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首页> 外文期刊>Journal of Molecular Biochemistry >Somatostatin and Epidermal Growth Factor Receptors: Implications in Breast Cancer
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Somatostatin and Epidermal Growth Factor Receptors: Implications in Breast Cancer

机译：生长抑素和表皮生长因子受体：对乳腺癌的影响。

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Despite several advances, the underlying mechanism of complexity of breast cancer progression still remains elusive. In addition to the genetic predisposition, several growth factor receptors including insulin growth factor receptor (IGF), platelet derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) relaying proliferative signals are accountable for disease progression. Epidermal growth factor receptors (EGFRs, or commonly known as ErbBs), members of the receptor tyrosine kinase family (RTKs), play a central role in tumor growth, progression and metastatic disease. Typically, agonist dependent activation of EGFR results in receptor phosphorylation, homo- and/or heterodimerization and modulation of signaling pathways leading to cell proliferation, survival and metastasis. Targeting one or multiple steps in EGFR-mediated tumor progression may serve as a better approach in drug therapies. Unlike EGFRs, G-protein coupled somatostatin receptors (SSTRs) have been recognized as negative regulators of breast tumors. The activation of SSTRs modulates downstream signaling responsible for tumor growth and consequent cytostatic or cytotoxic effects on tumor proliferation. SSTR subtypes are well characterized to form homo-and/or heterodimers within the same family as well as with other GPCRs. Clinically, the chimeric molecule targeting both SSTR5 and dopamine receptors (specifically dopamine receptor 2) is in use for the treatment of pituitary tumors. This review describes the interplay between SSTRs and EGFR and the potential role of such cross talk in attenuation of EGFR-mediated signaling pathways involved in tumorigenesis. Furthermore, recent findings supporting the role of SSTR in EGFR-mediated signaling in tumor biology are discussed in detail.
机译：尽管取得了一些进展，但是乳腺癌进展复杂性的潜在机制仍然难以捉摸。除了遗传易感性之外，包括增生信号的胰岛素生长因子受体（IGF），血小板衍生生长因子（PDGF）和血管内皮生长因子（VEGF）在内的几种生长因子受体也可用于疾病进展。表皮生长因子受体（EGFRs，或通常称为ErbBs）是受体酪氨酸激酶家族（RTKs）的成员，在肿瘤生长，进展和转移性疾病中起着核心作用。通常，EGFR的激动剂依赖性激活导致受体磷酸化，均二和/或异二聚化以及信号传导途径的调节，从而导致细胞增殖，存活和转移。在EGFR介导的肿瘤进展中靶向一个或多个步骤可以作为药物治疗中的更好方法。与EGFR不同，G蛋白偶联的生长抑素受体（SSTR）被认为是乳腺肿瘤的负调节剂。 SSTR的激活调节下游信号传导，所述下游信号传导负责肿瘤生长以及随之而来的对肿瘤增殖的细胞抑制或细胞毒性作用。 SSTR亚型已被很好地表征，可以在同一家族以及其他GPCR中形成同型和/或异型二聚体。临床上，靶向SSTR5和多巴胺受体（特别是多巴胺受体2）的嵌合分子可用于垂体肿瘤的治疗。这篇综述描述了SSTR和EGFR之间的相互作用以及这种串扰在涉及肿瘤发生的EGFR介导的信号通路衰减中的潜在作用。此外，详细讨论了支持SSTR在EGFR介导的信号传导在肿瘤生物学中的作用的最新发现。

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