Injectable platelet rich fibrin facilitates hair follicle regeneration by promoting human dermal papilla cell proliferation, migration, and trichogenic inductivity.

Hair follicle regeneration has been successful in mice but failed in human being for years. Dermal papilla cells, a specialized mesenchymal stem cell derived from dermal papilla within hair follicles, is considered the key cells for hair follicle regeneration function as both regeneration initiator and regulator. Injectable platelet rich fibrin (i-PRF), a novel biomaterial rich in a variety of growth factors and three-dimensional scaffolds, has shown promising effects on tissue regeneration. In this study, we aimed to evaluate the application of i-PRF in human hair follicle regeneration by examining the biological effects of i-PRF on human dermal papilla cells (hDPCs). Biomaterial compatibility, cell viability, proliferation, migration, alkaline phosphatase activity and trichogenic inductivity were assessed after exposing hDPCs to different concentrations of i-PRF extracts. In addition, we investigated the ultrastructure of i-PRF with all cell components filtered. The results revealed that i-PRF possessing excellent biocompatibility and could significantly promote hDPCs proliferation, migration, and trichogenic inductivity. Furthermore, the concentration of i-PRF is able to remarkably influence hDPCs behavior in a dose-dependent pattern. Different concentrations exhibited differential effects on hDPCs behavior. In general, lower concentration promotes cell proliferation better than higher concentration, while higher concentration promotes cell function better reversely. Best concentration for hDPCs in vitro expending is 1% concentration. 20% concentration is optimal for hair follicle regeneration. In summary, our findings concluded that i-PRF facilitates hair follicle regeneration by promoting human dermal papilla cell proliferation, migration, and trichogenic inductivity.

[Retracted] MicroRNA­675 inhibits cell proliferation and invasion in melanoma by directly targeting metadherin.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the western blotting data shown in Fig. 5A and the cell migration and invasion assay data shown in Fig. 5C were strikingly similar to data appearing in different form in other articles by different authors at different research institutes, several of which have been retracted. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 3372­3379, 2018; DOI: 10.3892/mmr.2017.8264].

MicroRNA­675 inhibits cell proliferation and invasion in melanoma by directly targeting metadherin.

Melanoma is derived from melanocytes and accounts for ~80% of skin cancer-associated fatalities worldwide. The dysregulation of microRNAs (miRNAs/miRs) is involved in the development and progression of melanoma. Therefore, miRNAs may be novel diagnostic or prognostic biomarkers and promising therapeutic targets in the treatment of patients with melanoma. miR­675 is differentially expressed in several types of human cancer and has important roles in the pathogenesis of several diseases. However, the expression levels and the biological roles of miR­675 in melanoma remain unclear. Therefore, the present study aimed to assess the expression of miR­675 in melanoma, explore the effects of miR­675 on melanoma cells and investigate the underlying molecular mechanisms that may be involved in the actions of miR­675. The present study indicated that miR­675 expression was downregulated in melanoma tissues and cell lines. Functional assays demonstrated that the upregulation of miR­675 impaired cell proliferation and invasion in melanoma. Bioinformatics analysis, luciferase reporter assay, reverse transcription­quantitative polymerase chain reaction and western blot analysis demonstrated that metadherin (MTDH) was a direct target of miR­675 in melanoma. The MTDH levels were upregulated in melanoma tissues and inversely correlated with the miR­675 expression. Furthermore, restored MTDH expression rescued the inhibition effects in melanoma cells caused by miR­675 overexpression. Thus, miR­675 may be a potential therapeutic target for melanoma.