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Guo, Q.

Publications and source records attributed to Guo, Q..

At least 55 records · Page 3Linked to original sources

Simultaneous profiling of native-state proteomes and transcriptomes of neural cell types using proximity labeling

Deep molecular phenotyping of cells at transcriptomic and proteomic levels is an essential first step to understanding cellular contributions to development, aging, injury, and disease. Since proteome and transcriptome level abundances only modestly correlate with each other, complementary profiling of both is needed. We report a novel method called simultaneous protein and RNA -omics (SPARO) to capture the cell type-specific transcriptome and proteome simultaneously from both in vitro and in vivo experimental model systems. This method leverages the ability of biotin ligase, TurboID, to biotinylate cytosolic proteins including ribosomal and RNA-binding proteins, which allows enrichment of biotinylated proteins for proteomics as well as protein-associated RNA for transcriptomics. We validated this approach first using well-controlled in vitro systems to verify that the proteomes and transcriptomes obtained reflect the ground truth, bulk proteomes and transcriptomes. We also show that the effect of a biological stimulus (e.g., neuroinflammatory activation by lipopolysaccharide) can be faithfully captured. We also applied this approach to obtain native-state proteomes and transcriptomes from two key neural cell types, astrocytes and neurons, thereby validating the in vivo application of SPARO. Next, we used these data to interrogate protein-mRNA concordance and discordance across these cell types, providing insights into groups of molecular processes that exhibit uniform or cell type-specific patterns of mRNA-protein discordance.

neuroscience↗

Proximity labeling of the Tau repeat domain enriches RNA-binding proteins that are altered in Alzheimer's disease and related tauopathies

In Alzheimers disease (AD) and other tauopathies, tau dissociates from microtubules and forms toxic aggregates that contribute to neurodegeneration. Although some of the pathological interactions of tau have been identified from postmortem brain tissue, these studies are limited by their inability to capture transient interactions. To investigate the interactome of aggregate-prone fragments of tau, we applied an in vitro proximity labeling technique using split TurboID biotin ligase (sTurbo) fused with the tau microtubule repeat domain (TauRD), a core region implicated in tau aggregation. We characterized sTurbo TauRD co-expression, robust enzyme activity and nuclear and cytoplasmic localization in a human cell line. Following enrichment of biotinylated proteins and mass spectrometry, we identified over 700 TauRD interactors. Gene ontology analysis of enriched TauRD interactors highlighted processes often dysregulated in tauopathies, including spliceosome complexes, RNA-binding proteins (RBPs), and nuclear speckles. The disease relevance of these interactors was supported by integrating recombinant TauRD interactome data with human AD tau interactome datasets and protein co-expression networks from individuals with AD and related tauopathies. This revealed an overlap with the TauRD interactome and several modules enriched with RBPs and increased in AD and Progressive Supranuclear Palsy (PSP). These findings emphasize the importance of nuclear pathways in tau pathology, such as RNA splicing and nuclear-cytoplasmic transport and establish the sTurbo TauRD system as a valuable tool for exploring the tau interactome.

neuroscience↗

Modular DNA Barcoding of Nanobodies Enables Multiplexed in situ Protein Imaging and High-throughput Biomolecule Detection

Current immunodetection methods using antibody-DNA conjugates enable multiplexed target detection through orthogonal DNA barcodes, but existing conjugation approaches are labor-intensive and often compromise antibody function. Here we present a modular, site-specific, and cost-efficient DNA tagging strategy -- multiplexed and modular barcoding of antibodies (MaMBA). Utilizing nanobodies as modular adaptors, MaMBA enables direct site-specific labeling of off-the-shelf IgG antibodies with a one-component design. We first applied MaMBA to develop the misHCR method for highly multiplexed in situ protein imaging via orthogonal hybridization chain reaction (HCR). Its cleavable variant, misHCRn, achieves simultaneous visualization of 12 different targets within the same mouse brain sections through iterative probe use. We further extended the cleavable MaMBA to develop the barcode-linked immunosorbent assay (BLISA) for multiplexed and high-throughput biomolecule detections. By combining BLISA with next-generation sequencing, we successfully measured SARS-CoV-2 IgG and HBV-associated antigens in a large number of human serum samples. Additionally, we demonstrated a small-scale drug screen by using BLISA to simultaneously detect eight protein targets. In conclusion, MaMBA offers a highly modular and easily adaptable approach for antibody DNA-barcoding, which can be broadly applied in basic research and clinical diagnostics.

