In summary, mutant SEMA3A is a vascular normalizing agent that can be exploited to treat cancer and, potentially, other diseases characterized by pathological angiogenesis.
Higher sema3A values were significantly correlated (P = 0.006) with presence of urothelial cancer, as determined by positive cystoscopy or urethroscopy and pathological biopsy.
The results indicate that miR-192-5p contributes to targeting SEMA3A in HCCLM3 cells, and this may be used as a target in targeted therapy and a marker for cancer behavior and prognosis.
In human breast cancer specimens, we found that immunohistochemical levels of SEMA3A correlated with the expression of genes characteristic of M1 macrophages, CD8(+) T cells, and NK cells, while inversely correlating with established characters of malignancy.
The expression levels of SEMA3A were lower in the cancer tissues with III/IV stage [the International Federation of Gynecology and Obstetrics (FIGO) stage], poor histological grade, lymph node metastasis and distant metastasis compared to that in the cancer tissues with I/II stage (FIGO), well histological grade, or without lymph node metastasis and distant metastasis (P<0.05).
Semaphorin3a (sema3a), a member of class 3 semaphorins, is a guidance protein that regulates angiogenesis, branching morphogenesis, axon growth, and cell migration, and has pleiotropic roles on organogenesis, immune response, and cancer.
Based on human tumor gene expression databases, HMGB1 was significantly inversely correlated with SEMA3A, suggesting that this mechanism may be more widely relevant in different cancer types.
Collapsin response mediator protein (CRMP) family proteins are cytosolic phosphoproteins involved in semaphorin 3A-mediated neuronal cell growth cone collapse and cancer invasion.
Although NP1 is expressed in carcinoma cells, its functions have remained elusive, and neither SEMA3A nor plexin expression has been explored in cancer.