MON-536 SPOCK1 Promotes the Progression of Papillary Thyroid Cancer ViaPI3K/Akt Signaling Activation

With the increasing incidence, thyroid cancer as one of the most common malignancy, has got widespread attention during the past few years. Papillary thyroid cancer (PTC) is the most common thyroid cancer type. Understanding the underlining molecular mechanisms of PTC is of great interest. The oncogenic role of SPARC/osteonectin, cwcv, and kazal-like domain proteoglycan 1 (SPOCK1) has been demonstrated in several cancers, however, the clinical and functional significance of SPOCK1 in PTC are largely unknown. Here, we found that the expression of SPOCK1 was upregulated in PTC tissues when comparing with the adjacent normal thyroid tissues. The overexpression of SPOCK1 was associated with the clinicopathological characteristics of the patients with PTC. We demonstrated that the proliferation of PTC cells was significantly promoted and the apoptosis of PTC cells was significantly inhibited in cells with overexpression of SPOCK1. Furthermore, we showed that knockdown of SPOCK1 arrested the cell cycle in G0/G1 phase and promoted the apoptosis in PTC cell lines. Importantly, our data suggested that SPOCK1 promoted the progression of PTC cell via regulating the PI3K/Akt signaling pathway. Taking together, our findings demonstrate that SPOCK1 enhances the activation of PI3K/Akt signaling pathway, thereby promoting the proliferation and inhibiting the apoptosis of PTC cells.