Researchers have reported that zinc finger CCHC domain containing 12 gene (ZCCHC12) plays a role in the progression and tumorigenesis of papillary thyroid cancer. However, the biological role of ZCCHC12 in osteosarcoma (OS) remains unknown. ZCCHC12 was highly upregulated in OS cell lines according to our present study. Also, our subsequent assays demonstrated that ZCCHC12 enhanced the proliferation, tumor growth and migration of OS cells. Moreover, the epithelial-mesenchymal transition (EMT) of OS cells was also promoted by ZCCHC12. In addition, downregulation of ZCCHC12 induced apoptosis and S-phase arrest in OS cells. Then, our study indicated that ZCCHC12 exerts its oncogenic function in OS cells by activating the PI3K/AKT pathway. Inhibition of the PI3K/AKT pathway greatly limits the oncogenic function of ZCCHC12 in OS cells. Also, overexpression of ZCCHC12 promotes tumor growth in vivo. Altogether, our study suggests ZCCHC12 promotes OS cells progression by activating the PI3K/AKT pathway. The ZCCHC12 gene may be a novel diagnostic and therapeutic target for OS.

中文翻译：

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ZCCHC12通过PI3K/AKT通路促进骨肉瘤进展

研究人员报道，含有 12 基因的锌指 CCHC 结构域 (ZCCHC12) 在甲状腺乳头状癌的进展和肿瘤发生中发挥作用。然而，ZCCHC12 在骨肉瘤 (OS) 中的生物学作用仍然未知。根据我们目前的研究，ZCCHC12 在 OS 细胞系中被高度上调。此外，我们随后的测定表明 ZCCHC12 增强了 OS 细胞的增殖、肿瘤生长和迁移。此外，ZCCHC12 还促进了 OS 细胞的上皮-间质转化 (EMT)。此外，下调 ZCCHC12 可诱导 OS 细胞凋亡和 S 期停滞。然后，我们的研究表明 ZCCHC12 通过激活 PI3K/AKT 通路在 OS 细胞中发挥其致癌作用。抑制 PI3K/AKT 通路极大地限制了 ZCCHC12 在 OS 细胞中的致癌功能。还，体内。总之，我们的研究表明 ZCCHC12 通过激活 PI3K/AKT 通路促进 OS 细胞进展。ZCCHC12 基因可能是 OS 的新诊断和治疗靶点。