Clinical significance of Laminin-332 and its potential as a therapeutic target

层粘连蛋白-332封闭抗体失活AKT通路可抑制食道癌细胞系的侵袭力。纯化的层粘连蛋白-332的加入激活了AKT途径，增加了细胞的侵袭力。这些结果提示层粘连蛋白-332可能通过AKT途径参与食道癌的恶性行为。MTOR是AKT途径中的一个关键分子，作为抗癌治疗的潜在靶点越来越重要。因此，我们致力于揭示mTOR抑制剂在食道癌中的临床应用价值。P-mTOR过表达与ESCC预后不良独立相关，支持mTOR作为ESCC治疗靶点的可能性。我们目前正在进行进一步的体外和体内研究，以阐明RAD001(mTOR抑制剂)对ESCC的抗肿瘤作用。

Inactivation of the AKT pathway by laminin-332 blocking antibody suppressed the invasiveness of esophageal cancer cell line. The addition of the purified laminin-332 activated the AKT pathway and increased the invasiveness of cell line. These results indicate that Laminin-332 could contribute to the malignant behavior of esophageal cancer through AKT pathway. mTOR is a key molecule in the AKT pathway and is increasingly important as a potential target for anticancer therapy. Thus, we focused on revealing clinical usefulness of mTOR inhibitor in esophageal cancer. p-mTOR overexpression was independently associated with poor prognosis in ESCC, supporting the potential for mTOR as a therapeutic target for ESCC. We are currently performing further in vitro and in vivo study to clarify the antitumor effect of RAD001 (mTOR inhibitor) on ESCC.