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SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study.

ABSTRACT: Serpin family D member 1 (SERPIND1) belongs to the serine protease inhibitor family. Its role in cancers has gradually attracted interest from researchers in recent years. However, the role of SERPIND1 in the development of epithelial ovarian cancer remains poorly understood. This studied aimed to investigate the expression and clinical significance of SERPIND1 in epithelial ovarian cancer, as well as its effect on the malignant biological behavior of ovarian cancer cells and the related regulatory mechanisms. We found that SERPIND1 expression was significantly elevated in epithelial ovarian cancer. Patients with higher expression of SERPIND1 in ovarian cancer tissues had poor prognoses. SERPIND1 promoted the proliferation, migration, invasion, G1-to-S phase transition, and epithelial-mesenchymal transition of ovarian cancer cells and inhibited their apoptosis by promoting phosphorylation in the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway. Meanwhile, the inhibition of SERPIND1 expression in ovarian cancer cells resulted in opposite effects. The addition of the PI3K/AKT pathway inhibitor LY294002 to SERPIND1-overexpressing cells could reverse the promoting effect of SERPIND1 on the malignant biological behavior of ovarian cancer cells. Further, nuclear factor kappa B subunit 1, a transcription factor could bind to the promoter region of SERPIND1 and regulate SERPIND1 expression. In conclusion, our results indicated that SERPIND1 could be an effective marker for assessing the prognosis of ovarian cancer. By elucidating its mechanism underlying the promotion of malignant biological behavior of ovarian cancer by SERPIND1, we demonstrated that SERPIND1 could potentially serve as a novel drug target.

SUBMITTER: Guo Q

PROVIDER: S-EPMC6788328 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study.

Guo Qian Q Zhu Liancheng L Wang Caixia C Wang Shuang S Nie Xin X Liu Juanjuan J Liu Qing Q Hao Yingying Y Li Xiao X Lin Bei B

Frontiers in oncology 20191004

Serpin family D member 1 (SERPIND1) belongs to the serine protease inhibitor family. Its role in cancers has gradually attracted interest from researchers in recent years. However, the role of SERPIND1 in the development of epithelial ovarian cancer remains poorly understood. This studied aimed to investigate the expression and clinical significance of SERPIND1 in epithelial ovarian cancer, as well as its effect on the malignant biological behavior of ovarian cancer cells and the related regulat ...[more]

PMID: 31637210

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Project description:BackgroundCC chemokine receptor 9 (CCR9), an organ-specific chemokine receptor, interacts with its exclusive ligand CCL25 to promote tumor proliferation and metastasis. However, the effect of CCR9 on salivary adenoid cystic carcinoma (SACC) malignant behavior remains unknown. This study aimed to investigate the specific molecular mechanism by which CCR9/CCL25 modulates malignant progression in SACC.MethodsImmunohistochemistry staining and RT-qPCR analyses were performed to detect the correlation of CCR9 expression and tumor progression-associated markers in SACC. In vitro, SACC cell proliferation and apoptosis were evaluated using Cell Counting Kit-8 and colon formation, and cell migration and invasion were detected by wound healing and transwell assays. Vercirnon was used as an inhibitor of CCR9, and LY294002 was used as an inhibitor of the PI3K/AKT pathway in this study. Western blot and RT-qPCR assays were carried out to measure the downstream factors of the interaction of CCL25 and CCR9. The effect of CCL25 on the development of SACC in vivo was examined by a xenograft tumor model in nude mice following CCL25, Vercirnon and LY294002 treatment.ResultsCCR9 was highly expressed in SACC compared with adjacent salivary gland tissues, and its level was associated with tumor proliferation and metastases. CCL25 enhanced cell proliferation, migration, and invasion through its interaction with CCR9 and exerted an antiapoptotic effect on SACC cells. Targeting CCR9 via Vercirnon significantly reduced the phosphorylation level of AKT induced by CCL25. CCL25/CCR9 could activate its downstream factors through the PI3K/AKT signaling pathway, such as cyclin D1, BCL2 and SLUG, thus promoting SACC cell proliferation, antiapoptosis, invasion and metastasis. The in vivo data from the xenograft mouse models further proved that CCL25 administration promoted malignant tumor progression by activating the PI3K/AKT pathway.ConclusionThe interaction of CCL25 and CCR9 promotes tumor growth and metastasis in SACC by activating the PI3K/AKT signaling pathway, offering a promising strategy for SACC treatment.

Dataset Information

SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study.

Publications

SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study.

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