Despite advances in wound closure techniques and devices, there is still a critical need for new methods of enhancing the healing process to achieve optimal outcomes. Recently, stem cell therapy has emerged as a new approach to accelerate wound healing. Adipose-derived stem cells (ASCs) hold great promise for wound healing, because they are multipotential stem cells capable of differentiation into various cell lineages and secretion of angiogenic growth factors. The aim of this study was to evaluate the benefit of ASCs on wound healing and then investigate the probable mechanisms. ASCs characterized by flow cytometry were successfully isolated and cultured. An excisional wound healing model in rat was used to determine the effects of locally administered ASCs. The gross and histological results showed that ASCs significantly accelerated wound closure in normal and diabetic rat, including increased epithelialization and granulation tissue deposition. Furthermore, we applied GFP-labeled ASCs on wounds to determine whether ASCs could differentiate along multiple lineages of tissue regeneration in the specific microenvironment. Immunofluorescent analysis indicated that GFP-expressing ASCs were costained with pan-cytokeratin and CD31, respectively, indicating spontaneous site-specific differentiation into epithelial and endothelial lineages. These data suggest that ASCs not only contribute to cutaneous regeneration, but also participate in new vessels formation. Moreover, ASCs were found to secret angiogenic cytokines in vitro and in vivo, including VEGF, HGF, and FGF2, which increase neovascularization and enhance wound healing in injured tissues. In conclusion, our results demonstrate that ASC therapy could accelerate wound healing through differentiation and vasculogenesis and might represent a novel therapeutic approach in cutaneous wounds.

A series of polyesters, which are comprised of aromatic main chain backbones and flexible aliphatic side chains with 4-cyanobiphenyl end groups, has been synthesized based on a polycondensation of 2,2‘-bis(trifluoromethyl)-4,4‘-biphenyldiyldicarbonyl chloride with 2,2‘-bis{ω-[(4-(4-cyanophenyl)phenoxy]-n-alkoxy)carbonyl]}-4,4‘-biphenyldiol (PEFBP). For a PEFBP polyester containing eleven methylene units in the side chains, PEFBP(n = 11), multiple phase transitions can be found via differential scanning calorimetry during cooling and heating at varying rates. Different phase structures are identified by wide-angle X-ray diffraction and electron diffraction experiments, while morphologies of these ordered states are observed by polarized light and transmission electron microscopy. During cooling, a high temperature nematic (N) phase is formed at 193 °C independent of the cooling rate due to the combined orientational order of the cyanobiphenyl groups in the side chains and the aromatic polyester backbones. At a temperature of 90 °C, a new ordered low-temperature phase with an orthorhombic lattice (KO) starts to form at a cooling rate equal to or slower than 10 °C/min. However, the formation temperature of this phase is too close to the glass transition temperature (60 °C) to proceed to completion. Only at very slow heating rates (e.g., 1 °C/min), can the KO phase further develop. This phase melts at around 120 °C during heating and returns to the N phase. A new crystalline phase with a triclinic lattice at high temperatures (KT1) appears at 130 °C. It then transfers to a second triclinic crystalline phase (KT2). This KT2 phase melts at around 180 °C and, again, returns to the N phase. At 193 °C, isotropization occurs. This complicated phase behavior can be explained by the monotropic origin of the KO and KT1 phases with respect to the KT2 phase, which are metastable in the whole temperature region.

In the past few decades, apoptosis has been regarded as the only form of programmed cell death. However, the traditional view has been challenged by the identification of several forms of regulated necrosis, including necroptosis. Necroptosis is typified by a necrotic cell death morphology and is controlled by RIP1, RIP3, and mixed lineage kinase domain-like protein. The physiological role of necroptosis is to serve as a "fail-safe" form of cell death for cells that fail to undergo apoptosis during embryonic development and disease defense. Currently, established studies have indicated that necroptosis is involved in cancer initiation and progression. Although elevated necroptosis contributes to cancer cell death, extensive cell death also increases the risk of proliferation and metastasis of the surviving cells by inducing the generation reactive oxygen species, activation of inflammation, and suppression of the immune response. Thus, questions regarding the overall impact of necroptosis on cancer remain open. In this review, we introduce the basic knowledge regarding necroptosis, summarize its dual effects on cancer progression, and analyze its advantages and disadvantages in clinical applications.

MicroRNAs play an important role in the regulation of cancer migration, invasion and metastasis. Patients with triple-negative breast cancer (TNBC) have a high incidence of early relapse and metastasis; however, the molecular basis for metastasis and recurrence in these individuals remains largely unknown. Herein, we demonstrate that miR-136 is an anti-invasive microRNA in TNBC and suppresses mesenchymal invasion and metastasis. Our results demonstrated that miR-136 was downregulated in TNBC and negative correlated with the WHO grades. However, RASAL2 was identified as a functional target of miR-136, and was overexpressed in TNBC and correlates with pathological grades. Moreover, overexpression of RASAL2 in a breast cancer cell line rescued miR-136-mediated cell migration and invasion. In conclusion, these results indicate that the miR-136/RASAL2/MET axis act as a suppressor of TNBC metastasis.

The expressions of the CSC markers ABCB1, ABCG2, and CD133 differed in the gastric cancers with various degrees of differentiation, with poorly differentiated gastric cancer expressing relatively more CSC markers.