Activation of EGFR promotes squamous carcinoma SCC10A cell migration and invasion via inducing EMT‐like phenotype change and MMP‐9‐mediated degradation of E‐cadherin

Zuo, Jianhong; Zhu, Wei; Li, Maoyu; Li, Xinhui; Yi, Hong; Zeng, Gu-Qing; Wan, Xun-Xun; He, Qianyu; Li, Jianhuang; Qu, Jia-Quan; Chen, Yu; Xiao, Zhi‐Qiang

doi:10.1002/jcb.23175

Cited by 223 publications

(186 citation statements)

References 46 publications

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“…2A). The constitutive expression of EGFR in metastatic tumor cells has previously been demonstrated to be associated with enhanced MMP-9 expression and induction of invasive capacity (25). In the present study, it was observed that CXCR4-overexpressing cells elevated MMP-9 production compared with controls (Fig.…”

Section: Cxcr4 Promotes Expression Of Egfr and Elevates Mmp-9 Productsupporting

confidence: 69%

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Overexpression of CXCR4 promotes invasion and migration of non‑small cell lung cancer via EGFR and MMP‑9

Zuo

Wen

et al. 2017

Oncol Lett

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Abstract. The aim of the present study was to verify whether overexpression of CXC receptor 4 (CXCR4) promotes the invasion and migration of non-small cell lung cancer (NSCLC) via epidermal growth factor receptor (EGFR) and matrix metallopeptidase-9 (MMP-9), and to detect the association between CXCR4, EGFR and MMP-9. The effects of overexpression of CXCR4 on lung cancer cell functions were investigated by migration and invasion assays. Western blotting and zymograph assays were used to analyze the protein expression levels of EGFR and the production of MMP-9, respectively. Immunohistochemistry was applied to analyze the expression of EGFR, CXCR4 and MMP-9 in NSCLC. Statistical analyses were used to detect the associations among EGFR, CXCR4 and MMP-9 in NSCLC. Finally, survival analyses were performed. CXCR4 overexpression enhanced cell motility and invasion. CXCR4 also promoted expression of EGFR and elevated MMP-9 production. CXCR4, EGFR and MMP-9 were highly expressed in NSCLC, and were not identified as associated with age and sex (P>0.05). However, they were associated with tumor differentiation and lymph node metastasis (P<0.05). CXCR4, EGFR and CXCR4 expression were positively associated with one another in NSCLC (P<0.05). In addition, patients with positive expression of CXCR4, EGFR or MMP-9 in tumors exhibited significantly shorter overall survival compared with those with negative expression (P<0.05). In conclusion, CXCR4 overexpression enhanced cell motility and invasion via EGFR and MMP-9. CXCR4, EGFR and MMP-9 were identified as highly expressed in NSCLC, and there was positive correlation among them.

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Section: Cxcr4 Promotes Expression Of Egfr and Elevates Mmp-9 Productsupporting

confidence: 69%

“…In the Transwell migration assay, as previously described (21,25), the underside of the Transwell insert (pore size, 8 µm; Costar; Corning Incorporated, Corning, NY, USA) was pre-coated with collagen type I (Col-I, 1 µg/ml) or fibronectin (10 µg/ml). Subsequently, 2x10…”

Section: Antibodiesmentioning

confidence: 99%

Overexpression of CXCR4 promotes invasion and migration of non‑small cell lung cancer via EGFR and MMP‑9

Zuo

Wen

et al. 2017

Oncol Lett

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“…Zhou et al (2014) showed that suppression of EGFR by miRNA-7 is able to inactivate the ERK-1/2/ATK signaling cascade, thus reversing EMT and attenuating metastasis in epithelial ovarian cancer cells. Zuo et al (2011) found that EGFR activation can induce EMT-like phenotype change and MMP-9-mediated degradation of E-cadherin in HNSCC SCC10A cells through the ERK-1/2 and PI3K signaling pathways. Based on these findings, the negative effects of LRIG1 on EMT are most likely attributed to inactivation of the EGFR/PI3K/AKT pathway triggered by the antagonistic interaction between EGFR and LRIG1, consequently suppressing VM formation and VM-dependent malignant behaviors in glioma cells (the hypothetical scheme is shown in Fig.…”

Section: Discussionmentioning

confidence: 93%

LRIG1 inhibits hypoxia-induced vasculogenic mimicry formation via suppression of the EGFR/PI3K/AKT pathway and epithelial-to-mesenchymal transition in human glioma SHG-44 cells

