Li Yanhua, Chen Xia, Lu Hong
Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, P.R. China.
Oncol Res. 2016 Oct 27;24(6):511-519. doi: 10.3727/096504016X14719078133483.
The gene solute carrier family 34 (sodium phosphate), member 2 (SLC34A2), is a member of the SLC34 family. Increasing evidence suggests that SLC34A2 is involved in the development of many human carcinomas. However, its role in hepatocellular carcinoma (HCC) is still unclear. Therefore, in this study we investigated the role of SLC34A2 in HCC and explored the underlying mechanism. We found that the expression of SLC34A2 is upregulated in HCC cell lines. Knockdown of SLC34A2 obviously inhibited HCC cell proliferation, migration/invasion, and the epithelial-mesenchymal transition (EMT) phenotype. Furthermore, knockdown of SLC34A2 significantly inhibited the expression of phosphorylated PI3K and AKT in HCC cells. Taken together, these results suggest that knockdown of SLC34A2 inhibits proliferation and migration by suppressing activation of the PI3K/AKT signaling pathway in HCC cells, and SLC34A2 may be a potential therapeutic target for the treatment of HCC.
溶质载体家族34（磷酸钠）成员2基因（SLC34A2）是SLC34家族的一员。越来越多的证据表明，SLC34A2参与多种人类癌症的发生发展。然而，其在肝细胞癌（HCC）中的作用仍不清楚。因此，在本研究中，我们探究了SLC34A2在HCC中的作用，并探讨了其潜在机制。我们发现，SLC34A2在HCC细胞系中的表达上调。敲低SLC34A2明显抑制HCC细胞增殖、迁移/侵袭以及上皮-间质转化（EMT）表型。此外，敲低SLC34A2显著抑制HCC细胞中磷酸化PI3K和AKT的表达。综上所述，这些结果表明，敲低SLC34A2通过抑制HCC细胞中PI3K/AKT信号通路的激活来抑制增殖和迁移，并且SLC34A2可能是治疗HCC的一个潜在治疗靶点。