bioengineering↗

Wnt/β-Catenin coordinates muscle spindle development by regulating capsule differentiation, intrafusal fiber nuclei aggregation and proprioceptive nerve endings

Proprioception is essential for the regulation of posture, movement, and musculoskeletal integrity. The muscle spindle, a mechanosensory organ composed of multiple specialized tissues, detects stretch and provides proprioceptive feedback. Despite its importance, the molecular mechanisms that orchestrate the development of the spindle components remain poorly understood. Here, we reveal the involvement of the Wnt/{beta}-catenin pathway in muscle spindle development. We show that Wnt ligands and their Frizzled receptors are expressed in the developing spindle and that {beta}-catenin is active throughout development in capsule cells and in bag2 intrafusal fibers. Embryonic deletion of {beta}-catenin from capsule and intrafusal fibers induced widespread transcriptomic changes, which led to significant malformations, including impaired capsule cell differentiation, disrupted nuclear organization in intrafusal fibers, and disorganized proprioceptive nerve endings. Postnatal deletion of {beta}-catenin from intrafusal fibers resulted in abnormal nerve endings and impaired proprioceptive function, indicating that the development of proprioceptive afferents is regulated by {beta}-catenin through a non-cell-autonomous mechanism acting in bag2 fibers. Collectively, our findings position the Wnt/{beta}-catenin pathway as a central regulator that acts through both cell-autonomous and non-cell-autonomous mechanisms to coordinate the development of the various spindle tissues into a functional organ.

developmental biology↗

Cavin1 binding nanobodies reveal structural flexibility and regulated interactions of the N-terminal coiled-coil domain

Caveolae are abundant plasma membrane structures that regulate signalling, membrane homeostasis, and mechanoprotection. Their formation is driven by caveolins and cavins and their coordinated interactions with lipids. We have developed nanobodies against the trimeric HR1 coiled-coil domain of Cavin1. We identify specific nanobodies that do not perturb Cavin1 membrane binding and localise to caveolae when expressed in cells. The crystal structure of a nanobody HR1 complex reveals a symmetric 3:3 architecture as validated by mutagenesis. In this structure, the C-terminal half of the HR1 domain is disordered suggesting the nanobody has stabilised an open conformation previously identified as important for membrane interactions. A phosphomimic mutation in a Thr-Ser pair proximal to this region reveals selective regulation of Cavin2/Cavin3 association. These studies provide new insights into Cavin domains required for assembly of multiprotein caveolar assemblies and describe new nanobody tools for structural and functional studies of caveolae. SUMMARY STATEMENTNanobodies are reported that can label the Cavin1 protein and caveola structures in cells.

cell biology↗

Mapping the endosomal proximity proteome reveals Retromer as a hub for RAB GTPase regulation.

Endosomal retrieval and recycling of integral cargo proteins is essential for cell, tissue and organism-level development and homeostasis and is orchestrated through a specialised retrieval sub-domain on the endosomal vacuole. However, although sub-domain dysfunction is associated with human disease our appreciation of the molecular details and functional components of the retrieval sub-domain(s) remains poorly described. Here, using comparative proximity proteomics of critical retrieval sub-domain components Retromer and Retriever, their cargo adaptors, and a component of the opposing ESCRT-degradative sub-domain, we provide a data-rich resource that identifies new molecular details of retrieval sub-domain composition and organization, including an unrecognised complexity in the interface of Retromer with RAB GTPases. Combining X-ray crystallography and in silico predictions with extensive biochemical and cellular analysis, we dissect the direct association of Retromer with RAB10 regulators DENND4A, DENND4C, TBC1D1, and TBC1D4, and the RAB35 regulator TBC1D13. Overall, we conclude that the Retromer retrieval sub-domain constitutes a major hub for the regulated switching of selected RAB GTPases and propose that this constitutes a major component of the role of Retromer in neuroprotection.

cell biology↗

Anti-HIV-1 HSPC-based gene therapy with safety kill switch to defend against and attack HIV-1 infection

