Most male dogs are castrated at young ages, making them easy to rear following androgen deprivation. Although the incidence of canine prostate cancer is low, several patients have resistance to androgen therapy and poor clinical prognosis. These outcomes are similar to those of end‐stage human androgen‐independent prostate cancer. The androgen receptor (AR) of canines has two polyglutamine (polyQ) sequences (Q × 10 and Q × 23) at its N‐terminal. The length of polyQ may be a risk factor for the development of prostate cancer in dogs; however, there is no evidence to support this. Hence, we artificially created polyQ deletion mutants of canine AR and evaluated their effects on AR signalling. The deletions of Q × 10 and Q × 23 were associated with significant reductions in AR signalling intensities. The Q × 10 mutants, which increase or decrease Q sequentially, also altered AR signalling. Furthermore, the Q × 10 deletion mutant, compared with the Q × 10 control, altered the intensities of the binding of polyQ to the C‐terminal of AR, which contains a ligand‐binding domain; this was not observed with the Q × 9, 11, and 12 variants. The number of glutamines in the N‐terminals of canine ARs may influence AR signalling intensities and contribute to the risk of prostate cancer in dogs.

中文翻译：

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犬雄激素受体 N 端谷氨酰胺的数量影响信号强度

大多数雄性狗在年轻时就被阉割，这使得它们在雄激素剥夺后很容易饲养。虽然犬前列腺癌的发病率很低，但一些患者对雄激素治疗有抵抗力，临床预后较差。这些结果与终末期人类雄激素非依赖性前列腺癌的结果相似。犬类的雄激素受体 (AR) 在其 N 端具有两个多聚谷氨酰胺 (polyQ) 序列（Q × 10 和 Q × 23）。polyQ 的长度可能是狗患前列腺癌的危险因素；但是，没有证据支持这一点。因此，我们人为地创建了犬 AR 的 polyQ 缺失突变体，并评估了它们对 AR 信号传导的影响。Q × 10 和 Q × 23 的缺失与 AR 信号强度的显着降低有关。Q × 10 突变体，依次增加或减少 Q，也改变了 AR 信号。此外，与 Q × 10 对照相比，Q × 10 缺失突变体改变了 polyQ 与包含配体结合结构域的 AR C 端的结合强度；这在 Q × 9、11 和 12 变体中没有观察到。犬 AR 的 N 末端中谷氨酰胺的数量可能会影响 AR 信号强度并导致犬患前列腺癌的风险。