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. Author manuscript; available in PMC: 2011 Feb 28.

Published in final edited form as: Head Neck. 2008 Jul;30(7):946–963. doi: 10.1002/hed.20833

Overview of the molecular mechanisms involved in nasopharyngeal carcinoma (NPC) development. NPC development begins with the upregulation of pathways that promote cellular proliferation: Akt pathway, mitogen-activated protein kinases (JNK, ERK), Wnt pathway, and EGFR signaling. Subsequent increases of transcription factors such as NF-κB and β-catenin lead to cellular proliferation via cell cycle dysregulation (high c-myc, cyclin D1, and cyclin E expression) and inhibition of tumor suppressors (p16, p27, and wild-type p53). In addition, cell adhesion abilities are compromised because of low E-cadherin levels and high expression of MMPs. Also, antiapoptotic mechanisms such as bcl-2, survivin, and telomerase are upregulated., Stimulatory effect; , inhibitory effect; orange color indicates apoptosis regulators; light blue color indicates cell adhesion proteins; yellow color indicates cell cycle regulators; dark blue color indicates proliferative pathways; green color indicates transcription factors; purple color indicates tumor suppressors; EGFR, epidermal growth factor receptor; ERK, extracellular signal related kinase; JNK, c-Jun N-terminal kinase; LMP1, latent membrane protein 1; MMP, matrix metalloproteinase; NPC, nasopharyngeal carcinoma; PTEN, phosphatase and tensin homolog; PI3K, phosphoinositol-3-kinase; RASSF, Ras association domain family; WIF, Wnt inhibitory factor; WT p53, wild-type p53. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]

Inline graphic — Overview of the molecular mechanisms involved in nasopharyngeal carcinoma (NPC) development. NPC development begins with the upregulation of pathways that promote cellular proliferation: Akt pathway, mitogen-activated protein kinases (JNK, ERK), Wnt pathway, and EGFR signaling. Subsequent increases of transcription factors such as NF-κB and β-catenin lead to cellular proliferation via cell cycle dysregulation (high c-myc, cyclin D1, and cyclin E expression) and inhibition of tumor suppressors (p16, p27, and wild-type p53). In addition, cell adhesion abilities are compromised because of low E-cadherin levels and high expression of MMPs. Also, antiapoptotic mechanisms such as bcl-2, survivin, and telomerase are upregulated., Stimulatory effect; , inhibitory effect; orange color indicates apoptosis regulators; light blue color indicates cell adhesion proteins; yellow color indicates cell cycle regulators; dark blue color indicates proliferative pathways; green color indicates transcription factors; purple color indicates tumor suppressors; EGFR, epidermal growth factor receptor; ERK, extracellular signal related kinase; JNK, c-Jun N-terminal kinase; LMP1, latent membrane protein 1; MMP, matrix metalloproteinase; NPC, nasopharyngeal carcinoma; PTEN, phosphatase and tensin homolog; PI3K, phosphoinositol-3-kinase; RASSF, Ras association domain family; WIF, Wnt inhibitory factor; WT p53, wild-type p53. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]