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Triple-negative breast cancers (TNBC) are a subtype of breast cancer lacking of estrogen receptor (ER), progesterone receptor (PR), and human EGF-like receptor 2 (HER2). MiR-193 always acted as an oncogene and promoted toxic aldehyde accumulation and tyrosine hydroxylase dysfunction. The purpose of this study is to explore the function of miR-193 in triple-negative breast cancer.Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the mRNA level of miR-193 expression in 50 cases of TNBC tissues and para-cancerous specimens. Also, the relation between miR-193 level and the overall survival of TNBC patient was analyzed. MiR-193 mimic and miR-193 inhibitor oligos, as well as the corresponding negative control, were synthesized from RiboBio (Guangzhou, China).MiR-193 expression was higher in triple-negative breast cancer tissues and cell lines than the corresponding adjacent non-tumor tissues and normal cell lines. Upregulation of miR-193 predicted poor prognosis of TNBC patients. Overexpression of miR-193 promoted cell proliferation and invasion, while that was suppressed by the knockdown of miR-193. MiR-193 binds to the 3'-UTR of an inhibitor of growth family member 5 (ING5) mRNA to mediate the expression of ING5 in TNBC cells. The knockdown of miR-193 inhibited cell invasion-mediated epithelial-mesenchymal transition (EMT). Furthermore, the knockdown of miR-193 suppressed cell proliferation through the ING5/phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) signal pathway.MiR-193 enhanced cell invasion-mediated EMT and improved cell proliferation through the ING5/PI3K/AKT signal pathway in triple-negative breast cancer. The newly identified miR-193/ING5/PI3K/AKT axis provides novel insight into the pathogenesis of triple-negative breast cancer.

Some circular RNAs (circRNAs) have been testified to play crucial roles in the regulation of skin melanoma, including circRNA_0016418 (circ0016418). However, the regulatory mechanism of circ0016418 in skin melanoma is undiscovered.The RNA expression was examined through quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and associated-proteins levels were measured via Western blot. Cell counting kit-8 (CCK-8) assay was used for detecting cell proliferation. Transwell assay was conducted to assess the abilities of migration and invasion. The target relation was analyzed by Dual-Luciferase reporter assay.The levels of circ0016418 and Yin Yang 1 (YY1) were up-regulated in skin melanoma tissues and cells. Knockdown of both circ0016418 and YY1 had suppressive effects on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of skin melanoma cells. YY1 overexpression reverted the inhibitory effects on skin melanoma cells caused by circ0016418 knockdown. Circ0016418 negatively modulated microRNA-625 (miR-625) expression and miR-625 directly targeted YY1. Circ0016418 functioned as a competitive endogenous RNA (ceRNA) of miR-625 to regulate YY1 expression.Circ0016418 regulated proliferation, migration, invasion, and EMT of skin melanoma cells through miR-625/YY1 axis. Circ0016418 might be a useful indicator of the therapeutic strategies of skin melanoma.

Accumulating evidence showed that dysregulation of cyclin-dependent kinases regulatory subunit 2 (CKS2) could contribute to tumor growth and metastasis of several tumors. However, its expression and function in epithelial ovarian cancer (EOC) have not been investigated. Here, we aimed to investigate the role of CKS2 in EOC.Real-time PCR and Western blotting were used to determine the mRNA and protein expression of CKS2 in EOC tissues and cell lines. Then, the associations of CKS2 expression with clinicopathological features and patient's overall survival were determined. Proliferation assay flow cytometric analysis and transwell assay were performed to detect the relation between CKS2 and malignant behaviors of EOC cells. We also evaluated the expression of related proteins of the Akt/mTOR pathway to determine the associated molecular mechanism.We found that CKS2 expression was significantly up-regulated in both EOC tissues and cell lines. Clinically, high expression of CKS2 was associated with advanced FIGO stage, histological grade and shorter overall survival of EOC patients. We also found that knockdown of CKS2 suppressed proliferation, invasion, and migration of EOC cells in vitro, and CKS2 could promote EMT progress by modulating EMT-related molecules. Finally, Western blot demonstrated that down-regulation of CKS2 suppressed the expression of p-Akt and p-mTOR.Our findings indicated that CKS2 might function as a tumor promoter by modulating Akt/mTOR pathway in EOC and could serve as a promising prognostic biomarker for EOC.

5-Aminolevulinic acid photodynamic therapy (5-ALA-PDT) for condylomata acuminate (CA) is effective and safe, but how this treatment affects immune reaction is poorly understood. We aimed to explore the effects of PDT on local immunity in CA.Immunohistochemical analysis before and after PDT was performed to analyze local changes in the distribution of T lymphocytes, CD123+ plasmacytoid dendritic cells (pDCs) and CD1a+ myeloid DCs. Quantitative Real-time PCR (qRT-PCR) was used to detect changes in mRNA levels of interferon (IFN), ISG-15, Mx-2, TLR9, and IRF7.Compared to the healthy foreskin, tissue from patient showed increased CD3+ and CD8+ cells but no significant changes in CD4+ cells or CD123+ pDCs, and a significantly decreased CD1a+ Langerhans cells (LCs). Twenty-four hours after a PDT session, local CD3+, CD4+, and CD123+ pDCs in lesions significantly increased and migrated to the superficial dermis. CD1a+ LCs in the epidermis gradually decreased, while DCs gradually increased. The number, distribution, and morphology of CD8+ cells did not change after a PDT session. The mRNA expressions of IFN-γ, IFN-α, IFN-β, ISG-15, Mx-2, TLR9, and IRF7 were all elevated. As compared to the patients without significantly increased IFN-a and IFN-b after a PDT session, patients with significant increases needed fewer sessions of PDT for a cure.These results suggest that PDT for CA can activate T-lymphocyte-meditated immunity, and pDC-related immunity is also activated. The clinical efficacy of 5-ALA-PDT against CA may be related to the increased IFN-α and IFN-β after treatment.