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Menebar Ilmu Pengetahuan

Epstein-Barr virus (EBV) dan NPC

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Nasopharyngeal carcinoma (NPC) adalah kanker yang paling umum berasal dari nasofaring, wilayah paling atas dari faring (“tenggorokan”), di belakang hidung dimana saluran hidung dan tabung pendengaran bergabung pada remainder saluran pernapasan bagian atas. Umumnya menyerang pada pria, di Asia Timur dan Afrika. Nasopharyngeal carcinoma (NPC) dikaitkan dengan infeksi Epstein-Barr virus (EBV).

Mechanisms of Epstein-Barr virus (EBV) latent proteins in nasopharyngeal carcinoma (NPC) development. NPC tumorigenesis depends on the activity of latent proteins LMP1 and 2 and EBNA 1 and 2. The majority of cancer development is propagated by LMP1, which is responsible for the activation of various molecular pathways and immune evasion. LMP1 is regulated positively by LMP2 and negatively by EBNA 2. The other functions of LMP2 include mediation of tumor cell survival and invasion. Finally, EBNA 1 is critical for viral DNA partitioning during replication; LMP, latent membrane protein; EBNA, EBV-determined nuclear antigen.

Gambar di bawah ini adalah mekanisme molekuler yang terlibat pada perkembangan nasopharyngeal carcinoma (NPC). NPC berkembang dimulai dengan upregulasi jalur yang mendorong proliferasi sel: jalur Akt, mitogen-activated protein kinases (JNK, ERK), jalur Wnt, dan jalur EGFR. Selanjutnya terjadi kenaikan faktor transkripsi seperti NF-κB dan β-catenin mendorong pada proliferasi seluler via disregulasi siklus sel (ekspresi tinggi c-myc, cyclin D1, dan cyclin E) dan penghambatan tumor suppressors (p16, p27, dan wild-type p53).

Selain itu, kemapuan sel adhesi dilemahkan karena rendahnya level E-cadherin dan ekspri tinggi MMP. Juga terjadi mekanisme anti-apoptosis melaui upregulasi bcl-2, survivin, dan telomerase.

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.

Referensi

Chou J, Lin YC, Kim J, You L, Xu Z, He B, Jablons DM. Nasopharyngeal carcinoma–review of the molecular mechanisms of tumorigenesis. Head Neck. 2008 Jul;30(7):946-63. doi: 10.1002/hed.20833.

Raab-Traub N. Epstein-Barr virus in the pathogenesis of NPC. Semin Cancer Biol. 2002 Dec;12(6):431-41.

Author: admin

menebar ilmu pengetahuan

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