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We further showed that mPRα mediates the ability of P4 to inhibit the growth of lung adenocarcinoma cells through the following lines of evidence P4/Org inhibited the proliferation of lung adenocarcinoma cells; mPRα mediated the ability of P4/Org to inhibit lung adenocarcinoma cell proliferation; mPRα mediated the ability of P4/Org to inhibit the PKA (cAMP-dependent protein kinase)/CREB (cAMP responsive element binding protein) and PKA/β-catenin signaling pathways; and P4/Org inhibited the growth of a lung adenocarcinoma tumor model in vi
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