Polydopamine Nanoparticles Loaded with EPB41L4A-AS2 Promote Ovarian Cancer Cell Apoptosis Through Activation of Mitogen-Activated Protein Kinase Signaling Pathway

Author:

Wu Xiao-Ying1,Xing Xue-Feng1,An Ming1

Affiliation:

1. Obstetrics and Gynecology Department, Sanya People’s Hospital, Sanya, Hainan, 572000, China

Abstract

Ovarian cancer (OC) is one of known gynecologic malignant tumors, posing a serious threat to women’s life, and this disorder is often not diagnosed until it’s more advanced. This study aimed to identify the efficacy of polydopamine (PDA) nanoparticles loaded with EPB41L4A-AS2 (EPB) on OC. PDA nanoparticles-loaded EPB (PDA-EPB) were prepared, and OC cells were administrated with 10 μmol/LPDA-EPB nanoparticles or 10 μmol LHBSS buffer (control group). Untreated cells were taken as control group, and CCK-8 assay was conducted 24 h after treatments, to detect cell proliferation, while Transwell assay was used to detect invasion. Apoptosis was evaluated by flow cytometry along with analysis of Bax, Bcl-2, and caspase-3 apoptosis genes expression as well as the expression of Erk1/2, JNK, and p38 proteins. PDA-EPB nanomaterials presented uniform nanoparticle size of 100 nm and hydrated particle size of 190 nm. Treatment with composite nanoparticles decreased proliferation of OC cells over time. The increased concentration of nanoparticles occurred with decreased proliferation activity and 10 μmol/L was the best intervention concentration. Besides, PDA-EPB nanomaterials resulted in decreased number of invaded and migrated cells (41.03±3.95%) and increased apoptosis rate (33.59±3.23%), compared with the other two groups. The apoptosis ability was significantly higher, P < 0.05. Meanwhile, in the presence of PDA-EPB nanoparticles, the experimental group presented low expressions of Bad (1.96 ±0.23), Bcl-2 (1.56± 0.34), Caspase-3 (2.89± 0.28) and (0.98 ±0.39), JNK (0.53±0.31), and p38 (0.79±0.26). PDA-EPB nanoparticles therefore decreased cell proliferation and induced apoptosis through specifically binding to the MAPK signaling pathway to activate the expression of Erk1/2, JNK, and p38 in OC.

Publisher

American Scientific Publishers

Subject

General Materials Science

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