Teijeiro Rosa, Rios Ramón, Costoya José A, Castro Ramón, Bello José L, Devesa Jesús, Arce Victor M
Departamento de Fisioloxía, Facultade de Medicina, Universidade de Santiago de Compostela, Rua San Francisco s/n, 15705 Santiago de Compostela, Spain.
Cell Physiol Biochem. 2002;12(1):31-8. doi: 10.1159/000047824.
The ability of both somatostatin (SS) and its stable analogues to inhibit cell growth depends on the stimulation of specific membrane receptors (SSTR1-5), which belong to the G protein-coupled receptor family. Accumulating evidence suggests that the SSTR2 plays a major role in mediating cell cycle arrest, and it is also clear that SHP-1, a cytoplasmic phosphotyrosine phosphatase (PTP), is an essential component of the SSTR2-mediated cytostatic effect. In contrast, the possibility that SSTR2 activation may also lead to increased apoptosis is still beyond debate, despite SHP-1 activation is also able to promote cell death in several cell types. In the present work we have investigated the ability of SSTR2 to induce apoptosis in HL-60 cells. We have found that HL-60 cells uniquely express the SSTR2 subtype, and that stimulation of SSTR2 with the SS analogue SMS 201-995 results in an increased cell death. In all, these findings demonstrate that activation of SSTR2 promotes apoptosis in HL-60 cells. Moreover, in contrast with the proapoptotic mechanism previously reported for SSTR3, cell death induced by activation of SSTR2 is independent from accumulation of p53.
生长抑素（SS）及其稳定类似物抑制细胞生长的能力取决于对特定膜受体（SSTR1 - 5）的刺激，这些受体属于G蛋白偶联受体家族。越来越多的证据表明，SSTR2在介导细胞周期停滞中起主要作用，并且很明显，SHP - 1，一种细胞质酪氨酸磷酸酶（PTP），是SSTR2介导的细胞生长抑制作用的重要组成部分。相比之下，尽管SHP - 1激活在几种细胞类型中也能够促进细胞死亡，但SSTR2激活也可能导致凋亡增加的可能性仍存在争议。在本研究中，我们研究了SSTR2在HL - 60细胞中诱导凋亡的能力。我们发现HL - 60细胞独特地表达SSTR2亚型，并且用SS类似物SMS 201 - 995刺激SSTR2会导致细胞死亡增加。总之，这些发现表明SSTR2的激活促进HL - 60细胞凋亡。此外，与先前报道的SSTR3的促凋亡机制相反，SSTR2激活诱导的细胞死亡与p53的积累无关。
