Ovarian cancer (OC) is one of the most common gynaecologic malignancies. Deleted in malignant brain tumors 1 (DMBT1) was considered as a tumour suppressor in multiple cancers, but there have been no systemic profiling studies of DMBT1 in OC until now. The aim of this study is to explore the role and the potential mechanism of DMBT1 in OC. mRNA levels and protein expressions of corresponding genes were detected by quantitative real‐time polymerase chain reaction and western blot. Cell proliferation was detected by CCK‐8 assay and cell colony formation. Cell migration and invasion were detected by wound healing and transwell assay. The combination between DMBT1 and galectin‐3 was demonstrated by immunoprecipitation. We demonstrated that DMBT1 was downregulated in OC cell lines, especially SKOV3 cells. Overexpression of DMBT1 significantly inhibited cell proliferation, colony formation, migration and invasion, as well as decreased Matrix Metalloproteinase‐2 (MMP‐2) and MMP‐7. DMBT1 caused a reduction of cell viability by treatment with cisplatin. Immunoprecipitation assay revealed a combination between DMBT1 and galectin‐3. DMBT1 could decrease the expression of galectin‐3 and inhibit the phosphorylation of PI3K and AKT, while overexpression of galectin‐3 reversed this effect. In summary, DMBT1 might inhibit the progression of OC and improve the sensitivity of SKOV3 cells to cisplatin through galectin‐3/PI3K/AKT pathway, giving a new insight into the role of DMBT1 in OC and enriching the potential strategies for OC treatment.

中文翻译：

---

DMBT1通过galectin-3 / PI3k / Akt途径抑制卵巢癌中的细胞增殖，迁移和侵袭，并增强对顺铂的敏感性。

卵巢癌（OC）是最常见的妇科恶性肿瘤之一。在恶性脑肿瘤中缺失1（DMBT1）被认为是多种癌症的肿瘤抑制因子，但迄今为止，在OC中尚未进行DMBT1的系统分析研究。这项研究的目的是探讨DMBT1在OC中的作用和潜在机制。通过定量实时聚合酶链反应和蛋白质印迹检测相应基因的mRNA水平和蛋白质表达。通过CCK-8测定和细胞集落形成来检测细胞增殖。通过伤口愈合和transwell分析检测细胞迁移和侵袭。免疫沉淀法证明了DMBT1和半乳凝素3之间的结合。我们证明了DMBT1在OC细胞系特别是SKOV3细胞中下调。DMBT1的过表达显着抑制细胞增殖，集落形成，迁移和侵袭，并降低基质金属蛋白酶-2（MMP-2）和MMP-7。DMBT1通过用顺铂处理导致细胞活力降低。免疫沉淀分析显示DMBT1和半乳凝素3之间存在结合。DMBT1可能会降低galectin-3的表达并抑制PI3K和AKT的磷酸化，而galectin-3的过表达则逆转了这种作用。综上所述，DMBT1可能通过galectin-3 / PI3K / AKT途径抑制OC的进程并提高SKOV3细胞对顺铂的敏感性，从而使DMBT1在OC中的作用有了新的认识，并丰富了OC治疗的潜在策略。以及基质金属蛋白酶-2（MMP-2）和MMP-7减少。DMBT1通过用顺铂处理导致细胞活力降低。免疫沉淀分析显示DMBT1和半乳凝素3之间存在结合。DMBT1可能会降低galectin-3的表达并抑制PI3K和AKT的磷酸化，而galectin-3的过表达则逆转了这种作用。综上所述，DMBT1可能通过galectin-3 / PI3K / AKT途径抑制OC的进程并提高SKOV3细胞对顺铂的敏感性，从而使DMBT1在OC中的作用有了新的认识，并丰富了OC治疗的潜在策略。以及基质金属蛋白酶-2（MMP-2）和MMP-7减少。DMBT1通过用顺铂处理导致细胞活力降低。免疫沉淀分析显示DMBT1和半乳凝素3之间存在结合。DMBT1可能会降低galectin-3的表达并抑制PI3K和AKT的磷酸化，而galectin-3的过表达则逆转了这种作用。综上所述，DMBT1可能通过galectin-3 / PI3K / AKT途径抑制OC的进程并提高SKOV3细胞对顺铂的敏感性，从而使DMBT1在OC中的作用有了新的认识，并丰富了OC治疗的潜在策略。DMBT1可能会降低galectin-3的表达并抑制PI3K和AKT的磷酸化，而galectin-3的过表达则逆转了这种作用。综上所述，DMBT1可能通过galectin-3 / PI3K / AKT途径抑制OC的进程并提高SKOV3细胞对顺铂的敏感性，从而使DMBT1在OC中的作用有了新的认识，并丰富了OC治疗的潜在策略。DMBT1可能会降低galectin-3的表达并抑制PI3K和AKT的磷酸化，而galectin-3的过表达则逆转了这种作用。综上所述，DMBT1可能通过galectin-3 / PI3K / AKT途径抑制OC的进程并提高SKOV3细胞对顺铂的敏感性，从而使DMBT1在OC中的作用有了新的认识，并丰富了OC治疗的潜在策略。