Breast cancer (BC) is a malignant breast tumor confronted with high invasion, metastasis and recurrence rate, and adipocytes are the largest components in breast tissue. The aberrant adipocytes, especially the BC-neighbored cancer-associated adipocytes (CAAs), are found in the invasive front of BC. CAAs present a vicious phenotype compared with mature mammary adipocytes and mediate the crosstalk network between adipocytes and BC cells. By releasing multiple adipokines such as leptin, adiponectin, interleukin (IL)-6, chemokine ligand 2 (CCL2) and chemokine ligand 5 (CCL5), CAAs play essential roles in favor of proliferation, angiogenesis, dissemination, invasion and metastasis of BC. This article reviews the recent existing CAAs studies on the functions and mechanisms of adipocytes in the development of BC, including adipokine regulating, metabolic reprogramming, extracellular matrix (ECM) remodeling, microRNAs (miRNAs) and immune cell adjusting. Besides, adipocyte secretome and cellular interactions are implicated in the intervention to BC therapy and autologous fat grafting of breast reconstruction. Therefore, the potential functions and mechanisms of CAAs are very important for unveiling BC oncogenesis and progress. Deciphering the complex network between CAAs and BC is critical for designing therapeutic strategies and achieving the maximum therapeutic effects of BC.

Intratumoral hypoxia significantly constrains the susceptibility of solid tumors to oxygen-dependent photodynamic therapy (PDT), and effort to reverse such hypoxia has achieved limited success to date. Herein, we developed a novel engineered bacterial system capable of targeting hypoxic tumor tissues and efficiently mediating the photodynamic treatment of these tumors. For this system, we genetically engineered Escherichia coli to express catalase, after which we explored an electrostatic adsorption approach to link black phosphorus quantum dots (BPQDs) to the surface of these bacteria, thereby generating an engineered E. coli/BPQDs (EB) system. Following intravenous injection, EB was able to target hypoxic tumor tissues. Subsequent 660 nm laser irradiation drove EB to generate reactive oxygen species (ROS) and destroy the membranes of these bacteria, leading to the release of catalase that subsequently degrades hydrogen peroxide to yield oxygen. Increased oxygen levels alleviate intratumoral hypoxia, thereby enhancing BPQD-mediated photodynamic therapy. This system was able to efficiently kill tumor cells in vivo, exhibiting good therapeutic efficacy. In summary, this study is the first to report the utilization of engineered bacteria to facilitate PDT, and our results highlight new avenues for BPQD-mediated cancer treatment.

Breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is an uncommon type of T-cell lymphoma. Although with a low incidence, the epidemiological data raised the biosafety and health concerns of breast reconstruction and breast augmentation for BIA-ALCL. Emerging evidence confirms that genetic features, bacterial contamination, chronic inflammation, and textured breast implant are the relevant factors leading to the development of BIA-ALCL. Almost all reported cases with a medical history involve breast implants with a textured surface, which reflects the role of implant surface characteristics in BIA-ALCL. With this review, we expect to highlight the most significant features on etiology, pathogenesis, diagnosis, and therapy of BIA-ALCL, as well as we review the physical characteristics of breast implants and their potential pathogenic effect and hopefully provide a foundation for optimal choice of type of implant with minimal morbidity.

Purpose: The first case of coronavirus disease 2019 (COVID-19) was identified and confirmed in December 2019 in Wuhan, China. COVID-19 is gradually posing a serious threat to global public health. In this review the characteristics and mechanism of kidney injury caused by SARS-CoV, MERS-CoV and SARS-CoV-2 infection are summarized and contrasted. In particular, urine-oral transmission, prevention and management of the kidney injury caused by SARS-CoV-2 are emphasized. Materials and Methods: We searched PubMedÒ for English language articles published since 2003 with the keywords "SARS," "MERS," "COVID-19" or "kidney injury." ClinicalTrials.gov was queried for ongoing studies. We also used relevant data from websites, including the Centers for Disease Control and Prevention and European Centre for Disease Prevention and Control. Results: Similar to 2 other coronaviruses including SARS-CoV and MERS-CoV, SARS-CoV-2 caused severe respiratory syndrome with rapid progression and kidney injury. The infection process of SARS-CoV-2 is mediated by specifically binding to angiotensin-converting enzyme 2. Cases of COVID-19 combined with kidney impairment are associated with a higher risk of mortality than those without comorbidities. The pathological changes of the kidney are mainly due to local SARS-CoV-2 replication or indirectly by pro-inflammatory cytokine response. In addition, studies have confirmed the isolation of infectious SARS-CoV-2 in urine, raising the possibility of urine-oral transmission. Ultimately this is significant for preventing potential urine-oral transmission and improving the cure rate of acute kidney injury with COVID-19. Conclusions: Emerging evidence supports that in patients with SARS-CoV-2 infections the prevalence of kidney injury is high and usually leads to a poor prognosis. Optimal prevention and management of kidney injury will benefit patients with COVID-19.

