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The latest progress on miR-374 and its functional implications in physiological and pathological processes.
Bian, H, Zhou, Y, Zhou, D, Zhang, Y, Shang, D, Qi, J
Journal of cellular and molecular medicine. 2019;(5):3063-3076
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Abstract
Non-coding RNAs (ncRNAs) have been emerging players in cell development, differentiation, proliferation and apoptosis. Based on their differences in length and structure, they are subdivided into several categories including long non-coding RNAs (lncRNAs >200nt), stable non-coding RNAs (60-300nt), microRNAs (miRs or miRNAs, 18-24nt), circular RNAs, piwi-interacting RNAs (26-31nt) and small interfering RNAs (about 21nt). Therein, miRNAs not only directly regulate gene expression through pairing of nucleotide bases between the miRNA sequence and a specific mRNA that leads to the translational repression or degradation of the target mRNA, but also indirectly affect the function of downstream genes through interactions with lncRNAs and circRNAs. The latest studies have highlighted their importance in physiological and pathological processes. MiR-374 family member are located at the X-chromosome inactivation center. In recent years, numerous researches have uncovered that miR-374 family members play an indispensable regulatory role, such as in reproductive disorders, cell growth and differentiation, calcium handling in the kidney, various cancers and epilepsy. In this review, we mainly focus on the role of miR-374 family members in multiple physiological and pathological processes. More specifically, we also summarize their promising potential as novel prognostic biomarkers and therapeutic targets from bench to bedside.
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Detention of copper by sulfur nanoparticles inhibits the proliferation of A375 malignant melanoma and MCF-7 breast cancer cells.
Liu, H, Zhang, Y, Zheng, S, Weng, Z, Ma, J, Li, Y, Xie, X, Zheng, W
Biochemical and biophysical research communications. 2016;(4):1031-1037
Abstract
Selective induction of cell death or growth inhibition of cancer cells is the future of chemotherapy. Clinical trials have found that cancer tissues are enriched with copper. Based on this finding, many copper-containing compounds and complexes have been designed to "copper" cancer cells using copper as bait. However, recent studies have demonstrated that copper boosts tumor development, and copper deprivation from serum was shown to effectively inhibit the promotion of cancer. Mechanistically, copper is an essential cofactor for mitogen-activated protein kinase (MAPK)/extracellular activating kinase (ERK) kinase (MEK), a central molecule in the BRAF/MEK/ERK pathway. Therefore, depleting copper from cancer cells by directly sequestering copper has a wider field for research and potential for combination therapy. Based on the affinity between sulfur and copper, we therefore designed sulfur nanoparticles (Nano-S) that detain copper, achieving tumor growth restriction. We found that spherical Nano-S could effectively bind copper and form a tighter surficial structure. Moreover, this Nano-S detention of copper effectively inhibited the proliferation of A375 melanoma and MCF-7 breast cancer cells with minimum toxicity to normal cells. Mechanistic studies revealed that Nano-S triggered inactivation of the MEK-ERK pathway followed by inhibition of the proliferation of the A375 and MCF-7 cells. In addition, lower Nano-S concentrations and shorter exposure stimulated the expression of a copper transporter as compensation, which further increased the cellular uptake and anticancer activities of cisplatin. Collectively, our results highlight the potential of Nano-S as an anticancer agent or adjuvant through its detention of copper.
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Forkhead box Q1: A key player in the pathogenesis of tumors (Review).
Li, Y, Zhang, Y, Yao, Z, Li, S, Yin, Z, Xu, M
International journal of oncology. 2016;(1):51-8
Abstract
As a member of the Forkhead box protein family, Forkhead box Q1 (FOXQ1) is a transcription factor that functions to regulate cell differentiation. Recently, an increasing number of studies have demonstrated that FOXQ1 is significantly associated with the pathogenesis of tumors. This review aims to predominantly discuss the relationship between FOXQ1 and various types of tumor. The FOXQ1 gene is located at human chromosome 6p25.3 and encodes a functional 403 amino acid protein, which has many physiological functions, including promoting epithelial differentiation, inhibiting smooth muscle differentiation, activating T cells and autoimmunity, and controlling mucin gene expression and granule content in stomach surface mucous cells. There are several modes of regulation of FOXQ1 expression that have been demonstrated in normal and tumor cells, such as microRNA and the Wnt signaling pathway. The activation of FOXQ1 affects downstream genes promoting the initiation, proliferation and invasion, in addition to the metastasis of tumor cells. Amongst these, the regulation of invasion and metastasis by FOXQ1 is the most extensively studied. The detailed mechanism involves angiogenesis, tumor re-initiation, alterations in the tumor microenvironment and epithelial-mesenchymal transition. In a number of studies, the expression of FOXQ1 has been reported to be upregulated in breast, colorectal, pancreatic, bladder and ovarian cancer, and glioma, amongst other tumor types. Together, these studies contribute to cancer diagnostics, prognostics and therapeutics. In conclusion, the application prospect of FOXQ1 in tumors is hopeful.