Hematopoietic stem/progenitor cell (HSPC)-based anti-HIV-1 gene therapy holds promise to provide life-long remission following a single treatment. Here we report a multi-pronged anti-HIV-1 HSPC-based gene therapy designed to defend against and attack HIV-1 infection. We developed a lentiviral vector capable of co-expressing three anti-HIV-1 genes. Two are designed to prevent infection, including a short-hairpin RNA (CCR5sh1005) to knock down HIV-1 co-receptor CCR5 and a membrane anchored HIV-1 fusion inhibitor (C46). The third gene is a CD4-based chimeric antigen receptor (CAR) designed to attack HIV-1 infected cells. Our vector also includes a non-signaling truncated human epidermal growth factor receptor (huEGFRt) which acts as a negative selection-based safety kill switch against transduced cells. Anti-HIV-1 vector-transduced human CD34+ HSPC efficiently reconstituted multi-lineage human hematopoietic cells in humanized bone marrow/liver/thymus (huBLT) mice. HIV-1 viral load was significantly reduced (1-log fold reduction, p <0.001) in transplanted huBLT mice. Anti-huEGFR monoclonal antibody Cetuximab (CTX) administration significantly reduced huEGFRt+ vector-modified cells (>4-fold reduction, p <0.01) in huBLT mice. These results demonstrate that our strategy is highly effective for HIV-1 inhibition, and that CTX-mediated negative selection can deplete anti-HIV-1 vector-modified cells in the event of unwanted adverse effects in huBLT mice.

microbiology↗

FOXP Genes Regulate Purkinje Cell Diversity in Cerebellar Development and Evolution

Mammalian cerebellar development is thought to be influenced by distinct Purkinje cell (PC) subtypes. However, the degree of PC heterogeneity and the molecular drivers of this diversity have remained unclear, hindering efforts to manipulate PC diversification and assess its role in cerebellar development. Here, we demonstrate the critical role of Foxp genes in cerebellar development by regulating PC diversification. We identified 11 PC subtypes in the embryonic mouse cerebellum through single-cell RNA sequencing. Using a novel unsupervised method, we mapped these subtypes in three-dimensional space, revealing discrete PC subtypes predictive of adult cerebellar organization, including longitudinal stripes and lobules. These subtypes exhibit unique combinations of Foxp1, Foxp2, and Foxp4 expression. Deletion of Foxp2 and Foxp1 disrupts PC diversification, leading to altered cerebellar patterning, including the loss of a specific Foxp1-expressing subtype and the cerebellar hemisphere. The Foxp1-expressing PC subtype is much more abundant in the fetal human cerebellum than in mice, but rare in the chick cerebellum, correlating with cerebellar hemisphere size in these species. This highlights the significance of Foxp1-expressing PCs in cerebellar hemisphere development and evolution. Therefore, our study identifies Foxp genes as key regulators of PC diversity, providing new insights into the developmental and evolutionary underpinnings of the cerebellum.

developmental biology↗

RING1 dictates GSDMD-mediated inflammatory response and host susceptibility to pathogen infection

RING1 is an E3 ligase component of the polycomb repressive complex 1 (PRC1) with known roles in chromatin regulation and cellular processes such as apoptosis and autophagy. However, its involvement in inflammation and pyroptosis needs to be better characterized. Here, we found that human RING1, but not RING2, promoted K48-linked ubiquitination of Gasdermin D (GSDMD) and acted as a negative regulator of pyroptosis and bacterial infection. Ring1 knockout mice increased the bacterial loads and mortality rate by treatment of S. typhimurium. Upon infection by M. tuberculosis (Mtb) H37Rv strain, RING1 deletion initially reduced bacterial loads but later increased lung inflammation and impaired immune defense responses in mice. Also, Ring1 knockout exacerbated acute sepsis induced by lipopolysaccharide (LPS). Mechanistically, RING1 directly interacts with GSDMD and ubiquitinates the K51 and K168 sites of GSDMD for K48-linked proteasomal degradation, thereby inhibiting pyroptosis. Inhibition of RING1 E3 ligase activity by mutation or small molecular compound increased GSDMD level and cell death during pyroptosis. Our findings reveal that RING1 dictates GSDMD-mediated inflammatory response and host susceptibility to pathogen infection, highlighting RING1 as a potential therapeutic target for combating infectious diseases. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/622030v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@e6d4a6org.highwire.dtl.DTLVardef@92f137org.highwire.dtl.DTLVardef@11a69c4org.highwire.dtl.DTLVardef@115dc0b_HPS_FORMAT_FIGEXP M_FIG Graphic Abstract C_FIG HighlightsO_LIE3 ubiquitin ligase RING1 targets GSDMD for proteasomal degradation. C_LIO_LIMice lacking RING1 are more vulnerable to S. typhimurium infection and LPS- induced sepsis. C_LIO_LIIn the early stages of M. tuberculosis (Mtb) infection, Ring1-/- mice exhibit efficient bacterial clearance. C_LIO_LIChronic inflammation in Ring1-/- mice impairs the ability to control Mtb in the late stages of infection. C_LI

cell biology↗

A Genomic Language Model for Chimera Artifact Detection in Nanopore Direct RNA Sequencing

