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Mo, X.

Publications and source records attributed to Mo, X..

At least 19 recordsLinked to original sources
bioRxiv2026

Carbon dioxide sequestration into biomineral armor by ants

Over geologic time, Earths climate has been shaped by the capture and conversion of atmospheric carbon dioxide (CO2) into stable carbonate minerals, including dolomite [CaMg(CO3)2]. Accelerating natural carbon mineralization offers significant potential for mitigating anthropogenic climate change. Using stable carbon isotope tracking, nano-scale secondary ion mass spectroscopy, and 13C SSNMR, we show that, paralleling global biosphere-level processes, Sericomyrmex amabilis fungus-farming ants rapidly convert CO2 in their nest chambers into a biomineral layer covering their exoskeletons. We further reveal that biogenic carbon mineralization by these ants produces partially ordered dolomite. This rapid sequestration of CO2 into defensive armor in ants provides a fascinating natural example of mediation of potentially toxic accumulation of atmospheric CO2 that could inform human efforts to mitigate climate change.

ecology↗
bioRxiv2025

BERT-T6: Towards High-accuracy T6SS Bacterial Toxin Identification Using Protein Language Model

Type VI secretion system effectors target the cell wall, membranes and nucleic acids, leading to the killing of bacteria or impairment of host cell defense mechanisms. Accurate identification of T6SEs will be beneficial to understand the virulence of these bacteria via type VI secretion systems as well as bacterial pathogenesis. Although some traditional machine learning-based and deep learning-based tools have been developed to distinguish T6SEs from non-T6SEs, we believe there is still room for further improvement. To obtain the robust feature for model construction, we successively investigate various classic sequence-based features and embeddings from pre-trained transformer-based protein language models. Building upon the model incorporating ProtBert embeddings, we employed a transfer learning approach to fine-tune the ProtBert protein language model with a downstream T6SE classification task. The resulting BERT-T6 model demonstrates performance significantly superior to baseline models. More importantly, with an accuracy of 0.959, a sensitivity of 0.909, a specificity of 0.973, a precision of 0.905, a F1-score of 0.907, MCC of 0.881, our model achieves performance competitive with state-of-the-art binary and multi-class predictors. This work highlights the effectiveness of utilizing BERT with transfer learning for T6SE prediction. BERT-T6 provides a robust and precise approach for identifying T6SEs, offering promise for enhancing studies of bacterial virulence mechanisms.

bioinformatics↗
bioRxiv2025

Lipid peroxidation intrinsically induces mitochondrial iron overload via Bach1-HO-1 signaling to promote cardiac ferroptosis

BackgroundLipid peroxidation and iron accumulation are hallmarks of ferroptosis, a form of cell death characterized by iron-dependent oxidative damage to cellular membranes. However, the molecular link between lipid peroxidation and iron overload in the execution of ferroptosis remains elusive. Moreover, the pathophysiological implications of the interaction between lipid peroxidation and iron overload in cardiac homeostasis and remodeling are also unknown. MethodsWe assessed the role of lipid peroxidation in mediating cardiac iron overload and ferroptosis using genetic mouse models. We also performed molecular and cellular biology studies to elucidate the mechanisms by which lipid peroxidation regulates iron homeostasis and ferroptosis signaling in cardiomyocytes. ResultsCardiomyocyte-specific ablation of Gpx4 (glutathione peroxidase 4), a key suppressor of lipid peroxidation, promoted iron overload and ferroptosis in the heart, leading to dilated cardiomyopathy. Mice with heterozygous Gpx4 knockout were also predisposed to adverse cardiac remodeling and dysfunction following pressure overload. Mechanistically, elevated lipid peroxidation due to GPX4 inactivation intrinsically induced iron overload by promoting the nuclear export of Bach1 and subsequent induction of heme oxygenase-1 (HO-1). Genetic and pharmacologic inhibition of HO-1 markedly attenuated iron overload and ferroptosis in cardiomyocytes and rescued dilated cardiomyopathy associated with Gpx4 deficiency. Moreover, we identified HO-1 mitochondrial translocation as a key mechanism driving mitochondrial iron overload and ferroptosis. Targeted inhibition of mitochondrial iron overload or lipid peroxidation abrogated cardiac ferroptosis and pathological remodeling induced by Gpx4 deficiency. ConclusionsThese findings identified a mechanistic link between lipid peroxidation and iron overload via the Bach1-HO-1 signaling pathway, revealing new regulators and molecular targets for cardiac ferroptosis.

