Semen affects the biological behavior of HeLa cells by altering ERK signaling

Abstract

The aim of the study was to investigate the effects of human semen on the proliferation, survival, migration and invasion of HeLa cervical cancer cells by analyzing the extracellular regulated protein kinase (ERK) pathway. Material and methods: HeLa cells were stimulated with different concentrations of human semen. MTT assay was used to analyze the effects on cell proliferation. Apoptosis in the different experimental groups was quantified by Annexin V-FITC/PI staining. The effect of seminal plasma on in vitro invasiveness of cells was evaluated using transwell assay. Western blotting was used to evaluate ERK pathway activation. Results: Human semen promoted HeLa cell proliferation; ERK1/2 phosphorylation and c-myc expression also increased with increasing semen concentration. U0126 inhibited semen-induced ERK1/2 phosphorylation, c-myc upregulation and cell proliferation. Compared with the control group, semen did not significantly affect the apoptotic rate of HeLa cells (p > 0.05). The transwell assays showed that compared with the control group, the number of invading cells increased significantly with increasing semen concentration, and the difference was significant (p < 0.05) when 1 : 50 semen was added, suggesting that semen promotes the invasion of cervical cancer cells. Western blotting indicated that ERK1/2 phosphorylation began to increase when 1 : 100 semen was added; with increasing semen concentration, ERK1/2 phosphorylation was significantly up-regulated, and the expression of its downstream target gene, c-myc, was also up-regulated (p < 0.05). Conclusions: Semen promoted the proliferation of HeLa cells by activating the ERK pathway and showed increased tumorigenic potential in vivo. Human seminal plasma might be a potential factor contributing to the development of cervical cancer.

Anti-tumor effects of isoliquiritigenin in Bcl-2/Bax and PCNA expression of T24 human bladder cancer cells

“…T24 cells exhibit typical morphology of apoptosis after treatment with ISL, including nuclear shrinkage, nuclear fragmentation, chromosome edge set, etc. It is speculated that the anti-tumor mechanism of ISL might be associated with the increase of CDK2 viability, the down-regulation of inner mitochondrial membrane potential (DeltaPsim), and activation of the caspase-3/9-mediated mitochondrial apoptotic signaling pathway [15][16][17][18], but the specific molecular mechanism of ISL in cancer treatment remains unclear.…”