肺癌的发病率和死亡率在国内外均高居各类癌症榜首，且临床治疗效果不佳。因而抑制肺癌的发生和早癌进展成为肿瘤干预的重要关口。糖代谢在肺癌的发生发展中起重要作用。我们的前期研究结果提示同源异形盒转录因子HOXB9可以通过自身的磷酸化感受肺癌细胞中糖代谢信号的改变。本研究中我们将详细研究细胞的能量感受器AMPK对HOXB9的磷酸化，明确HOXB9的磷酸化位点，并阐明HOXB9磷酸化和泛素化之间的关系；采用基因敲入动物验证HOXB9磷酸化关键位点的突变体与肺腺癌发生发展的关系。在肺腺癌病人组织水平上建立HOXB9磷酸化作用与肺腺癌进展和预后之间的关系。利用AMPKαβ双敲鼠验证HOXB9的磷酸化是肿瘤细胞能量代谢变化的感受器，可以将肿瘤能量代谢信号转换成肿瘤发生发展的促进因素。本研究首次将葡萄糖代谢与肺癌发生发展相关转录因子HOXB9紧密联系起来，将为抑制肺癌发生发展提供新的可能的干扰靶点。

The incidence and mortality of lung cancer are among the highest in all types of cancer at home and abroad, and the clinical treatment effect is not good. Therefore, inhibiting the occurrence of lung cancer and early cancer progression has become an important barrier for tumor intervention. Glucose metabolism plays an important role in the development of lung cancer. Our preliminary results suggest that the homeobox transcription factor HOXB9 can sense changes of glucose metabolism signals in lung cancer cells through its own phosphorylation. In this study, we will study the phosphorylation of HOXB9 by the cellular energy metabolism receptor AMPK, clarify the phosphorylation site of HOXB9, and elucidate the relationship between HOXB9 phosphorylation and ubiquitination. The knock-in animals were used to verify the relationship between the mutants of the key site of HOXB9 phosphorylation and the development of lung adenocarcinoma. The relationship between HOXB9 phosphorylation and progression and prognosis of lung adenocarcinoma was established at the tissue level of lung adenocarcinoma patients. Using AMPKαβ double knock out-mouse to verify that phosphorylation of HOXB9 is a receptor for changes in energy metabolism of tumor cells, it can convert tumor energy metabolism signals into facilitators of tumor development. For the first time, this study closely linked glucose metabolism with the transcription factor HOXB9, which is involved in the development of lung cancer, and will provide a new possible interference target for inhibiting the development of lung cancer.