cell biology↗
bioRxiv2025

A Bioinformatic Investigation into the Role of ITGB1 in Cancer Prognosis and Therapeutic Resistance

Integrin {beta} 1 is a crucial transmembrane protein that regulates cellular adhesion, migration, and signal transduction, processes essential for cancer progression. This study investigates the role of ITGB1, the gene that encodes Integrin {beta}1, in various cancers using bioinformatics tools. By analyzing gene expression data across different cancer types and normal tissues, the study identifies significant upregulation of ITGB1 in 12 cancer types. We find elevated expression of ITGB1 is associated with poor prognosis in multiple tumors, suggesting its potential as a biomarker for cancer progression and therapeutic resistance. Further analysis reveals ITGB1s correlation with chemoresistance and immunoresistance genes, highlighting its involvement in cancer treatment evasion. The study also explores the expression and role of genes that are highly related to ITGB1 in tumor and patient prognosis, offering insights into potential molecular pathways and therapeutic targets. These findings underscore the clinical relevance of ITGB1 in cancer prognosis and therapy.

bioinformatics↗
bioRxiv2025

Epigenetic Modulation, Intra-tumoral Microbiome and Immunity in Early Onset Colorectal Cancer

BackgroundThe incidence of colorectal cancer (CRC) in young adults (age of diagnosis < 50 years old) has been rapidly increasing. Although [~]20% of early-onset (EO) CRC cases are due to germline mutations, the etiology of the majority of EOCRC cases remains poorly understood. Non-genetic factors such as environmental exposure and lifestyle changes are likely to have a direct link to the increased incidence of sporadic EOCRC. We hypothesize that such factors may be observable as differences in the EOCRC epigenome, microbiome and immunome. We sought to address this by comparing differences in DNA methylation from the cohort of colorectal cancer patients in The Cancer Genome Atlas (TCGA). Further, we carefully identified intra-tumoral microbes from TCGA and two other datasets and then related the microbes to EOCRC status and deconvolved immune cell abundances. We found that DNA methylation (DNAm) age acceleration by12 years when compared with average-onset CRC (AOCRC) patients. Differentially methylated sites associated with genes are related to CREB signaling in neurons, G protein coupled receptor signaling, phagosome formation and S100 family signaling. These differences were validated in the gene expression from TCGA and a second, larger real-world dataset from the Oncology Research Information Exchange Network (ORIEN). However, no consistent differences were observed in the intra-tumor microbes between EOCRC and AOCRC. Interestingly, the most abundant microbes interacted with the immune systems differently between the EOCRC and AOCRC tumors, characterized by more, larger, positive correlations in EOCRC. These data suggest epigenetic modulation and accelerated aging may play a key role in the development of EOCRC. SIGNIFICANCEWe investigated whether environmentally driven factors contribute to early-onset colorectal cancer (EOCRC). We observed accelerated epigenetic aging in EOCRC and epigenetic changes associated with chronic inflammation. Tumor immune cell abundances correlated more strongly with microbes in EOCRC than average-onset CRC. These data suggest a dysregulation of immune response in EOCRC, driving chronic inflammation and tissue aging.

cancer biology↗
bioRxiv2024

TET2-mediated epigenetic modification promotes stress senescence of pancreatic β cells in type 2 diabetes mellitus

Epigenetic modification plays a key role in {beta} cell senescence. In the regulation of gene expression, there is a complex and close relationship between DNA methylation and histone modification. In order to explore its specific mechanism in T2DM {beta} cell senescence, we used postbisulfite aptamer labeling of genome-wide bisulfite-SEQ, chromatin immunocoprecipitation-SEQ, RNA-SEQ, CRISPR/Cas9 TETs knockout, RNA interference, TET2 inhibitors, lentiviral overexpression, and gene knockout mouse models. Our study found that demethylase TET2 was localized in the islets of mice, and the expression level increased with age. TET2 knockout in pancreatic {beta} cells can hypermethylate PTEN, up-regulate MOF and enrich H4K16ac, and reduce the level of aging markers. This study confirmed that TET2-mediated PTEN DNA methylation can promote a new mechanism of {beta} cell senescence by regulating H4K16ac, providing a new molecular mechanism and therapeutic target for T2DM {beta} cell senescence therapy.

