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"Yang, Xian"
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Targeting CD39 in cancer
The ATP–adenosine pathway functions as a key modulator of innate and adaptive immunity within the tumour microenvironment. Consequently, multiple clinical strategies are being explored to target this pathway for the treatment of cancer; in particular, recent clinical data with CD73 antagonists and inhibitors of A2A receptors have demonstrated the therapeutic potential of modulating this pathway. Now, inhibitors of the ectonucleotidase CD39, the rate-limiting enzyme in the conversion of ATP to immunomodulatory adenosine, are entering clinical trials. Consequently, there is currently a focus on understanding the impact of CD39 enzymatic function on innate and adaptive immunity and how therapeutic modulation of this pathway alters their functional potential within the tumour microenvironment. Recent findings reveal multipronged mechanisms of action of CD39 antagonism that rely not only on preventing the accumulation of adenosine but also on the stabilization of pro-inflammatory extracellular ATP to restore antitumour immunity. Here, we review the impact of CD39 expression and ectonucleotidase activity on immunity with a focus on the setting of oncology. Additionally, we discuss the implications for immunotherapy strategies targeting CD39, including their inclusion in rational combination therapies.The ATP–adenosine pathway plays an important role in modulating innate and adaptive immune responses in the tumour microenvironment. Here, the authors focus on CD39, a key enzyme in the ATP–adenosine pathway, and examine immunotherapeutic strategies that target it.
Journal Article
أفكار حول تعميق الإصلاح
يناقش الكتاب سلسلة من الإيضاحات الهامة قدمها الرئيس الصيني والأمين العام للجنة المركزية للحزب الشيوعي الصيني، شي جين بينغ، وتدور حول أفكار الإصلاح وتوسيع الانفتاح على نحو شامل في الصين. يضم الكتاب أكثر من 70 وثيقة هامة على صورة كلمات شي جين بينغ وخطاباته وتعليقاته وتوجيهاته وينقسم الكتاب إلى 12 موضوعا خاصا تتضمن 274 قطعة من مقتطفات الأقوال، نشر بعضها لأول مرة.
Book
Prevalence of Depression among Chinese University Students: A Meta-Analysis
Depression is a major mental health issue worldwide, and university students with heavy burdens of study are at a high risk for depression. While a number of studies have been conducted regarding depression among university students in China, there is a lack of information regarding the national prevalence of depression among Chinese university students. Therefore, we performed a meta-analysis to statistically pool the prevalence of depression among Chinese university students.
A systematic search of scientific databases was conducted, including Chinese Web of Knowledge, Embase, PubMed, Wanfang (a Chinese database) and Weipu (a Chinese database) to find relevant publications published between 1995 and December 2015. This was supplemented by a secondary review of the reference lists of all retrieved papers to find additional relevant citations. Studies published in either English or Chinese that provided prevalence estimates of depression in Chinese university students were considered. Prevalence estimates of each eligible study were extracted and pooled in our meta-analysis using a random-effects model.
A total of 39 studies conducted between 1997 and 2015 including 32,694 university students were analyzed. Our results indicate that the overall prevalence of depression among Chinese university students is 23.8% (95% CI: 19.9%-28.5%). Substantial heterogeneity in prevalence estimates was noted. Subgroup analysis revealed that the prevalence of depression among medical students is higher than among other students.
Overall, the prevalence of depression among Chinese university students is exceedingly high. This suggests that it is imperative that more attention be given to the development of appropriate mental healthcare strategies for university students in China.
Journal Article
Proactive Intervention and Multidimensional Collaboration: Prevention and Comprehensive Management of Osteoporosis in Perimenopausal and Postmenopausal Women
The clinical burden of osteoporosis in perimenopausal and postmenopausal women is becoming increasingly prominent. The disease has a well-defined onset stage: perimenopause is a critical window for accelerated bone loss, while the five to ten years after menopause are a peak period for fractures. Epidemiological surveys show that the prevalence in Chinese women over 50 years old is nearly half, and the disease continues to rise with age. Its core mechanism is enhanced bone resorption and insufficient bone formation caused by a sudden drop in estrogen levels. Combined with calcium and vitamin D deficiency and genetic susceptibility, this ultimately leads to a sharp increase in the risk of vertebral and hip fractures. Clinical treatment primarily involves drugs such as bisphosphonates and denosumab, which can reduce fracture incidence, but poor adherence to treatment and long-term adverse effects limit their widespread use. Lifestyle interventions such as resistance training and calcium and vitamin D supplementation, while effective adjunctively, are rarely effective alone in high-risk populations. Emerging therapies, such as drugs targeting the RANKL pathway and stem cell therapy, are being explored, but the evidence remains insufficient to support routine use. This review aims to clarify the epidemiology, molecular mechanisms, and progress in prevention and treatment of this disease, and to propose possible approaches for individualized and multidisciplinary management in the future.
