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Curcumin [(1E,6E)‑1,7‑bis(4‑hydroxy‑3‑-methoxyphenyl) hepta‑1,6‑diene‑3,5‑dione] is a natural polyphenol that is derived from the turmeric plant (curcuma longa L.). Curcumin is widely used in food coloring, preservatives, and condiments. Curcumin possesses anti‑tumor, anti‑oxidative and anti‑inflammatory efficacy, as well as other pharmacological effects. Emerging evidence indicates that curcumin alters microRNAs (miRNAs) and long non‑coding RNAs (lncRNAs) in various types of cancers. Both miRNAs and lncRNAs are non‑coding RNAs that can epigenetically modulate the expression of multiple genes via post‑transcriptional regulation. In the present review, the interactions between curcumin and non‑coding RNAs are summarized in numerous types of cancers, including lung, colorectal, prostate, breast, nasopharyngeal, pancreatic, blood, and ovarian cancer, and the vital non‑coding RNAs and their downstream targets are described.

The inherent heterogeneity of individual cells in cell populations plays significant roles in disease development and progression, which is critical for disease diagnosis and treatment. Substantial evidences show that the majority of traditional gene profiling methods mask the difference of individual cells. Single cell sequencing can provide data to characterize the inherent heterogeneity of individual cells, and reveal complex and rare cell populations. Different microfluidic technologies have emerged for single cell researches and become the frontiers and hot topics over the past decade. In this review article, we introduce the processes of single cell sequencing, and review the principles of microfluidics for single cell analysis. Also, we discuss the common high-throughput single cell sequencing technologies along with their advantages and disadvantages. Lastly, microfluidics applications in single cell sequencing technology for the diagnosis of cancers and immune system diseases are briefly illustrated.

Exosomes play critical roles in regulating various physiological and pathological processes, including immune stimulation, immune suppression, cardiovascular diseases, and cancers. Recent studies show that exosomes that transport specific microRNAs (miRNAs) are involved in tumor development. However, the molecular mechanism by which tumor invasion and migration are regulated by exosomes from non-small cell lung cancer (NSCLC) is not well understood. Here, we show that exosomes shuttling low levels of miR-34c-3p are involved in NSCLC progression. Our results showed that exosomes derived from NSCLC cells carrying low levels of miR-34c-3p could be transported into the cytoplasm of NSCLC cells and accelerate NSCLC invasion and migration by upregulating integrin α2β1. A luciferase assay revealed that integrin α2β1 was the direct target of miR-34c-3p, and overexpression of integrin α2β1 could promote the invasion and migration of NSCLC cells. The analysis of exosomes derived from clinical serum samples indicated that the expression of miR-34c-3p was significantly downregulated in exosomes from NSCLC patients compared with that of normal controls. A549-derived exosomes promoted NSCLC cells lung metastases in vivo. Exosomes shuttling low levels of miR-34c-3p were associated with the progression of NSCLC in vitro and in vivo. Our data demonstrate that exosomes shuttling low levels of miR-34c-3p can accelerate the invasion and migration of NSCLC by upregulating integrin α2β1. MiR-34c-3p can be a diagnostic and prognostic marker for NSCLC. High expression of integrin α2β1 is positively related to the migration and metastasis of NSCLC cells.

Background: Non-small cell lung cancer (NSCLC) is considered one of the leading causes of cancer-related death. Despite the availability of drugs for the treatment of NSCLC, the need for the development of novel agents with high efficiency and fewer adverse effects remains unmet. The natural compound bruceine D (BD) is widely recognized for its notable anti-inflammatory, antiparasitic, and hypoglycemic activities. However, it is unclear whether BD can be used as a novel agent for NSCLC treatment. Materials and Methods: MTT and colony formation assays were used to assess the antiproliferative effect of BD on NSCLC cells. Wound healing and transwell assays were performed to determine the effect of BD on the migration and invasion of H1299 cells, respectively. Western blotting assay was used to detect the expression levels of proteins. Results: We demonstrated that BD significantly inhibited the proliferation of H1299, A549, and H226 cells with respective IC50 values of 6.06 ± 0.52, 7.15 ± 0.90, and 7.21 ± 0.75 μM. In addition, BD suppressed colony formation of H1299 cells in a dose-dependent manner. Following treatment with BD, the migration and invasive capabilities of H1299 cells were significantly inhibited in a dose- and time-dependent manner. Moreover, the results of Western blotting demonstrated that BD treatment resulted in the upregulation of the protein expression of E-cadherin and downregulation of the expression of N-cadherin, twist, snail, integrin αv, integrin β4, matrix metalloproteinase-7, and β-catenin proteins. Conclusion: BD inhibits proliferation, migration, and invasion of NSCLC cells; therefore, BD may be considered for its potential in adjuvant therapy for NSCLC.

Objective To compare the effect of cast immobilization with that of early Kiymil arkili emdew (Kazakh exercise therapy) on the post-operative healing of Achilles tendon rupture in rabbits, and to observe the influence of early Kiymil arkili emdew on the differentially expressed proteins in the healing tendon. Methods Forty-five New Zealand white rabbits were randomly divided into three groups (Arm A: control group; Arm B: postoperative immobilization group; and Arm C: postoperative early Kiymil arkili emdew group). After tenotomy, the rabbits of the two experimental groups received microsurgery to repair the ruptured tendons, and then received either cast immobilization or early Kiymil arkili emdew treatment. Achilles tendon tissue samples were collected 7 days after the surgery, and two-dimensional gel electrophoresis and MALDI-TOF-MS technique were used to analyze differentially expressed proteins in the tendon tissue of the three Arms. Results A total of 462.67±11.59, 532.33±27.79, and 515.33±6.56 protein spots were detected by the two-dimensional polyacrylamide gels in the Achilles tendon samples of the rabbits in Arms A, B, and C, respectively. Nineteen differentially expressed protein spots were randomly selected from Arm C. Among them, 7 were unique, and 15 had five times higher abundance than those in Arm B. These included annexin A2, gelsolin isoforms and a-1 Type III collagen. It was confirmed by western blot that gelsolin isoform b, annexin A2, etc. had specific and incremental expression in Arm C. Conclusion The self-protective instincts of humans were overlooked in the classical postoperative treatment for Achilles tendon rupture with cast immobilization. Kiymil arkili emdew induced the specific and incremental expression of proteins in the repaired Achilles tendon in the early healing stage in a rabbit model, compared with those treated with postoperative cast immobilization. These differentially expressed proteins may contribute to the healing of the Achilles tendon via a mechanobiological mechanism caused by the application of Kiymil arkili emdew.