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SDC2 Stabilization by USP14 Promotes Gastric Cancer Progression through Co-option of PDK1

文献类型： 外文期刊

作者： You, Li 1 ; Dou, Yi 1 ; Zhang, Yu 1 ; Xiao, Hongwei 3 ; Lv, Hong 2 ; Wei, Gong-Hong 1 ; Xu, Dazhi 1 ;

作者机构： 1.Fudan Univ, Dept Gastr Surg, Shanghai Canc, Shanghai 200032, Peoples R China

2.Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China

3.Hubei Acad Agr Sci, Inst Anim Husb & Vet, Key Lab Anim Embryo Engn & Mol Breeding Hubei Prov, Wuhan 430064, Peoples R China

4.Fudan Univ, Dept Pathol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China

5.Fudan Univ, MOE Key Lab Metab & Mol Med, Shanghai 200032, Peoples R China

6.Fudan Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Shanghai 200032, Peoples R China

7.Fudan Univ, Shanghai Med Coll Fudan Univ, Shanghai Canc Ctr, Shanghai 200032, Peoples R China

8.138 Med Coll Rd, Shanghai, Peoples R China

9.270 Dongan Rd, Shanghai, Peoples R China

关键词： Gastric cancer; SDC2; PDK1; FGF2; USP14

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES （ 影响因子：9.2； 五年影响因子：8.5 ）

ISSN： 1449-2288

年卷期： 2023 年 19 卷 11 期

页码：

收录情况： SCI

摘要： Gastric cancer (GC) is a common malignancy and remains the fourth-leading cause of cancer-related deaths worldwide. Oncogenic potential of SDC2 has been implicated in multiple types of cancers, yet its role and underlying molecular mechanisms in GC remain unknown. Here, we found that SDC2 was highly expressed in GC and its upregulation correlated with poor prognosis in GC patients. Depletion of SDC2 significantly suppressed the growth and invasive capability of GC cells, while overexpressing SDC2 exerts opposite effects. Combined bioinformatics and experimental analyses substantiated that overexpression of SDC2 activated the AKT signaling pathway in GC, mechanistically through the interaction between SDC2 and PDK1-PH domain, thereby facilitating PDK1 membrane translocation to promote AKT activation. Moreover, SDC2 could also function as a co-receptor for FGF2 and was profoundly involved in the FGF2-AKT signaling axis in GC. Lastly, we revealed a mechanism on the USP14-mediated stabilization of SDC2 that is likely to contribute to SDC2 upregulation in GC tissues. Furthermore, we showed that IU1, a potent USP14 inhibitor, decreased the abundance of SDC2 in GC cells. Our findings indicate that SDC2 functions as a novel GC oncogene and has potential utility as a diagnostic marker and therapeutic target for GC.

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