The expression and activation of ERK/MAPK pathway in human esophageal cancer cell line EC9706

Huo, Qi; Tuerxun, Aerziguli; Ma, Wu; Lv, Guo-dong; Huang, Chongmei; Liu, Qing; Wang, Xing; Lin, Renyong; Sheyhidin, Ilyar; Lü, Xiaomei

doi:10.1007/s11033-010-0178-z

Cited by 14 publications

(7 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, ERK, a widely expressed signaling molecular, is pivotal for cellular proliferation, differentiation and survival in various cells, including EPCs [ 30 – 32 ], which can be activated during cell angiogensis induced by Toll-like receptor 2 in endothelial cells [ 33 ]. Our data demonstrated that phosphorylated ERK expression in EOCs from CAD patients was significantly lower compared with healthy subjects, and upregulation of CXCR7 by gene transfer can reverse the decreased phosphorylated ERK level in EOCs from CAD patients, indicating that ERK was the downstream signaling of CXCR7 pathway in EOCs.…”

Section: Discussionmentioning

confidence: 99%

CXCR7/p-ERK-Signaling Is a Novel Target for Therapeutic Vasculogenesis in Patients with Coronary Artery Disease

et al. 2016

View full text Add to dashboard Cite

Coronary artery disease (CAD) is characterized by insufficient vasculogenic response to ischemia, which is typically accompanied by dysfunction of endothelial outgrowth cells (EOCs). CXC chemokine receptor 7 (CXCR7) is a key modulator of the neovascularization of EOCs to perfusion defect area. However, the mechanism underlying the role of EOCs in CAD-related abnormal vasculogenesis is still not clear. Here, we investigated the alteration of EOCs-related vasculogenic capacity in patients with CAD and its potential mechanism. Compared with EOCs isolated from healthy subjects, EOCs from CAD patients showed an impaired vasculogenic function in vitro. CXCR7 expression of EOCs from CAD patients was downregulated. Meanwhile, the phosphorylation of extracellular signal-regulated kinase (ERK), downstream of CXCR7 signaling, was also reduced. CXCR7 expression introduced by adenovirus increased the phosphorylation of ERK, which was parallel to improved function of EOCs. The enhanced adhesion and vasculogenesis of EOCs can be blocked by short interfering RNA (siRNA) against CXCR7 and ERK inhibitor PD098059. Therefore, our study demonstrates that the upregulation of CXCR7 signaling contributes to increased vasculogenic capacity of EOCs from CAD patients, indicating that CXCR7 signaling may be a novel therapeutic vasculogenic target for CAD.

show abstract

Section: Discussionmentioning

confidence: 99%

CXCR7/p-ERK-Signaling Is a Novel Target for Therapeutic Vasculogenesis in Patients with Coronary Artery Disease

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The other crucial cell survival pathway is MAPK. The MAPK family, which is well known to be involved in the occurrence, progression, and metastasis of tumors, includes ERK1/2, p38, and JNK [25][26][27]. ERK1/2 was found to be expressed more highly in ESCC tissues than in adjacent normal esophageal tissues [28].…”

Section: Discussionmentioning

confidence: 99%

Multiple Signal Pathways Involved in Crocetin-Induced Apoptosis in KYSE-150 Cells