Journal Article
Lipid desaturation-associated endoplasmic reticulum stress regulates MYCN gene expression in hepatocellular carcinoma cells
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide due to its high rate of recurrence, in part because of cancer stem cell (CSC)-dependent “field cancerization”. Recently, we identified that the oncogene v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) marked CSC-like subpopulations in heterogeneous HCC and served as a therapeutic target and prognostic marker for HCC. In this study, we explored the molecular basis of upregulated
MYCN
gene expression in HCC cells. Liquid chromatograph time-of-flight mass spectrometry-based metabolome analysis demonstrated that the content of unsaturated fatty acids was increased in MYCN high expression (MYCN
high
) CSC-like HCC cells. Inhibition of lipid desaturation using either the chemical inhibitor or siRNA/shRNA against stearoyl-CoA desaturase-1 (SCD1) suppressed cell proliferation as well as
MYCN
gene expression in MYCN
high
HCC cells, grown as both monolayer and spheres. Further mechanistic study using RNA-seq based transcriptome analysis revealed that endoplasmic reticulum (ER) stress related signaling networks such as endocannabinoid cancer inhibition pathway were under the control of SCD1 in MYCN
high
HCC cells. Furthermore, the expression of ER stress-inducible transcription suppressor cyclic AMP-dependent transcription factor (
ATF3
) was downregulated in MYCN
high
CSC-like HCC cells and CSC-rich spheroids, which was upregulated by inhibition of lipid desaturation or treatment with acyclic retinoid (ACR). Lipid profiling using NMR spectroscopy revealed that the ACR dramatically reduced the content of unsaturated fatty acids in HCC cells. The chemical inducer of ER stress inhibited
MYCN
gene expression, while the chemical inhibitor of ER stress or knockdown of
ATF3
gene expression partially rescued the suppression of
MYCN
gene expression by ACR in MYCN
high
HCC cells. These data suggested that lipid desaturation-mediated ER stress signaling regulates
MYCN
gene expression in HCC cells and serves as a promising therapeutic target for the treatment and prevention of HCC.
Journal Article
Immunotherapeutic approaches in EBV-associated nasopharyngeal carcinoma
Epstein–Barr virus (EBV) was the first tumor virus in humans. Nasopharyngeal carcinoma (NPC) accounts for approximately 60% of the 200,000 new tumor cases caused by EBV infection worldwide each year. NPC has an insidious onset and is highly malignant, with more than 70% of patients having intermediate to advanced disease at the time of initial diagnosis, and is strongly implicated in epithelial cancers as well as malignant lymphoid and natural killer/T cell lymphomas. Over 90% of patients with confirmed undifferentiated NPC are infected with EBV. In recent decades, much progress has been made in understanding the molecular mechanisms of NPC and developing therapeutic approaches. Radiotherapy and chemotherapy are the main treatment options for NPC; however, they have a limited efficacy in patients with locally advanced or distant metastatic tumors. Tumor immunotherapy, including vaccination, adoptive cell therapy, and immune checkpoint blockade, represents a promising therapeutic approach for NPC. Significant breakthroughs have recently been made in the application of immunotherapy for patients with recurrent or metastatic NPC (RM-NPC), indicating a broad prospect for NPC immunotherapy. Here, we review important research findings regarding immunotherapy for NPC patients and provide insights for future research.
Journal Article
The role of lysosomes in cancer development and progression
Lysosomes are an important component of the inner membrane system and participate in numerous cell biological processes, such as macromolecular degradation, antigen presentation, intracellular pathogen destruction, plasma membrane repair, exosome release, cell adhesion/migration and apoptosis. Thus, lysosomes play important roles in cellular activity. In addition, previous studies have shown that lysosomes may play important roles in cancer development and progression through the abovementioned biological processes and that the functional status and spatial distribution of lysosomes are closely related to cancer cell proliferation, energy metabolism, invasion and metastasis, immune escape and tumor-associated angiogenesis. Therefore, identifying the factors and mechanisms that regulate the functional status and spatial distribution of lysosomes and elucidating the relationship between lysosomes and the development and progression of cancer can provide important information for cancer diagnosis and prognosis prediction and may yield new therapeutic targets. This study briefly reviews the above information and explores the potential value of lysosomes in cancer therapy.
Journal Article
Anti-interleukin-6 receptor antibody treatment ameliorates postoperative adhesion formation
Postoperative adhesion formation often ruins the quality of life or is an obstacle to illnesses with curative operation such as cancer. Previously we demonstrated that interferon-γ-promoted fibrin deposition drove postoperative adhesion formation. However, its underlying cellular and molecular mechanisms remain poorly understood. We found that myofibroblasts of the adhesion predominantly expressed signature molecules of mesothelial cells that line the serosa. Microarray analysis revealed IL-6 as a key underlying player, supported by elevated IL-6 levels in the peritoneal fluid of post-laparotomy human subjects. Injured serosa of cecum-cauterized mice also exhibited induction of
Il6
, which was followed by
Tnf
, concomitant with rapid accumulation of neutrophils, substantial population of which expressed TGF-β1, a master regulator of fibrosis. Besides, neutrophil-ablated mice showed reduction in induction of the adhesion, suggesting that TGF-β1
+
neutrophils triggered the adhesion. Human neutrophils expressed
TGFB
1 in response to TNF-
α
and
TNF
in response to IL-6. Moreover, anti-IL-6 receptor monoclonal antibody abrogated neutrophil recruitment and adhesion formation. Thus, IL-6 signaling represents a potential target for the prevention of postoperative adhesions.
Journal Article