The antiproliferative action of [D-ARG1,D-PHE5,D-TRP7,9,LEU11] substance p analogue antagonist against small cell- and non-smallcell lung cancer cells could be due to the pharmacological profile of its tachykinin receptor antagonist

It is known that in human lung cancer samples,both small-cell lung cancer (sclc) and non-small-cell lung cancer (nsclc) cells express the neurokinin-1 (nk-1) receptor; that after binding to the nk-1 receptor the peptide substance p (sp) elicits tumour cell proliferation and an antiapoptotic effect. by contrast,it has been demonstrated that non-peptide nk-1 receptor antagonists,after binding to the nk-1 receptor and hence by blocking the sp action in sclc/nsclc,exert an antiproliferative action (inhibit lung cancer cell proliferation and induce the death of tumour cells by apoptosis). it is also known that sp peptide nk-1 receptor antagonists also called sp analogue antagonists (broad-spectrum gpcr antagonists,broad-spectrum neuropeptide antagonists or synthetic analogues of sp),also exert antiproliferative actions against sclc/nsclc. however,the underlying mechanisms involved in this antiproliferative action remain unknown. by using competition assays with sp,here we demonstrate that the antiproliferative action exerted by the [d-arg1,dphe5,d-trp7,9,leu11] sp analogue on human h-69 sclc and cor-l23 nsclc cell lines,occurs at least through the nk-1 receptor. © 2015 polish physiological society. all rights reserved.