Zn(II) porphyrin-encapsulated MIL-101 for photodynamic therapy of breast cancer cells.

The photodynamic treatment is a non-aggressive and clinically accepted procedure for removing selected cancer cells with the activation of a photosensitizer agent at a specific light. In this study, the zinc porphyrin (Zn[TPP]) was prepared and encapsulated into the MIL-101 (Zn[TPP]@MIL-101). It was used in photodynamic therapy (PDT) against MCF-7 breast cancer cells under a red light-emitting diode. The structure, morphology, surface area, and compositional changes were investigated using conventional characterization methods including FTIR, FESEM, EDX, and BET analyses. The MTT assay was performed under light and dark conditions to explore the ability of Zn[TPP]@MIL-101 in PDT. The results have demonstrated the IC50 of 14.3 and 81.6 mg/mL for light and dark groups, respectively. As the IC50 revealed, the Zn[TPP]@MIL-101 could efficiently eradicate cancer cells using PDT.

Current concepts of microRNA-mediated regulatory mechanisms in human pulp tissue-derived stem cells: a snapshot in the regenerative dentistry.

One of the most studied class of non-coding RNAs is microRNAs (miRNAs) which regulate more than 60% of human genes. A network of miRNA gene interactions participates in stem cell self-renewal, proliferation, migration, apoptosis, immunomodulation, and differentiation. Human pulp tissue-derived stem cells (PSCs) are an attractive source of dental mesenchymal stem cells (MSCs) which comprise human dental pulp stem cells (hDPSCs) obtained from the dental pulp of permanent teeth and stem cells isolated from exfoliated deciduous teeth (SHEDs) that would be a therapeutic opportunity in stomatognathic system reconstruction and repair of other damaged tissues. The regenerative capacity of hDPSCs and SHEDs is mediated by osteogenic, odontogenic, myogenic, neurogenic, angiogenic differentiation, and immunomodulatory function. Multi-lineage differentiation of PSCs can be induced or inhibited by the interaction of miRNAs with their target genes. Manipulating the expression of functional miRNAs in PSCs by mimicking miRNAs or inhibiting miRNAs emerged as a therapeutic tool in the clinical translation. However, the effectiveness and safety of miRNA-based therapeutics, besides higher stability, biocompatibility, less off-target effects, and immunologic reactions, have received particular attention. This review aimed to comprehensively overview the molecular mechanisms underlying miRNA-modified PSCs as a futuristic therapeutic option in regenerative dentistry.

An in vitro model for investigation of vitamin A effects on wound healing.

Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1-5 µM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

Gold Nanoparticles Conjugated L-Lysine for Improving Cisplatin Delivery to Human Breast Cancer Cells.

INTRODUCTION: Nano drug delivery is a broad field of research on the development of novel nano- carrier systems for effective therapeutic delivery of drugs. Here, an anticancer drug, cisplatin (CDDP) conjugated Gold Nanoparticles (GNPs) via L-Lysine (Lys) linker. METHODS: The produced nanodrug (GNPs-Lys-CDDP) was characterized by UV-Vis spectroscopy, Dynamic Light Scattering (DLS), Zeta potentials and electron force microscopy. The cytotoxic efficacy of the GNPs-Lys-CDDP against human breast cancer cells (SKBR3) and normal cells (MCF- 10A) was evaluatedby MTT assay. Cell apoptosis and morphology changes were assessed by flowcytometery and Acridine Orange/Ethidium Bromide (AO/EtBr) staining, respectively. RESULTS: It was found that the GNPs-Lys-CDDP with a size of 85 nm and negatively charged with a zeta-potential of about -25 mV could be taken up by tumor cells. A marked change in the UV spectrum of GNPs-Lys-CDDP compare to GNPs showed a strong absorption shift in the 525 nm region. The LD 50 of GNPs-Lys-CDDP against SKBR3 (1 µg.mL -1), was found to be 8 times lower than that of naked CDDP against SKBR3 (8 µg.mL -1). The nanocomplex GNPs-Lys-CDDP also significantly increased the apoptosis of SKBR3 with the lowest cytotoxic effects on normal cells. DISCUSSION: This work indicates that GNPs effectively could decrease the lethal dose of CDDP to 87%. Hence, GNPs modified by Lys, could be a good nano-carrier for chemotherapeutic drugs.

Angioregulatory microRNAs in Colorectal Cancer.

Colorectal cancer (CRC) is one of the leading causes of cancer mortality. Angiogenesis is a rate-determining step in CRC development and metastasis. The balance of angiogenic and antiangiogenic factors is crucial in this process. Angiogenesis-related genes can be regulated post-transcriptionally by microRNAs (miRNAs) and some miRNAs have been shown to shuttle between tumor cells and the tumor microenvironment (TME). MiRNAs have context-dependent actions and can promote or suppress angiogenesis dependent on the type of cancer. On the one hand, miRNAs downregulate anti-angiogenic targets and lead to angiogenesis induction. Tumor suppressor miRNAs, on the other hand, enhance anti-angiogenic response by targeting pro-angiogenic factors. Understanding the interaction between these miRNAs and their target mRNAs will help to unravel molecular mechanisms involved in CRC progression. The aim of this article is to review the current literature on angioregulatory miRNAs in CRC.