanisms of action. The regulation of this pathway for targeted oral cancer therapy is explored and the challenges confronting this, as well as corresponding potential solutions, are discussed. Exploring this pathway with an emphasis on its components, subfamilies, sub-pathways, interactions with other pathways and clinical practice modes may improve oral cancer treatment.

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Signaling pathway of MAPK/ERK in cell proliferation, differentiation, migration, senescence and apoptosis

Cited by 1,423 publications

References 71 publications

Psoralen stimulates osteoblast proliferation through the activation of nuclear factor-κB-mitogen-activated protein kinase signaling

Psoralen stimulates osteoblast proliferation through the activation of nuclear factor-κB-mitogen-activated protein kinase signaling

The role of epithelial cell adhesion molecule N-glycosylation on apoptosis in breast cancer cells

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

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