Estrogen receptor β2 inhibits growth of lung transplantation tumors in mice by upregulating P38 mitogen-activated protein kinase

Objective: The purpose of this study was to further observe the function of ER beta 2 in lung cancer, examining its relationship with p38MAPK in vivo. Methods: A549/H358/LTEP-a2 cells were used to construct nude mice transplanted tumor models by subcutaneous implantation. Moreover, hER beta 2, iER beta 2, hp38MAPK, hER beta 2+SB, iER beta 2+hp38MAPK, and empty groups were set. The weights of the mice and volumes of the transplanted tumors were measured each week. Growth curve was also measured. Expression of relevant proteins in the transplanted tumors was detected by IHC and WB. Results: Tumors in the hER beta 2 group had slow growth, significantly more than that of empty and iER beta 2 groups. The specific inhibitor of p38MAPK could reverse the effects of hER beta 2 on tumor growth. Compared with the empty group, weights and transplanted tumor volumes of nude mice in the iER beta 2 group had a significant increase. This effect could be reversed by increasing expression of p38MAPK. Accordingto IHC and WB analysis, p38MAPK expression was significantly increased and bcl-2 expression was decreased in the hER beta 2 group, compared to the empty group. p38MAPK specific inhibitor increased bcl-2 expression in the hER beta 2 group, whereas in the iER beta 2 group, the reverse effects were observed. p38MAPK was decreased and bcl-2 protein was significantly increased, which was also disturbed by p38MAPK. Conclusion: ER beta 2 high expression may have the function of inhibiting the progression of lung cancer through the upregulation of p38MAPK and inhibition of bcl-2 expression.