Chimera artifacts in nanopore direct RNA sequencing (dRNA-seq) can significantly distort transcriptome analyses, yet their detection and removal remain challenging due to limitations in existing basecalling models. We present Deep-Chopper, a genomic language model that precisely identifies and removes adapter sequences from base-called dRNA-seq long reads at single-base resolution, operating independently of raw signal or alignment information to effectively eliminate chimeric read artifacts. By removing these artifacts, DeepChopper substantially improves the accuracy of critical downstream analyses, such as transcript annotation and gene fusion detection, thereby enhancing the reliability and utility of nanopore dRNA-seq for transcriptomics research.

genomics↗

Long deletion signatures in repetitive genomic regions track somatic evolution and enable sensitive detection of microsatellite instability

Deficiency in the mismatch repair system (MMRd) causes microsatellite instability (MSI) in cancers and determines eligibility for immunotherapy. Here, we show that MMRd tumours harbour long-deletion signatures ([&ge;]2-5+ base pairs deleted in repetitive regions), which provide new insights into MSI evolution and enable sensitive MSI detection particularly in challenging clinical samples. Long deletions, accumulated through stepwise DNA slippage errors, are significantly more prevalent in metastatic MMRd tumours compared to primary tumours. Importantly, we show that long-deletion signatures harbour features that are distinct from background noise, making them robustly detectable even in shallow whole genome sequencing (sWGS, [~]0.1X coverage) of formalin-fixed samples. We constructed a machine learning classifier that uses these distinct features to detect Microsatellite Instability in LOw-quality (MILO) samples. MILO achieved 100% accuracy in detecting MSI in sWGS data with only 2%-15% tumour purity and demonstrated promise in identifying MMRd clones in precancerous intestinal lesions. We propose that MILO could be clinically used for the sensitive monitoring of MMRd cancer evolution from early to late stages, using minimal sequencing data from both archival and fresh-frozen samples with low tumour content. SignificanceMutational signatures characterised by long deletions in repetitive genomic regions provide a sensitive route to detect and track MMRd clone evolution, even with low purity shallow whole genome sequencing data.

bioinformatics↗

An all-in-one AAV vector for cardiac-specific gene silencing by an adenine base editor

ABE editing outcomes are highly variable and unpredictable, depending on various factors. Therefore, the success rate of creating targeted A*T-to-G*C conversions using ABE is not high. But utilizing ABE to target RNA splicing sites for gene silencing has a higher success rate. Another challenge for base editing in the heart is that traditional ABE is too large in size, necessitating dual AAV delivery. Whether single AAV delivery can be achieved remains to be explored. In this study, we demonstrated how the diversity of Cas9 homologs and screening of sgRNAs can facilitate cardiac base editing. Single-AAV base editing outperformed dual-AAV systems in the heart, potentially benefiting from chromatin accessibility-guided sgRNA selection. These findings have important implications for the development of more effective and predictable base editing tools for cardiac gene therapy.

molecular biology↗

Metabolic Stress Accelerates Dysregulated Synovial Macrophage-Fibroblast Communication and Htra1 Overproduction in Osteoarthritis

Biomechanical and metabolic factors increase the risk for osteoarthritis (OA) by causing supraphysiological stresses on joint tissues. Chronic exposure to these stresses contributes to failure of the joint organ system, resulting in pain and loss of function for patients with OA. The synovium is vital for joint organ health but during OA, synovial inflammation and damage are associated with worse outcomes including pain. Unfortunately, the separate and combined effects of metabolic and biomechanical stresses on synovial tissues are not well understood. In this study, metabolic syndrome (MetS) was associated with worse knee pain in patients with early-stage knee OA, suggesting that metabolic stress may act on synovial tissues during early-stage OA, exacerbating outcomes. In a rat model of experimental knee OA, the combined effects of biomechanical and metabolic stresses induced worse knee pain, cartilage damage, and synovial inflammation than biomechanical stress alone. Further, single-cell RNA sequencing of synovial macrophages and fibroblasts identified earlier metabolic (glycolytic and respiratory) shifts, neurogenesis, dysregulated communication, and cell activation when metabolic and biomechanical stresses were combined. Lastly, using a direct contact co-culture system, we showed that metabolic stress alters macrophage-fibroblast communication leading to increased expression of Htra1, a pathogenic protease in OA. This study identifies novel mechanisms that may represent amenable therapeutic targets for patients experiencing MetS and OA. One-sentence summary: Metabolic stress may cause worse outcomes in OA through dysregulated synovial cell communication that activates synovial fibroblasts and increases Htra1 production.

