Myo1b是基于肌动蛋白的一种分子马达。课题组前期研究发现，Myo1b在宫颈癌中发挥癌基因的功能，并与淋巴结转移相关。此外，Myo1b高表达与头颈鳞癌、垂体腺瘤、脑胶质瘤、前列腺癌的恶性表型有关。然而，Myo1b在其他肿瘤（包括乳腺癌）中的作用却鲜有报道，且相关调控机制及信号转导途径仍不完全清楚。我们前期预实验结果提示：Myo1b在乳腺癌中高表达，沉默Myo1b能有效抑制细胞的增殖、迁移和侵袭能力，机制上可能通过Akt/mTOR通路影响自噬和糖酵解。在此基础上，我们认为“Myo1b可能通过Akt/mTOR通路调控自噬和糖酵解促进乳腺癌进展”。本项目拟采用分子病理学及分子生物学的技术方法，结合体内外研究，旨在获得Myo1b调控自噬和糖酵解发挥生物学功能的可靠证据，阐明Myo1b促进乳腺癌侵袭转移的分子机制，为确立Myo1b作为临床治疗的新靶点提供更为充分的科学依据。

Myosin 1b (Myo1b), a class I myosin, is a widely expressed, single-headed, actin-associated molecular motor. Our previous study has identified Myo1b as a novel tumor promotor in cervical cancer, and its high expression is associated with lymph node metastasis. And other evidence suggests an important role of Myo1b in the progression of several cancers, including head and neck squamous cell carcinoma (HNSCC), pituitary adenoma, glioma and prostate cancer. However, the roles of Myo1b in other cancers remain elusive, and the underlying mechanisms and signal transduction pathways involved in carcinogenesis are still unknown. Our preliminary experimental results indicate that Myo1b is highly expressed in breast cancer, and silencing Myo1b can effectively inhibit cell proliferation, invasion and migration, which may affect autophagy and glycolysis through the Akt/mTOR pathway. On basis of this, we wondered whether Myo1b could contribute to the progression of breast cancer by regulating autophagy and glycolysis via the Akt/mTOR pathway. Here we aim to obtain reliable evidence that Myo1b regulate autophagy and glycolysis to exert its biological functions in breast cancer using proteomic technique, molecular pathological and biological strategy. Our study may illustrate biological mechanism of how Myo1b promote tumor malignant progression by regulating Akt/mTOR pathway, and provide the scientific basis for establishing Myo1b as a novel target for clinical therapy of tumor invasion and metastasis.