宫颈癌（cervical carcinoma）是女性第二大恶性肿瘤，并且在年轻女性中发病率高。2002年全世界的新发病例为50万人，死亡病例为27万人。根据中国疾病预防与控制中心公布的数据，我国每年宫颈癌新发病例为13.15 万人，约占世界总数的26%，死亡病例为5.3 万人，约占世界总数的20%。因此，我国的宫颈癌防治形势非常严峻。
在99.8%的宫颈癌患者中均可检测到HPV感染。但单独的HPV 感染不足以引起宫颈癌，细胞本身必须发生相应的变化，才能最终引起宫颈癌。清华大学的程京教授与新疆医科大学第一附属医院的温浩教授合作，利用生物芯片平台研究了宫颈癌组织中microRNA的表达变化，发现了20种microRNA在宫颈癌的发生和发展过程中表达量发生了改变。其中microRNA-133b在从宫颈上皮内瘤样病变到侵润癌的发展过程中，表达量逐步升高。功能学实验结果表明，这一microRNA具有促进宫颈癌发生和发展的作用。该microRNA有可能作为临床早期诊断的新型宫颈癌标志物。
上述研究成果已申请ZL，研究论文已在Oncogene杂志网站在线发表。其中的博奥生物晶芯®哺乳动物miRNA芯片服务与Real time RT-PCR服务在博奥生物有限公司完成。
原文摘要：
MicroRNA-133b is a key promoter of cervical carcinoma development through the activation of the ERK and AKT1 pathways
We
report that elevated microRNA-133b (miR-133b) acts as an oncogene in
human cervical carcinoma to promote tumorigenesis and metastasis. In
situ hybridization confirmed that miR-133b is localized in proliferating
human cervical carcinoma cells with levels progressively elevating
throughout advancing stages. Cellular studies showed that miR-133b
enhances cell proliferation and colony formation by targeting mammalian
sterile 20-like kinase 2 (MST2), cell division control protein 42
homolog (CDC42) and ras homolog gene family member A (RHOA), which
subsequently results in activation of the tumorigenic protein kinase B
alpha (AKT1) and mitogenactivated protein kinase (ERK1 and ERK2, here
abbreviated as ERK) signaling pathways. Mouse experiments revealed that
upregulation of miR-133b in cervical carcinoma cells strongly promotes
both in vivo tumorigenesis and independent metastasis to the mouse lung.
The data indicates that upregulation of miR-133b shortens the latency
of cervical carcinoma. Together, these findings suggest that miR-133b
could be a potent marker for the early onset of cervical carcinoma.
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