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In contrast, cyclin D1 had been upregulated in NSCLC, and cyclin D1 and MIR503HG were inversely correlated. In NSCLC cells, overexpression experiments disclosed that MIR503HG functioned as an upstream inhibitor of cyclin D1. MIR503HG overexpression led to G1 cell cycle arrest, while overexpression of cyclin D1 attenuated the consequences of MIR503HG overexpression. Similarly, MIR503HG overexpression resulted in decreased mobile proliferation price, while overexpression of cyclin D1 caused the increased
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