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LRIG1 exerts important tumor-suppressive effects in EGFR-mutant NSCLC.
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proposed LRIG1 protein interaction network
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MiR-183 overexpression promoted radioresistance of glioblastoma via down-regulating LRIG1 and increasing the activity of EFGR/Akt.
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LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in papillary and medullary thyroid carcinoma
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LRIG1 expression in human GC tissues is inversely correlated with miR-20a and EGFR.
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Role of LRIG1 in cancer [review]
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LRIG1 expression may represent a barrier to EMT
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LRIG1 role in the atrophic epidermis
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Downregulation of LRIG1 expression in oral verrucous carcinoma tissue is reported.
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LRIG1, as a negative mediated gene of tumor, can inhibit biological function of PAs via inhibiting PI3K/AKT and Ras/Raf/ERK pathways, and it might be a new target for gene therapy ofPituitary adenomas
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LRIG1 and Fascin-1 were differently expressed in cancer and normal lung tissue in patients with NSCLC, which could be a biomarker for mediastinal lymph node metastasis in NSCLC patients.
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Results suggest that the LRIG1could negatively control MRP-1 and the apoptosis to improve the sensitivity of VP16-related chemotherapy.
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ERa-dependent expression of LRIG1 dampens ErbB3 signaling in luminal breast cancer cells, and by blocking ERa activity with fulvestrant, LRIG1 is decreased thus permitting ErbB3 accumulation, enhanced ErbB3 signaling to cell survival pathways
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These findings demonstrate that LRIG1 is an independent prognostic factor in patients with non-small cell lung cancer
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LRIG1 expression was associated with pathological type, differentiation status, and stage of Non-small Cell Lung Cancer. The result showed that LRIG1 was an independent prognostic factor for OS of NSCLC patients.
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The inhibitory effects of LRIG1 are most likely mediated by suppression of the EGFR/PI3K/AKT pathway and epithelial-mesenchymal transition (EMT) process.
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LRIG1 can enhance chemosensitivity in glioblastoma by inhibition of BCL-2 and MnSOD
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Results showed that leucine-rich repeats and immunoglobulin-like domains can reverse multidrug resistance in glioblastoma, by negatively regulating epidermal growth factor receptor.
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MiR-20a mediated temozolomide-resistance in glioblastoma cells through negatively regulating LRIG1 expression.
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Based on these results, we concluded that the upregulation of LRIG1 expression inhibited the EGFR signaling pathway, activated the mitochondrial pathway of apoptosis and eventually increased the sensitivity of bladder cancer cells to CDDP.