Gα13 和 Gα12 分别由 GNA13 和 GNA12 基因编码，是 Gα 蛋白 G12 家族的成员，与其相关的 Gβγ 亚基一起介导来自特定 G 蛋白偶联受体 (GPCR) 的信号传导。晚期前列腺癌的 GPCR 表达增加，例如 CXC 基序趋化因子受体 4 (CXCR4)、溶血磷脂酸受体 (LPAR) 和蛋白酶激活受体 1 (PAR-1)。这些 GPCR 通过 G12 家族或专门通过 Gα13 发出信号，通常除了其他 G 蛋白之外。 Gα13 的作用可能与 Gα12 的作用不同，并且 Gα13 在前列腺癌发生和进展中的作用很大程度上尚未被探索。 Gα13 对前列腺癌细胞迁移和侵袭的致癌作用已得到表征，但人们对线粒体功能和氧化应激等其他生物过程知之甚少。目前关于 Gα13 与氧化应激之间联系的知识基于动物研究，其中 GPCR-Gα13 信号传导降低了超氧化物水平，而组成型活性 Gα13 的过度表达促进了抗氧化基因激活。在人类样本中，线粒体超氧化物歧化酶 2 (SOD2) 与前列腺癌风险和预后格里森分级相关。然而，前列腺癌细胞中 SOD2 的过度表达在基础应激条件与氧化应激条件下对细胞生长和存活产生了相互矛盾的结果。因此，有必要探讨Gα13对前列腺癌肿瘤发生的影响，以及氧化应激条件下Gα13对前列腺癌细胞生长中SOD2的影响。

Gα13 and Gα12, encoded by the GNA13 and GNA12 genes, respectively, are members of the G12 family of Gα proteins that, along with their associated Gβγ subunits, mediate signaling from specific G protein-coupled receptors (GPCRs). Advanced prostate cancers have increased expression of GPCRs such as CXC Motif Chemokine Receptor 4 (CXCR4), lysophosphatidic acid receptor (LPAR), and protease activated receptor 1 (PAR-1). These GPCRs signal through either the G12 family, or through Gα13 exclusively, often in addition to other G proteins. The effect of Gα13 can be distinct from that of Gα12, and the role of Gα13 in prostate cancer initiation and progression is largely unexplored. The oncogenic effect of Gα13 on cell migration and invasion in prostate cancer has been characterized, but little is known about other biological processes such as mitochondrial function and oxidative stress. Current knowledge on the link between Gα13 and oxidative stress is based on animal studies in which GPCR-Gα13 signaling decreased superoxide levels, and the overexpression of constitutively active Gα13 promoted antioxidant gene activation. In human samples, mitochondrial superoxide dismutase 2 (SOD2) correlates with prostate cancer risk and prognostic Gleason grade. However, overexpression of SOD2 in prostate cancer cells yielded conflicting results on cell growth and survival under basal versus oxidative stress conditions. Hence, it is necessary to explore the effect of Gα13 on prostate cancer tumorigenesis, as well as the effect of Gα13 on SOD2 in prostate cancer cell growth under oxidative stress conditions.