Zhang

Song

Wei

et al. 2015

Cell Stress and Chaperones

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Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a pan-negative regulator of the epidermal growth factor receptor (EGFR) signaling pathway. The aim of this study was to investigate the underlying mechanism of LRIG1 in the regulation of vasculogenic mimicry (VM) formation in glioma cells. We constructed an enhanced green fluorescent protein plasmid (pEGFP) system, pEGFP-C1-LRIG1, for overexpression of LRIG1, and transfected it into human glioma cell line SHG-44. Under hypoxic conditions induced by CoCl 2 , we investigated the effects of LRIG1 overexpression on VM formation and VM-dependent malignant behaviors including migration, invasion, and proliferation. Additionally, we explored the effects of LRIG1 on the expression levels of major components of the EGFR/PI3K/AKT pathway as well as E-cadherin and vimentin. We found that LRIG1 overexpression is able to inhibit hypoxia-induced VM formation, migration, invasion, and proliferation. Furthermore, LRIG1 overexpression counteracts hypoxiainduced increase in the expression of phosphorylated EGFR (pEGFR), PI3K (pPI3K), and AKT (pAKT) and reverts hypoxia-induced alteration in E-cadherin and vimentin expression levels. In LRIG1 knockdown SHG-44 cells, however, hypoxia-induced VM formation and alteration in E-cadherin and vimentin expression levels were exacerbated. These results suggest that the inhibitory effects of LRIG1 are most likely mediated by suppression of the EGFR/PI3K/AKT pathway and epithelial-mesenchymal transition (EMT) process. Our findings provide compelling evidence implicating LRIG1 in glioma pathophysiology, suggesting that gene therapy using LRIG1 may serve as a treatment for this disease.

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“…Similarly, Wang et al indicated that overexpression of activated Erk1/2 and cyclin D1 proteins are involved in oral tongue carcinogenesis (51). Finally, Judd et al (59) reported that MEK1 activation enhances CD44 expression and promotes aggressiveness in HNSCC, while Katada et al (60) and Zuo et al (61) suggested that Erk1/2 activation correlates with increased cell migration and invasion in HNSCC.…”

Section: Discussionmentioning

confidence: 99%

Erk1/2 activation and modulation of STAT3 signaling in oral cancer

et al. 2014

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Abstract. Constitutive activation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway possesses confirmed oncogenic potential in oral squamous cell carcinoma (OSCC). Crosstalk with other molecular pathways contributes to STAT3 regulation in cancer. The effects of mitogen-activated protein kinases (MAPKs) and particularly extracellular signal-regulated kinase 1/2 (Erk1/2) on STAT3 signaling in OSCC have not been thoroughly investigated. The present study examined the effects of Erk1/2 modulation on STAT3 signaling and cell growth in OSCC cells. Constitutive expression levels of phosphorylated (tyrosine and serine) and total STAT3, Erk1/2 and cyclin D1 were assessed in OSCC cell lines. Erk1/2 modulation was achieved by pharmacological agents; siRNA silencing against Erk1/2 was also performed. Cell proliferation and viability were assessed. Erk1/2 inhibition with either U0126 treatment or specific siRNA silencing resulted in decreases in p-ser STAT3 and cyclin D1 levels and increases in p-tyr STAT3 in OSCC cells. Moreover, Erk1/2 inhibition resulted in a dose-dependent reduction in OSCC cell growth and viability. Erk1/2 induction had the opposite effects. Taken together, these results are supportive of an active crosstalk between the oncogenic Erk1/2 and STAT3 pathways in OSCC, the significance of which requires further investigation.

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Activation of EGFR promotes squamous carcinoma SCC10A cell migration and invasion via inducing EMT‐like phenotype change and MMP‐9‐mediated degradation of E‐cadherin

Cited by 223 publications

References 46 publications

Overexpression of CXCR4 promotes invasion and migration of non‑small cell lung cancer via EGFR and MMP‑9

Overexpression of CXCR4 promotes invasion and migration of non‑small cell lung cancer via EGFR and MMP‑9

LRIG1 inhibits hypoxia-induced vasculogenic mimicry formation via suppression of the EGFR/PI3K/AKT pathway and epithelial-to-mesenchymal transition in human glioma SHG-44 cells

Erk1/2 activation and modulation of STAT3 signaling in oral cancer

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