Shen

et al. 2019

Pharmacology

View full text Add to dashboard Cite

Background: Crocetin is a carotenoid extracted from the traditional Chinese medical herb saffron. Previous studies have demonstrated that crocetin possesses anticancer properties that are effective against various cancers. As an extension of our earlier study, the present study explored the underlying mechanisms in crocetin’s anticancer effect on KYSE-150 cells. The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT), Mitogen-activated protein kinases (MAPK), and p53/p21 signal pathways play an important role in carcinogenesis, progression, and metastasis of carcinoma cells. Thus, we investigated crocetin’s effects on the PI3K/AKT, MAPK, and p53/p21 pathways in esophageal squamous carcinoma cell line KYSE-150 cells. Methods: KYSE-150 cells were treated with various concentrations of crocetin. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltertrazolium bromide assay, Annexin V/PI stain as well as Rh123 stain were used to evaluate the cell viability, apoptosis, and MMP. Western blot was used to detect the expression of PI3K, AKT, ERK1/2, p38, c-Jun NH-terminal kinase (JNK), P53, P21, Bcl-2, Bax, and cleaved caspase-3, which were associated with cell proliferation and apoptosis. Results: Our results showed that crocetin significantly inhibited the proliferation of KYSE-150 cells in a dose- and time-dependent manner. Crocetin also markedly induced cell apoptosis. Furthermore, we have found that crocetin not only inhibited the activation of PI3K/AKT, extracellular signal–regulated kinase-1/2 (ERK1/2), and p38 but also upregulated the p53/p21 level. These regulations ultimately triggered the mitochondrial-mediated apoptosis pathway with an eventual disruption of MMP, increased levels of Bax and cleaved caspase-3, and decreased levels of Bcl-2. Conclusions: These findings suggested that crocetin interfered with multiple signal pathways in KYSE-150 cells. Therefore, this study suggested that crocetin could potentially be used as a therapeutic candidate for the treatment of esophageal cancer.

show abstract

“…The ERK/MAPK signaling pathway is widely expressed in many tissues and cells, and can regulate cell proliferation, the cell cycle, apoptosis, migration and invasion, and many other biological processes (22,23). Excessive activation of the ERK/MAPK signaling pathway can cause abnormal proliferation, apoptosis and differentiation of cells, and thus is associated with tumor occurrence, progression and metastasis, including gallbladder carcinoma (22), esophageal cancer (24), and breast cancer (24)(25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

miR‑101 regulates the cell proliferation and apoptosis in diffuse large B‑cell lymphoma by targeting MEK1 via regulation of the ERK/MAPK signaling pathway

et al. 2018

View full text Add to dashboard Cite

MAPK kinase 1 (MEK1) is an upstream protein kinase of extracellular signal regulated kinase (ERK), which activates the ERK/MAPK (mitogen activated protein kinase) pathway. Importantly, bioinformatic analysis has shown that there is a target complementary binding site between miR-101 and MEK1. The present study aimed to ascertain whether or not miR-101 plays a role in regulating MEK1 expression, ERK/MAPK pathway activity, and the proliferation and apoptosis in a diffuse large B cell lymphoma (DLBCL) cell line. DLBCL tumor samples were collected from patients in our hospital, and lymphatic tissues with reactive lymphoid hyperplasia were selected as controls. The patients were divided into high and low expression groups, and then the survival rate of the two groups was compared using Kaplan-Meier method, as well the effect of miR-101 and MEK1 mRNA expression on survival and prognosis was analyzed. The expression of miR-101, MEK1 and p-MEK1 between normal lymphoblastic cell lines (HCC1954 BL and NCI-BL2009) and lymphoma cell lines (SU-DHL-4 and Farage) was compared. Lymphoma SU-DHL-4 and Farage cells were cultured in vitro, and then divided into the following groups: miR-NC group; miR-101 mimic group; siRNA-NC group; and siRNA-MEK1 group. The expression of miR-101, MEK1, p-MEK1, p-ERK1/2 and Bcl-2 was compared. Cell apoptosis was detected by flow cytometry, and cell proliferation was detected by EdU staining. The results showed that targeted regulation existed between miR-101 and MEK1, and the decreased expression of miR-101 was related to the pathogenesis and prognosis of DLBCL. Upregulation of miR-101 inhibited DLBCL cell proliferation and facilitated apoptosis by inhibiting the expression of MEK1.

show abstract

The expression and activation of ERK/MAPK pathway in human esophageal cancer cell line EC9706

Cited by 14 publications

References 22 publications

CXCR7/p-ERK-Signaling Is a Novel Target for Therapeutic Vasculogenesis in Patients with Coronary Artery Disease

CXCR7/p-ERK-Signaling Is a Novel Target for Therapeutic Vasculogenesis in Patients with Coronary Artery Disease

Multiple Signal Pathways Involved in Crocetin-Induced Apoptosis in KYSE-150 Cells

miR‑101 regulates the cell proliferation and apoptosis in diffuse large B‑cell lymphoma by targeting MEK1 via regulation of the ERK/MAPK signaling pathway

Contact Info

Product

Resources

About