Antagonist of Growth Hormone-Releasing Hormone Potentiates the Antitumor Effect of Pemetrexed and Cisplatin in Pleural Mesothelioma.
Iacopo GesmundoFrancesca PedrolliNicoletta VitaleAlessia BertoldoGiulia OrlandoDana BanfiGiuseppina GranatoRamesh KasarlaFederico BalzolaSilvia DeaglioRenzhi CaiWei ShaMauro PapottiEzio GhigoAndrew V SchallyRiccarda GranataPublished in: International journal of molecular sciences (2022)
Pleural mesothelioma (PM) is an aggressive cancer with poor prognosis and no effective therapies, mainly caused by exposure to asbestos. Antagonists of growth hormone-releasing hormone (GHRH) display strong antitumor effects in many experimental cancers, including lung cancer and mesothelioma. Here, we aimed to determine whether GHRH antagonist MIA-690 potentiates the antitumor effect of cisplatin and pemetrexed in PM. In vitro, MIA-690, in combination with cisplatin and pemetrexed, synergistically reduced cell viability, restrained cell proliferation and enhanced apoptosis, compared with drugs alone. In vivo, the same combination resulted in a strong growth inhibition of MSTO-211H xenografts, decreased tumor cell proliferation and increased apoptosis. Mechanistically, MIA-690, particularly with chemotherapeutic drugs, inhibited proliferative and oncogenic pathways, such as MAPK ERK1/2 and cMyc, and downregulated cyclin D1 and B1 mRNAs. Inflammatory pathways such as NF-kB and STAT3 were also reduced, as well as oxidative, angiogenic and tumorigenic markers (iNOS, COX-2, MMP2, MMP9 and HMGB1) and growth factors (VEGF and IGF-1). Overall, these findings strongly suggest that GHRH antagonists of MIA class, such as MIA-690, could increase the efficacy of standard therapy in PM.
Keyphrases
- growth hormone
- cell proliferation
- pi k akt
- cell cycle arrest
- poor prognosis
- small cell lung cancer
- oxidative stress
- signaling pathway
- particulate matter
- air pollution
- cell cycle
- advanced non small cell lung cancer
- long non coding rna
- polycyclic aromatic hydrocarbons
- heavy metals
- endoplasmic reticulum stress
- cell death
- squamous cell carcinoma
- cell migration
- endothelial cells
- vascular endothelial growth factor
- transcription factor
- squamous cell
- bone marrow
- lps induced
- nuclear factor
- immune response
- inflammatory response
- nitric oxide synthase
- binding protein