physiology↗

A near-complete genome assembly of the bearded dragon Pogona vitticeps provides insights into the origin of Pogona sex chromosomes

BackgroundThe agamid dragon lizard Pogona vitticeps is one of the most popular domesticated reptiles to be kept as pets worldwide. The capacity of breeding in captivity also makes it emerging as a model species for a range of scientific research, especially for the studies of sex chromosome origin and sex determination mechanisms. ResultsBy leveraging the CycloneSEQ and DNBSEQ sequencing technologies, we conducted whole genome and long-range sequencing for a captive-bred ZZ male to construct a chromosome-scale reference genome for P. vitticeps. The new reference genome is [~]1.8 Gb in length, with a contig N50 of 202.5 Mb and all contigs anchored onto 16 chromosomes. Genome annotation assisted by long-read RNA sequencing greatly expanded the P. vitticeps lncRNA catalog. With the chromosome-scale genome, we were able to characterize the whole Z sex chromosome for the first time. We found that over 80% of the Z chromosome remains as pseudo-autosomal region (PAR) where recombination is not suppressed. The sexually differentiated region (SDR) is small and occupied mostly by transposons, yet it aggregates genes involved in male development, such as AMH, AMHR2 and BMPR1A. Finally, by tracking the evolutionary origin and developmental expression of the SDR genes, we proposed a model for the origin of P. vitticeps sex chromosomes which considered the Z-linked AMH as the master sex-determining gene. ConclusionsOur study provides novel insights into the sex chromosome origin and sex determination of this model lizard. The near-complete P. vitticeps reference genome will also benefit future study of amniote evolution and may facilitate genome-assisted breeding.

genomics↗

Vibrio alginolyticus is the pathogen of 'Baotou disease causing serious damage to Gracilariopsis lemaneiformis cultivation in China

Gracilariopsis lemaneiformis and Saccharina japonica, the two very important cultivated economic seaweeds, are often co-cultured in China due to their growth periods overlapped for about 3 months. These two seaweeds are often plagued with bleaching diseases during their high-density commercial cultivation. In recent years, a disease called Baotou has been causing large-scale yield reductions of G. lemaneiformis in China. Interestingly, Vibrio alginolyticus once reported to be beneficial to S. japonica by reducing the bleaching disease risk, was strongly proved to be the pathogen causing Baotou disease in this study. Analysis of 16S rRNA gene profiling revealed that V. alginolyticus was the most abundant and dominant bacterium on the algal thalli suffering from Baotou disease, whereas its presence was scarcely detected on healthy thalli. Scanning electron microscope (SEM) analysis revealed that a large number of V. alginolyticus cells were found to be attached to the algal thalli with Baotou disease and the rotten thalli acquired by the lab infection treatment. V. alginolyticus could cause the rotten symptoms which were consistent with those of Baotou disease. According to Kochs postulates, V. alginolyticus was identified as the pathogen causing Baotou disease. IMPORTANCEA highly contagious disease known as Baotou disease has persistently triggered significant yield reductions in G. lemaneiformis throughout China. The pathogen of Baotou disease was isolated and identified as V. alginolyticus which was once reported to be beneficial to S. japonica by reducing the bleaching disease risk. The study indicates that V. alginolyticus is closely involved in the competition or co-existence between G. lemaneiformis and S. japonica co-cultured in China, and provides a novel perspective and evidence that bacteria are closely involved in the competition or co-existence among different species of seaweeds that grow together.

microbiology↗

CLCC1 Governs Bilayer Equilibration at the Endoplasmic Reticulum to Maintain Cellular and Systemic Lipid Homeostasis