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Reconciling Estimates of Cell Proliferation from Stable Isotope Labeling Experiments.
Ahmed, R, Westera, L, Drylewicz, J, Elemans, M, Zhang, Y, Kelly, E, Reljic, R, Tesselaar, K, de Boer, RJ, Macallan, DC, et al
PLoS computational biology. 2015;(10):e1004355
Abstract
Stable isotope labeling is the state of the art technique for in vivo quantification of lymphocyte kinetics in humans. It has been central to a number of seminal studies, particularly in the context of HIV-1 and leukemia. However, there is a significant discrepancy between lymphocyte proliferation rates estimated in different studies. Notably, deuterated (2)H2-glucose (D2-glucose) labeling studies consistently yield higher estimates of proliferation than deuterated water (D2O) labeling studies. This hampers our understanding of immune function and undermines our confidence in this important technique. Whether these differences are caused by fundamental biochemical differences between the two compounds and/or by methodological differences in the studies is unknown. D2-glucose and D2O labeling experiments have never been performed by the same group under the same experimental conditions; consequently a direct comparison of these two techniques has not been possible. We sought to address this problem. We performed both in vitro and murine in vivo labeling experiments using identical protocols with both D2-glucose and D2O. This showed that intrinsic differences between the two compounds do not cause differences in the proliferation rate estimates, but that estimates made using D2-glucose in vivo were susceptible to difficulties in normalization due to highly variable blood glucose enrichment. Analysis of three published human studies made using D2-glucose and D2O confirmed this problem, particularly in the case of short term D2-glucose labeling. Correcting for these inaccuracies in normalization decreased proliferation rate estimates made using D2-glucose and slightly increased estimates made using D2O; thus bringing the estimates from the two methods significantly closer and highlighting the importance of reliable normalization when using this technique.
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Optimized Extraction of Polysaccharides from Grateloupia livida (Harv.) Yamada and Biological Activities.
Ye, D, Jiang, Z, Zheng, F, Wang, H, Zhang, Y, Gao, F, Chen, P, Chen, Y, Shi, G
Molecules (Basel, Switzerland). 2015;(9):16817-32
Abstract
Polysaccharides from Grateloupia livida (Harv.) Yamada (GL) were extracted by a heating circumfluence method. Single-factor experiments were performed for the three parameters: extraction time (X₁), extraction temperature (X₂) and the ratio of water to raw material (X₃) and their test range. From preliminary experimental results, one type of the response surface methodology, the Box-Behnken design was applied for the optimizing polysaccharide extraction conditions. The experimental data obtained were fitted to a second-order polynomial equation. The optimal conditions were extraction time 5 h, extraction temperature 100 °C and ratio of water to raw material 70 mL/g. Under these conditions, the experimental yield was 39.22% ± 0.09%, which well matched the predicted value (39.25%), with 0.9774 coefficient of determination (R²). GL polysaccharides had scavenging activities for DPPH and hydroxyl radicals in vitro. The scavenging rates for both radicals peaked at 20 mg/mL GL concentration. However, the positive standard, VC (ascorbic acid), possessed stronger antioxidant activities than GL polysaccharides. Furthermore, the anticancer activity of GL polysaccharides on HepG2 cell proliferation increased dose- and time-dependently, but the positive standard, 5-fluorouracil (5-fu) showed more significant anticancer activity in this study. Overall, GL polysaccharides may have potential applications in the medical and food industries.
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Study on optimisation of extraction process of tanshinone IIA and its mechanism of induction of gastric cancer SGC7901 cell apoptosis.
Hou, J, He, J, Jin, X, Hu, T, Zhang, Y
African journal of traditional, complementary, and alternative medicines : AJTCAM. 2013;(6):456-8
Abstract
The objective of this paper was to investigate the extraction process of tanshinone IIA and its mechanism of induction of gastric cancer SGC7901 cell apoptosis. Extraction process of tanshinone IIA was optimised by orthogonal experimental method, and its effect on gastric cancer SGC7901 cell apoptosis was observed using MTT assay and electron microscopy. The optimum extraction process of tanshinone IIA was as follows: addition of a 10-fold amount of 80% ethanol, one-time extraction, and extraction time of 45 minutes. The study concluded that tanshinone IIA can induce apoptosis of gastric cancer SGC7901 cells.