Ricerc@Sapienza

One of the major limits of chemotherapy is depending on the ability of the cancer cells
to elude and adapt to dierent drugs. Recently, we demonstrated how the activation of the M2
muscarinic receptor could impair neuroblastoma cell proliferation. In the present paper, we investigate
the possible eects mediated by the preferential M2 receptor agonist arecaidine propargyl ester (APE)
on drug resistance in two neuroblastoma cell lines, SK-N-BE and SK-N-BE(2C), a sub-clone presenting

Glioblastomas (GBM) are the most aggressive form of primary brain tumors in humans.
A key feature of malignant gliomas is their cellular heterogeneity. In particular, the presence of
an undierentiated cell population of defined Glioblastoma Stem cells (GSCs) was reported. Increased
expression of anti-apoptotic and chemo-resistance genes in GCSs subpopulation favors their high
resistance to a broad spectrum of drugs. Our previous studies showed the ability of M2 muscarinic

Glioblastoma (GBM) is the most aggressive human brain tumor. The high growth potential and decreased susceptibility to apoptosis of the glioma cells is mainly dependent on genetic amplifications or mutations of oncogenic or pro-apoptotic genes, respectively. We have previously shown that the activation of the M2 acetylcholine muscarinic receptors inhibited cell proliferation and induced apoptosis in two GBM cell lines and cancer stem cells. The aim of this study was to delve into the molecular mechanisms underlying the M2-mediated cell proliferation arrest.