Nuclear accumulation of epidermal growth factor receptor and acceleration of G1/S stage by Epstein–Barr-encoded oncoprotein latent membrane protein 1

Tao, Yongguang; Song, Xing; Deng, Xiyun; Xie, Daxin; Lee, Leo M.; Liu, Yiping; Li, Wei; Li, Lili; Deng, Lin; Wu, Qiao; Gong, Jianping; Cao, Yang

doi:10.1016/j.yexcr.2004.09.030

Cited by 62 publications

(64 citation statements)

References 38 publications

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“…Correlation analysis further revealed a significant inverse correlation between the level of cyclin E2 and three of its cognate miRNAs, miR-34c, miR-200a, and miR-9. These results suggest that the aberrant cell cycle control in NPC tissues may be tightly linked to the dysregulated expression of miRNAs (Hwang et al, 2002;Tao et al, 2005;Chou et al, 2008).…”

Section: Discussionmentioning

confidence: 88%

MicroRNA deregulation and pathway alterations in nasopharyngeal carcinoma

et al. 2009

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MicroRNAs (miRNAs) are a family of small non-coding RNA molecules of about 20 -23 nucleotides in length, which negatively regulate protein-coding genes at post-transcriptional level. Using a stem-loop real-time-PCR method, we quantified the expression levels of 270 human miRNAs in 13 nasopharyngeal carcinoma (NPC) samples and 9 adjacent normal tissues, and identified 35 miRNAs whose expression levels were significantly altered in NPC samples. Several known oncogenic miRNAs, including miR-17-92 cluster and miR-155, are among the miRNAs upregulated in NPC. Tumour suppressive miRNAs, including miR-34 family, miR-143, and miR-145, are significantly downregulated in NPC. To explore the roles of these dysregulated miRNAs in the pathogenesis of NPC, a computational analysis was performed to predict the pathways collectively targeted by the 22 significantly downregulated miRNAs. Several biological pathways that are well characterised in cancer are significantly targeted by the downregulated miRNAs. These pathways include TGF-Wnt pathways, G1-S cell cycle progression, VEGF signalling pathway, apoptosis and survival pathways, and IP3 signalling pathways. Expression levels of several predicted target genes in G1-S progression and VEGF signalling pathways were elevated in NPC tissues and showed inverse correlation with the down-modulated miRNAs. These results indicate that these downregulated miRNAs coordinately regulate several oncogenic pathways in NPC.

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Section: Discussionmentioning

confidence: 88%

MicroRNA deregulation and pathway alterations in nasopharyngeal carcinoma

et al. 2009

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“…It has been previously demonstrated that in non-transformed cells, the cyclin D1 gene senses the mitogenic potential of the microenvironment because its induction requires coordinated signaling from the extracellular matrix and soluble growth factors [44]. Activators of cyclin D1 gene transcription are mitogenic growth factors, and, it has been described that also nuclear EGFR is able to bind the cyclin D1 promoter, promoting the gene transcription [47]. Interestingly, also vandetanib inhibited cell proliferation in a dose-dependent manner, by blocking cell progression at the G0-G1 stage, through the downregulation of expression of cyclin D1 and cyclin E [37].…”

Section: Discussionmentioning

confidence: 99%

Antiproliferative and proapoptotic activity of CLM3, a novel multiple tyrosine kinase inhibitor, alone and in combination with SN-38 on endothelial and cancer cells

Bocci¹,

Fioravanti²,

Motta³

et al. 2011

Biochemical Pharmacology

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Aims. To demonstrate the antiproliferative and pro-apoptotic activity of the novel pyrazolopyrimidine derivative multiple tyrosine kinase inhibitor CLM3, alone and in combination with SN-38 (the active metabolite of irinotecan), on endothelial and tumour cells and to show its mechanism of action.Methods. Proliferation and apoptotic assays were performed on microvascular endothelial (HMVECd) and lung (A549) and thyroid cancer (8305C, TT) cell lines exposed to CLM3 and to the simultaneous combination with SN38 for 72h. Cell-based phospho-VEGFR-2, phospho-EGFR and phospho-RET inhibition assays were performed and ERK1/2 and Akt phosphorylation were quantified by ELISA kits. Conclusions.The pyrazolopyrimidine derivative CLM3 demonstrated a highly significant and promising antiproliferative and proapoptotic activity, alone and in combination with SN-38, for activated endothelial and cancer cell cells. These effects are mainly due to its inhibition of phosphorylation of VEGFR-2, EGFR and RET tyrosine kinases and their related signalling pathways.

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“…The nuclear receptor is reported to recognize the promoter of cyclin D1 and to transactivate this promoter in a reporter system. Other promoters are also reported to be recognized by the EGF receptor (Lo et al 2005(Lo et al , 2010Tao et al 2005;Hanada et al 2006). However, direct and specific binding to any promoter remains to be shown.…”

Section: Erbb-1mentioning

confidence: 99%

Receptor Tyrosine Kinases in the Nucleus

Carpenter

Liao

2013

Cold Spring Harbor Perspectives in Biology

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To date, 18 distinct receptor tyrosine kinases (RTKs) are reported to be trafficked from the cell surface to the nucleus in response to ligand binding or heterologous agonist exposure. In most cases, an intracellular domain (ICD) fragment of the receptor is generated at the cell surface and translocated to the nucleus, whereas for a few others the intact receptor is translocated to the nucleus. ICD fragments are generated by several mechanisms, including proteolysis, internal translation initiation, and messenger RNA (mRNA) splicing. The most prevalent mechanism is intramembrane cleavage by g-secretase. In some cases, more than one mechanism has been reported for the nuclear localization of a specific RTK. The generation and use of RTK ICD fragments to directly communicate with the nucleus and influence gene expression parallels the production of ICD fragments by a number of non-RTK cell-surface molecules that also influence cell proliferation. This review will be focused on the individual RTKs and to a lesser extent on other growth-related cell-surface transmembrane proteins.

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Nuclear accumulation of epidermal growth factor receptor and acceleration of G1/S stage by Epstein–Barr-encoded oncoprotein latent membrane protein 1

Cited by 62 publications

References 38 publications

MicroRNA deregulation and pathway alterations in nasopharyngeal carcinoma

MicroRNA deregulation and pathway alterations in nasopharyngeal carcinoma

Antiproliferative and proapoptotic activity of CLM3, a novel multiple tyrosine kinase inhibitor, alone and in combination with SN-38 on endothelial and cancer cells

Receptor Tyrosine Kinases in the Nucleus

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