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"Chen, Cao"
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Stabilization of interdependent networks with two sub-networks of non-identical nodes
This paper explores the stabilization of interdependent networks comprising two sub-networks with non-identical nodes, in which one of the sub-networks is connected to the other in one-to-many mode. Firstly, we establish a mathematical model where the sub-networks possess different number of nodes. Besides, the outer coupling matrix is not required to satisfy the diffusive coupling condition. Then, based on some useful assumptions, adaptive decentralized controllers are designed to realize asymptotic stabilization of the system, the validity of the proposed controllers is rigorously established using Lyapunov stability methods. Finally, their effectiveness is demonstrated through two simulation examples.
Journal Article
MIR497HG‐Derived miR‐195 and miR‐497 Mediate Tamoxifen Resistance via PI3K/AKT Signaling in Breast Cancer
Tamoxifen is commonly used for the treatment of patients with estrogen receptor‐positive (ER+) breast cancer, but the acquired resistance to tamoxifen presents a critical challenge of breast cancer therapeutics. Recently, long noncoding RNA MIR497HG and its embedded miR‐497 and miR‐195 are proved to play significant roles in many types of human cancers, but their roles in tamoxifen‐resistant breast cancer remain unknown. The results indicate that MIR497HG deficiency induces breast cancer progression and tamoxifen resistance by inducing downregulation of miR‐497/195. miR‐497/195 coordinately represses five positive PI3K‐AKT regulators (MAP2K1, AKT3, BCL2, RAF1, and CCND1), resulting in inhibition of PI3K‐AKT signaling, and PI3K‐AKT inhibition in tamoxifen‐resistant cells restored tamoxifen responsiveness. Furthermore, ER α binds the MIR497HG promoter to activate its transcription in an estrogen‐dependent manner. ZEB1 interacts with HDAC1/2 and DNMT3B at the MIR497HG promoter, resulting in promoter hypermethylation and histone deacetylation. The findings reveal that ZEB1‐induced MIR497HG depletion contributes to breast cancer progression and tamoxifen resistance through PI3K‐AKT signaling. MIR497HG can be used as a biomarker for predicting tamoxifen sensitivity in patients with ER+ breast cancer. This work presents a novel mechanism underlying tamoxifen resistance caused by ZEB1‐mediated histone deacetylation and DNA methylation of the MIR497HG promoter. The derivatives of MIR497HG, miR‐497, and miR‐195, work together to inhibit PI3K‐AKT signaling by downregulating the five positive regulators of PI3K‐AKT signaling, indicating MIR497HG can serve as a prognostic factor for tamoxifen sensitivity in patients with ER+ breast cancer.
Journal Article
المغامرون الصغار : ملحمة عالمية : استكشاف الطاقة النفط
ليث ولين وزياد. المغامرون الصغار بانتظار المغامرات دوما لكن سرعان ما يجدون أنفسهم أمام قضية غامضة وشائقة بسبب اختفاء البروفيسور أديب. المتهم الرئيسي في قضية انفجار مصنع شركة إنيرجيز وسيسعون معا إلى كشف الحقيقة بالبحث عنه وإثبات براءته.
Book
CircLONP2 enhances colorectal carcinoma invasion and metastasis through modulating the maturation and exosomal dissemination of microRNA-17
Background
Metastasis causes the vast majority of colorectal carcinoma (CRC)-related deaths. However, little is known about the specific traits and underlying mechanisms of metastasis-initiating cells in primary CRC. And whether or not circular RNAs (circRNAs) take part in this particular event remain not adequately stated yet.
Methods
A screening method based on Transwell assay was first applied to build CRC subgroups with different metastatic potential. High throughput RNA sequencing was used to find out novel metastatic drivers in CRC metastasis-initiating step. A series of in vitro and in vivo assays were further applied to elucidate the functions and underlying molecular mechanisms of circRNAs in CRC metastasis.
Results
A circRNA consisting of exon 8–11 of LONP2, termed as circLONP2, was upregulated in metastasis-initiating CRC subgroups. Aberrant higher expression of circLONP2 was observed in primary CRC tissues with established metastasis, and along the invasive margin in metastatic site. High expression of circLONP2 predicted unfavorable overall survival. Functional studies revealed that circLONP2 could enhance the invasiveness of CRC cells in vitro, and targeting circLONP2 through anti-sense oligonucleotide (ASO) dramatically reduced the penetrance of metastasis to foreign organs in vivo
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Mechanically, circLONP2 directly interacted with and promoted the processing of primary microRNA-17 (pri-miR-17), through recruiting DiGeorge syndrome critical region gene 8 (DGCR8) and Drosha complex in DDX1-dependent manner. Meanwhile, upregulated mature miR-17-5p could be assembled into exosomes and internalized by neighboring cells to enhance their aggressiveness.
Conclusions
Our data indicate that circLONP2 acts as key metastasis-initiating molecule during CRC progression through modulating the intracellular maturation and intercellular transfer of miR-17, resulting in dissemination of metastasis-initiating ability in primary site and acceleration of metastasis formation in foreign organs. circLONP2 could serve as an effective prognostic predictor and/or novel anti-metastasis therapeutic target in CRC treatment.
