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人LKB1(Liver Kinase B1,或Serine-Threonine Kinase 11,STK11)基因的胚系失活突变可导致癌症易感病皮杰氏综合征(Peutz-Jeghers syndrome,PJS),该病患者多发错构瘤息肉且患癌症风险增加。LKB1基因的体细胞突变还广泛地存在于众多类型的恶性肿瘤中,如肺癌、结肠癌和乳腺癌等,因此,LKB1被普遍认为是抑癌基因。LKB1基因的编码产物LKB1是一种丝氨酸/苏氨酸激酶,调节多种细胞生理病理过程。虽然LKB1的抑癌机制尚不完全清楚,但现有的研究表明,对细胞生长增殖、能量代谢和细胞极性等的调控是其抑制肿瘤发生和发展的重要方面。本文就目前已知的LKB1的抑癌机制作一综述。
Germline inactivation mutations in the human LKB1 (Liver Kinase B1, or Serine-Threonine Kinase 11, STK11) gene lead to Peutz-Jeghers syndrome (PJS), a disease of the patient that has multiple hamartomas Polyps and increased risk of cancer. Somatic mutations of the LKB1 gene are also widely found in many types of malignancies such as lung cancer, colon cancer and breast cancer. Therefore, LKB1 is generally considered as a tumor suppressor gene. LKB1 gene encoding product LKB1 is a serine / threonine kinase, regulating a variety of cell physiological and pathological processes. Although the mechanism of LKB1 tumor suppressor is not completely understood, the existing research shows that the regulation of cell growth and proliferation, energy metabolism and cell polarity are important aspects of tumorigenesis and development. This article reviews the currently known mechanism of tumor suppressor of LKB1.