Unipotent basal and luminal stem cells maintain prostate homeostasis, with an intermediate cell population emerging during prostate inflammation or cancer. However, the identities of basal stem cell and intermediate cell population remain unclear. Here we identified a rare intermediate cell population expressing luminal markers (termed Basal-B) with enhanced organoid formation capacity, and a larger basal population (termed Basal-A). Genetic lineage tracing revealed Basal-B cells represented a transient basal stem cell state during prostate homeostasis and androgen-mediated regeneration. Activated JAK/STAT signaling was identified in Basal-B cells, and its inhibition significantly reduced Basal-B markers expression. Inflammation increased Basal-B-to-luminal cell transdifferentiation, but JAK/STAT inhibition notably attenuated this effect. Pten gene deletion increased Nkx3.1-expressing Basal-B-like cell population and led to neoplasia. In humans, h-Basal-B cells were more prevalent in benign prostate hyperplasia. This study reveals the identities of intermediate Basal-B cells and underscores the role of JAK/STAT signaling in prostate cell fate determination.

单能基础干细胞和管腔干细胞维持前列腺稳态，在前列腺炎症或癌症期间出现中间细胞群。然而，基底干细胞和中间细胞群的身份仍不清楚。在这里，我们鉴定了一个罕见的中间细胞群，表达腔内标志物（称为 Basal-B），具有增强的类器官形成能力，以及一个更大的基础细胞群（称为 Basal-A）。遗传谱系追踪显示，基础 B 细胞在前列腺稳态和雄激素介导的再生过程中代表瞬时基础干细胞状态。在 Basal-B 细胞中鉴定出激活的 JAK/STAT 信号，其抑制显著降低 Basal-B 标志物的表达。炎症增加了基底 B 到管腔细胞的转分化，但 JAK/STAT 抑制显着减弱了这种影响。Pten 基因缺失增加了表达 Nkx3.1 的基础 B 样细胞群并导致肿瘤形成。在人类中，h-基础 B 细胞在良性前列腺增生中更为普遍。本研究揭示了中间基础 B 细胞的身份，并强调了 JAK/STAT 信号转导在前列腺细胞命运决定中的作用。