![]() ![]() ![]() Hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) are two key angiogenic regulatory factors. Although a recent report showed that Myo1b is a pro-invasive regulator marker of membrane protrusion in CRC, the studies of Myo1b on CRC tumorigenesis are still limited, and their functional mechanisms remain poorly understood. Our previous study suggested a potential role of Myo1b in cervical carcinogenesis and its over-expression was significantly correlated with FIGO Stage, HPV infection, lymph node metastasis and pathological grade. Furthermore, miR-363 and miR-145-3p were found to be a tumor-suppressor in HNSCC or ESCC via targeting Myo1b. demonstrated that silencing Myo1b suppressed the migration and invasion of HNSCC cells by inhibiting large protrusion formation of cell membranes. Recently, aberrant expression of Myo1b has been detected in various cancers, including prostate cancer, head and neck squamous cell carcinoma (HNSCC), cervical cancer, esophageal squamous cell carcinoma (ESCC) and glioma. ![]() Myo1b, an important member of class I myosins, is a single-headed membrane-associated motor that binds to actin filaments with a catch-bond behavior in response to load and participates in many critical physiological and pathological processes. Emerging evidence has revealed that myosins function as essential regulators of tumorigenesis, playing either oncogenic or tumor-suppressing roles. Myosins represent a large family of actin motor proteins that play key roles in regulating actin cytoskeleton architecture and dynamics. Moreover, tumor-induced angiogenesis is a key hallmark of carcinogenesis, which is also responsible for cancer cell growth and metastasis in CRC, and thus targeted antiangiogenic therapies have been a promising option for CRC treatment. In spite of the standard treatment including surgery, radiation, chemotherapy, there is still no valid and reliable means to improve the survival rate of CRC patients in advanced stages. Together, our study provided novel insights into the role of Myo1b in CRC progression and revealed that it might be a feasible predictive biomarker and promising therapeutic target for CRC patients.Ĭolorectal cancer (CRC) is the third most common cancer and the second leading cause for cancer-related death worldwide and its incidence is rising rapidly in young and middle-aged adults. Mechanistically, Myo1b blocked the autophagic degradation of HIF-1α and then led to the accumulation of HIF-1α, thus enhancing VEGF secretion and then promoting tumor angiogenesis in CRC. Further studies indicated that Myo1b inhibited the autophagosome-lysosome fusion and potentiated the VEGF secretion of CRC cells to promote angiogenesis. Conversely, silencing of Myo1b suppressed tumor progression both in vitro and in vivo. The overexpression of Myo1b promoted the proliferation, migration and invasion of CRC cells. ![]() Herein, we found that the expression of Myo1b was upregulated in CRC tissues and its high expression was correlated with worse survival. However, the functional mechanism of Myo1b in CRC angiogenesis and autophagy progression remains unclear. Mounting evidence suggests that the dysregulation of Myo1b expression has been extensively investigated in the development and progression of several tumors. Myosin 1b (Myo1b) is an important single-headed membrane-associated motor of class I myosins that participate in many critical physiological and pathological processes. ![]()
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