BackgroundRefractory surface of wound and dermal chronic ulcer are largely attributed to poor neovascularization. We have previously shown that E2F1 suppresses VEGF expression in the ischemic heart, and that genetic deletion of E2F1 leads to better cardiac recovery. However, whether E2F1 has a role in dermal wound healing is currently not known.Methods and ResultsSkin wounds were surgically induced in E2F1-null (E2F1–/–) mice and WT littermates. E2F1–/– displayed an accelerated wound healing including wound closure, dermal thickening and collagen deposition, which was associated with an increased endothelial cell proliferation and greater vessel density in the border zone of the wound. Furthermore, more macrophages were recruited to the skin lesions and the level of VEGF expression was markedly higher in E2F1–/– than in WT mice.ConclusionsE2F1 hinders skin wound healing by suppressing VEGF expression, neovascularization, and macrophage recruitment. Strategies that target E2F1 may enhance wound healing.

Skin cancer is one of the primary causes of mortality worldwide. With an increasing frequency of skin cancers, there is an urgent requirement for the development of numerous treatment options. The present study investigated the anticancer activity of caffeic acid n-butyl ester (CAE) against the A431 skin cancer cell line. Antiproliferative effects were investigated using an MMT assay. Apoptosis was examined by DAPI and Annexin V/fluorescein isothiocyanate and propidium iodide staining. Reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cell cycle analyses were performed via flow cytometry. Protein expression was determined by western blotting. The findings of the present study demonstrated that among a variety of cancer cell lines, CAE exhibited significant anticancer activity against the A431 skin cancer cell line with a half-maximal inhibitory concentration of 20 µM. CAE was associated with apoptosis and cell cycle arrest of A431 cells, and induced ROS-mediated alterations in MMP. In addition, CAE considerably suppressed the expression of some of the important proteins of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) cascade. The results of the present study indicated that CAE exerted anticancer effects on the A431 skin carcinoma cell line via the induction of apoptosis and suppression of the PI3K/AKT/mTOR signaling pathway. Therefore, CAE may be beneficial for the development of chemotherapy for skin cancers.

Sonosensitizer-mediated sonodynamic therapy (SDT) has emerged as a promising anti-tumor strategy. However, this strategy of continuous oxygen consumption further exacerbates the hypoxic tumor microenvironment, which limits its therapeutic efficacy. In this study, we designed a multifunctional hydrogel (PB+Ce6@Hy) that simultaneously co-delivers nanozyme prussian blue (PB) and sonosensitizer chlorin e6 (Ce6) for the realization of photothermal therapy (PTT) and enhanced SDT. When the hydrogel reaches the tumor tissue through local injection, the 808 nm laser can induce the hydrogel to warm up and soften, thereby triggering the release of PB and Ce6. PB can interact with endogenous H2O2in situ and generate sufficient oxygen to promote the Ce6-mediated SDT effect. Besides, due to the good encapsulation ability of the hydrogel, the nanomaterials can be released in a controlled manner by changing laser parameter, irradiation time, etc. The experimental results show that the PB+Ce6@Hy system we developed can generate a large amount of reactive oxygen species (ROS), which can be combined with the photothermal effect to kill tumor cells, as a result, tumor proliferation has been adequately inhibited. This combined PTT/SDT dynamic strategy provides a new perspective for Ce6-induced cancer therapy, showing great potential for clinical application.

Wound healing is one of the most complex physiological regulation mechanisms of the human body. Stem cell technology has had a significant impact on regenerative medicine. Adipose stem cells (ASCs) have many advantages, including their ease of harvesting and high yield, rich content of cell components and cytokines, and strong practicability. They have rapidly become a favored tool in regenerative medicine. Here, we summarize the mechanism and clinical therapeutic potential of ASCs in wound repair.