The intricate orchestration of lipid production, storage, and mobilization is vital for cellular and systemic homeostasis1,2. Dysfunctional plasma lipid control represents the major risk factor for cardio-metabolic diseases, the leading cause of human mortality3,4. Within the cellular landscape, the endoplasmic reticulum (ER) is the central hub of lipid synthesis and secretion, particularly in metabolically active hepatocytes in the liver or enterocytes in the gut5,6. Initially assembled in the ER lumen, lipid-ferrying lipoproteins necessitate the cross-membrane transfer of both neutral and phospho-lipids onto the lumenal apolipoprotein B (APOB), in a poorly-defined process7-10. Here we show that trans-bilayer equilibration of phospholipids, regulated by the ER protein CLCC1, determines lipid partition across the ER membrane and consequently systemic lipid homeostasis. CLCC1 partners with the phospholipid scramblase TMEM41B11,12 to recognize imbalanced bilayers and promote lipid scrambling, thereby licensing lipoprotein biogenesis and the subsequent bulk lipid transport. Strikingly, loss of CLCC1 or TMEM41B leads to the emergence of giant lumenal lipid droplets enclosed by extensively imbalanced ER bilayers, and consequently drastically accelerated pathogenesis of metabolic-dysfunction-associated liver steatohepatitis (MASH). The above results establish phospholipid scrambling at the ER as the lynchpin to maintain a dynamic equilibrium. Considering the requirement of trans-bilayer phospholipid equilibration in numerous biological processes, ranging from catabolic autophagy to viral infection13-16, our study may enable further elucidation of a previously under-appreciated homeostatic control mechanism intrinsic to the ER function in lipid biogenesis and distribution.

cell biology↗

Molecular mechanism of the flotillin complex in membrane microdomain organization

Flotillin-1 and flotillin-2 form hetero-oligomers to create flotillin membrane microdomains essential for endocytosis and protein sorting. However, the mechanisms of flotillin oligomerization and microdomain organization remain incompletely understood. Here, we present the cryo-EM structure of human flotillin complex, showing that flotillin-1 and -2 form a 44-mer, membrane attached, and dome-shaped structure that defines a 30-nm circular membrane domain. The cryo-ET data demonstrates that while attached to the cytoplasmic leaflet in situ, flotillin complexes possess intrinsic structural plasticity on the native membrane. Each flotillin complex may represent a fundamental unit of membrane microdomains, with their clustering enabling the formation of larger and more elaborate domains. We further reveal that phosphorylation at residues Y160 (flotillin-1) and Y163 (flotillin-2) may act as a molecular switch to modulate complex assembly, potentially regulating its function in endocytosis. These findings demonstrate the molecular mechanism of flotillin-mediated membrane segregation and microdomain formation, and suggest a previously unrecognized role of flotillin in sequestrating membrane proteins.

biochemistry↗

Identification of Candidate Diagnostic gene CDC25C for Trametinib-induced Cardiotoxicity by Integrating Bioinformatics and Machine Learning

Trametinib is a MEK inhibitor that has been shown to have considerable efficacy in retarding melanoma progression. However, the exact mechanism of cardiotoxicity induced by trametinib remains unclear. Our study was designed to investigate the underlying mechanisms by which trametinib-induced cardiotoxicity (TIC) might exist, offering novel perspectives and guidance for potential prediction, diagnosis, and treatment of TIC. The GSE217421 dataset indicated 574 up-regulated and 705 down-regulated DEGs. According to the KEGG analysis, these genes were implicated in several pathways and functions, including Cell Cycle, Axon Guidance, Cellular Senescence, and Dilated Cardiomyopathy. The GO analysis suggested their association with Mitotic Cell Cycle, Microtubule Cytoskeleton and Adenyl Nucleotide Binding. The hub genes (CDC25C) for TIC were screened through Multiple machine learning algorithms. Next, The expression level of CDC25C was verified using the GSE217423 validation set. Nomogram model based on CDC25C demonstrated excellent diagnostic capability according to three different evaluation measures. To further explore the regulatory mechanism of CDC25C in TIC, we constructed a multi-regulatory network using miRNAs-lncRNAs-TFs-CDC25C and conducted an immunoinfiltration analysis. Our study suggests that CDC25C may be a candidate diagnostic gene and a potential therapeutic target for the early occurrence and development of TIC. This provides new ideas for the prediction, diagnosis and treatment strategies for TIC.

cancer biology↗