Sox11 has also been found to be expressed in multipotent stromal stem cells, and Sox11 knockdown leads to reduced proliferation and promotes differentiation. In contrast, knockdown of Sox11 in mantle cell lymphoma cell lines actually increases cell proliferation and promotes tumorigenesis when injected into nude mice. Therefore, while it is clear that Sox11 is involved in the regulation of the cell cycle, its ability to promote or inhibit Ruxolitinib cellular proliferation may in fact be influenced by the specific cellular environment in which it is expressed. In the case of spermatogonia, the reduction in Sox11 expression may increase cell proliferation by up regulating the expression of the downstream target Cyclin D1. Interestingly, this same protein also appears as a downstream target of the PTEN signalling cascade, suggesting convergence or cross-talk between these pathways may be important in driving the differentiation of gonocytes. The PTEN tumour suppressor Carfilzomib pathway was also predicted to contain members which were potential targets of differentially expressed miRNA. One of the possible outcomes from the PTEN signalling pathway is the modification of the cell cycle via the post translational regulation of Cyclin D1. Cyclin D1 is known to promote cell cycle progression from G1 to S phase, and its expression has previously been shown to occur in spermatogonia at post natal day 4 when the cell cycle has resumed. After post natal day 4 in the mouse testis, we propose that post-translational control of the activity of Cyclin D1 could be required to fine tune the cell cycle. The seven significantly different miRNA molecules between gonocytes and spermatogonia identified in this study have the potential to influence the activity of Cyclin D1. One down-regulated miRNA molecule targets the negative regulator of Cyclin D1 allowing its expression and therefore limiting the effect of Cyclin D1. At the same time the positive regulator of Cyclin D1, ERK1/2, is also theoretically targeted by an up-regulated miRNA molecule, which may result in a reduction of expression to limit the effect of Cyclin D1 on the cell cycle. Cyclin D1 has previously been shown to be an indirect target of miRNA via a different pathway. Using epithelial cells transformed by c-Myc, Feng et al demonstrated miR-378 was a direct target of c-Myc. miR-378 in turn cooperates with either RAS or HER2 to target the cell cycle repressor TOB2 which directly controls the expression of Cyclin D1. As Cyclin D1 is frequently over expressed in testicular germ cell tumours which have become resistant to cisplatin therapies, we concur with the hypothesis that the high levels of Cyclin D1 cause an accelerated cell cycle transition and limit the cells sensitivity to the chemotherapy agent.