Abstract
Prostate carcinoma is a common malignant tumor of the male genitourinary system. Toosendanin can inhibit the biological behavior of a variety of malignant tumor cells (such as ovarian carcinoma, lung carcinoma, and breast carcinoma, etc.), but its effect on the malignant behavior of prostate carcinoma cells and its mechanism are not yet understood. Therefore, this article discusses the influence of toosendanin on the multiplication, apoptosis, migration, and invasion of prostate carcinoma cells and its possible mechanism. Different doses (0.125, 0.25, 0.5 ^M) of toosendanin can reduce the cell viability, number of colonies, number of migrating cells, number of invasive cells, and Bcl-2 protein and FOXC2-AS1 levels of prostate carcinoma cells, as well as increase the apoptosis rate and Bax protein level. Overexpression of FOXC2-AS1 can increase the cell viability, number of colonies formed, number of migrating cells, number of invasive cells, and Bcl-2 protein expression, as well as reduce the rate of apoptosis and Bax protein level after toosendanin treatment of prostate carcinoma cells. It was demonstrated that toosendanin may inhibit the multiplication, migration, and invasion of prostate carcinoma cells and promote its apoptosis by down-regulating FOXC2-AS1 expression.
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