Journal Article
Advances in 3D-printed scaffold technologies for bone defect repair: materials, biomechanics, and clinical prospects
The treatment of large bone defects remains a significant clinical challenge due to the limitations of current grafting techniques, including donor site morbidity, restricted availability, and suboptimal integration. Recent advances in 3D bioprinting technology have enabled the fabrication of structurally and functionally optimized scaffolds that closely mimic native bone tissue architecture. This review comprehensively examines the latest developments in 3D-printed scaffolds for bone regeneration, focusing on three critical aspects: (1) material selection and composite design encompassing metallic; (2) structural optimization with hierarchical porosity (macro/micro/nano-scale) and biomechanical properties tailored; (3) biological functionalization through growth factor delivery, cell seeding strategies and surface modifications. We critically analyze scaffold performance metrics from different research applications, while discussing current translational barriers, including vascular network establishment, mechanical stability under load-bearing conditions, and manufacturing scalability. The review concludes with a forward-looking perspective on innovative approaches such as 4D dynamic scaffolds, smart biomaterials with stimuli-responsive properties, and the integration of artificial intelligence for patient-specific design optimization. These technological advancements collectively offer unprecedented opportunities to address unmet clinical needs in complex bone reconstruction.
Journal Article
Impaired meningeal lymphatic drainage in patients with idiopathic Parkinson’s disease
Animal studies implicate meningeal lymphatic dysfunction in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease (PD). However, there is no direct evidence in humans to support this role
1
–
5
. In this study, we used dynamic contrast-enhanced magnetic resonance imaging to assess meningeal lymphatic flow in cognitively normal controls and patients with idiopathic PD (iPD) or atypical Parkinsonian (AP) disorders. We found that patients with iPD exhibited significantly reduced flow through the meningeal lymphatic vessels (mLVs) along the superior sagittal sinus and sigmoid sinus, as well as a notable delay in deep cervical lymph node perfusion, compared to patients with AP. There was no significant difference in the size (cross-sectional area) of mLVs in patients with iPD or AP versus controls. In mice injected with α-synuclein (α-syn) preformed fibrils, we showed that the emergence of α-syn pathology was followed by delayed meningeal lymphatic drainage, loss of tight junctions among meningeal lymphatic endothelial cells and increased inflammation of the meninges. Finally, blocking flow through the mLVs in mice treated with α-syn preformed fibrils increased α-syn pathology and exacerbated motor and memory deficits. These results suggest that meningeal lymphatic drainage dysfunction aggravates α-syn pathology and contributes to the progression of PD.
Reduced meningeal lymphatic flow detected in patients with idiopathic Parkinson’s disease compared to patients with atypical Parkinsonian disorders and cognitively normal controls.
Journal Article
TBX20 inhibits colorectal cancer tumorigenesis by impairing NHEJ‐mediated DNA repair
DNA high methylation is one of driving force for colorectal carcinoma (CRC) pathogenesis. Transcription factors (TFs) can determine cell fate and play fundamental roles in multistep process of tumorigenesis. Dysregulation of DNA methylation of TFs should be vital for the progression of CRC. Here, we demonstrated that TBX20, a T‐box TF family protein, was downregulated with hypermethylation of promoter in early‐stage CRC tissues and correlated with a poor prognosis for CRC patients. Moreover, we identified PDZRN3 as the E3 ubiquitin ligase of TBX20 protein, which mediated the ubiquitination and degradation of TBX20. Furthermore, we revealed that TBX20 suppressed cell proliferation and tumor growth through impairing non‐homologous DNA end joining (NHEJ)‐mediated double‐stranded break repair by binding the middle domain of both Ku70 and Ku80 and therefore inhibiting their recruitment on chromatin in CRC cells. Altogether, our results reveal the tumor‐suppressive role of TBX20 by inhibiting NHEJ‐mediated DNA repair in CRC cells, and provide a potential biomarker for predicting the prognosis of patients with early‐stage CRC and a therapeutic target for combination therapy. Our study highlights the dysregulation of TBX20 in early‐stage CRC tissues and the mechanism suppressing NHEJ‐mediated DSBs repair by inhibiting the interaction of Ku70 and Ku80, which indicates the potential of TBX20 as an effective biomarker for predicting the prognosis of patients with early‐stage CRC.
Journal Article
miR-190-5p in human diseases
miRNAs, a major class of small noncoding RNAs approximately 18–25 nucleotides in length, function by repressing the expression of target genes through binding to complementary sequences in the 3′-UTRs of target genes. Emerging evidence has highlighted their important roles in numerous diseases, including human cancers. Recently, miR-190 has been shown to be dysregulated in various types of human cancers that participates in cancer-related biological processes, including proliferation, apoptosis, metastasis, drug resistance, by regulating associated target genes, and to predict cancer diagnosis and prognosis. In this review, we summarized the roles of miR-190-5p in human diseases, especially in human cancers. Then we classified its target genes in tumorigenesis and progression, which might provide evidence for cancer diagnosis and prognosis, promising tools for cancer treatment, or leads for further investigation.
Journal Article