Ibanez-Costa, AlejandroRivero-Cortes, EstherVazquez-Borrego, Mari C.Gahete, Manuel D.Jimenez-Reina, LuisVenegas-Moreno, Evade la Riva, AndresAngel Arraez, MiguelGonzalez-Molero, InmaculadaSchmid, Herbert A.Maraver-Selfa, SilviaGavilan-Villarejo, InmaculadaAntonio Garcia-Arnes, JuanJapon, Miguel A.Soto-Moreno, AlfonsoGalvez, Maria A.Luque, Raul M.Castano, Justo P.2023-02-122023-02-122016-09-01Ibáñez-Costa A, Rivero-Cortés E, Vázquez-Borrego MC, Gahete MD, Jiménez-Reina L, Venegas-Moreno E, et al. Octreotide and pasireotide (dis)similarly inhibit pituitary tumor cells in vitro. J Endocrinol. 2016 Nov;231(2):135-1450022-0795http://hdl.handle.net/10668/19187Somatostatin analogs (SSA) are the mainstay of pharmacological treatment for pituitary adenomas. However, some patients escape from therapy with octreotide, a somatostatin receptor 2 (sst2)-preferring SSA, and pasireotide, a novel multi-sst-preferring SSA, may help to overcome this problem. It has been proposed that correspondence between sst1-sst5 expression pattern and SSA-binding profile could predict patient's response. To explore the cellular/molecular features associated with octreotide/pasireotide response, we performed a parallel comparison of their in vitro effects, evaluating sst1-sst5 expression, intracellular Ca2+ signaling ([Ca2+](i)), hormone secretion and cell viability, in a series of 85 pituitary samples. Somatotropinomas expressed sst5>sst2, yet octreotide reduced [Ca2+](i) more efficiently than pasireotide, while both SSA similarly decreased growth hormone release/expression and viability. Corticotropinomas predominantly expressed sst5, but displayed limited response to pasireotide, while octreotide reduced functional endpoints. Non-functioning adenomas preferentially expressed sst3 but, surprisingly, both SSA increased cell viability. Prolactinomas mainly expressed sst1 but were virtually unresponsive to SSA. Finally, both SSA decreased [Ca2+](i) in normal pituitaries. In conclusion, both SSA act in vitro on pituitary adenomas exerting both similar and distinct effects; however, no evident correspondence was found with the sst1-sst5 profile. Thus, it seems plausible that additional factors, besides the simple abundance of a given sst, critically influence the SSA response.enGrowth-hormoneReceptor subtypesQuantitative-analysisAggressive featuresMedical-treatmentCushings-diseaseActh releaseAdenomasPituitaryPituitary adenomaSomatostatinGene expressionCell signalingSomatostatin analog som230Gene-expression levelsresearch articleopen accessExpresión génicaGenesNeoplasias hipofisariasSomatostatinaTransducción de señal10.1530/JOE-16-03321479-6805https://joe.bioscientifica.com/downloadpdf/journals/joe/231/2/135.pdf385951600005