The stem cell niche normally prevents aberrant stem cell behaviors that lead to cancer formation. Recent studies suggest that some cancers are derived from endogenous populations of adult stem cells that have somehow escaped from normal control by the niche. However, the molecular mechanisms by which the niche retains stem cells locally and tightly controls their divisions are poorly understood. Here, we demonstrate that the presence of heparan sulfate (HS), a class glygosaminoglycan chains, in the Drosophila germline stem cell niche prevents tumor formation in the testis. Loss of HS in the niche, called the hub, led to gross changes in the morphology of testes as well as the formation of both somatic and germline tumors. This loss of hub HS resulted in ectopic signaling events in the Jak/Stat pathway outside the niche. This ectopic Jak/Stat signaling disrupted normal somatic cell differentiation, leading to the formation of tumors. Our finding indicates a novel non-autonomous role for niche HS in ensuring the integrity of the niche and preventing tumor formation.

中文翻译：

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生态位中硫酸乙酰肝素的损失导致果蝇睾丸中的肿瘤样生殖细胞生长

干细胞小生境通常可防止导致癌症形成的异常干细胞行为。最近的研究表明，某些癌症源自成年干细胞的内源性种群，这些成年干细胞以某种方式脱离了正常控制。但是，关于生态位使干细胞局部保留并严格控制其分裂的分子机制了解甚少。在这里，我们证明了果蝇中一类糖胺聚糖链硫酸乙酰肝素（HS）的存在种系干细胞生态位可防止睾丸中的肿瘤形成。在称为枢纽的小生境中，HS的丧失导致睾丸形态的重大变化以及体细胞和种系肿瘤的形成。集线器HS的这种损失导致利基外Jak / Stat通路中的异位信号事件。这种异位的Jak / Stat信号传导破坏了正常的体细胞分化，导致了肿瘤的形成。我们的发现表明，小生境HS在确保小生境的完整性和防止肿瘤形成方面具有新型的非自治作用。