cell biology↗
bioRxiv2024

Early-life antibiotic exposure leads to gut microbial dysbiosis associated with neurodevelopment and neuroregeneration

Early-life is a critical period for neurodevelopment and establishment of gut microbiota, which are highly susceptible to antibiotic exposure. Here, we aimed to investigate association between gut microbiota and metabolites with neurodevelopment and neuroregeneration in early-life after antibiotic exposure. To induce microbial dysbiosis in offspring, a broad-spectrum antibiotic cocktail was administered to mice dams. The prefrontal lobe, spinal cord tissues and gut sample of offspring were collected at different time with or without spinal cord crush injury. 16S rRNA sequencing and metabolomics were performed to analyze the gut microbiota and metabolites. NG2 glia were cultured and treated by mitochondrial fusion and fission compounds and metabolites. Maternal antibiotic exposure significantly affected neuronal maturation, NG2 glia proliferation, prefrontal cortex myelination and injured spinal cord neuroregeneration of offspring. Mice in antibiotic exposure group exhibited disruption of gut microbiota and metabolites, along with lower Ace, Chao and Shannon indexes, higher relative abundance of Enterobacter and Escherichia_Shigella, lower lactobacillus and Streptococcus genus, and downregulated Cyclo(Arg-Gly-Asp-D-Phe-Val), Ampicilloyl, DG(8:0/i-19:0/0:0), Petasinine and 6-Hydroxymelatonin glucuronide. These metabolites were enriched in alpha-Linolenic acid metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, linoleic acid metabolism. 6-Hydroxymelatonin glucuronide, PC(20:3/0:0), PC(20:2/0:0), Ameltolide, DG(8:0/i-19:0/0:0), Inproquone, and Chorismate were the cores of networks between gut microbiota and metabolites and negatively associated with neurodevelopment and neuroregeneration. Additionally, gut microbiota metabolites promoted NG2 glia differentiation, partly through reversing the effects of mitochondrial fusion/fission compounds. Totally, antibiotic exposure in early-life changed the composition, abundance, and metabolites of gut microbiota in offspring, which was associated with neurodevelopment and neuroregeneration.

microbiology↗
bioRxiv2024

Identification and predictive machine learning models construction of gut microbiota associated with lymph node metastasis in colorectal cancer

This study focuses on the significant role between gut microbiota and lymph node metastasis (LNM) in colorectal cancer (CRC). By conducting 16S rRNA sequencing on fecal samples from 147 CRC patients and combining it with the linear discriminant analysis effect size (LEfSe) algorithm, we successfully identified significant differences in the gut microbiota between patients with LNM and those with none lymph node metastasis (NLNM). Furthermore, using transcriptome data from 9 CRC patients, we constructed an immune cell infiltration matrix to deeply explore the biological functions associated with LNM. Eventually, using the characteristics of the gut microbiota associated with LNM, we developed random forest (RF) and multilayer perceptron (MLP) machine learning models to predict the lymph node metastasis status of CRC patients. We identified 21 differentially abundant gut microbes between the two groups, among which Bacteroides plebeius, significantly enriched in LNM group, is closely related to the upregulation of resting NK cells and chemokine CXCL8 expression, and this bacterial species is also positively correlated with the enhancement of fructose metabolism. The RF and MLP models constructed based on the LNM-associated gut microbiota showed good predictive efficacy in predicting LNM status in CRC. This study reveals that Bacteroides plebeius may play an important role in the progression of CRC, with its mechanism potentially involving changes in immune modulation and metabolic pathways. The classification model constructed based on gut microbiota characteristics can predict LNM status of CRC, providing a new perspective for personalized and precision treatment of CRC patients. ImportanceThis study highlights the pivotal role of gut microbiota in lymph node metastasis (LNM) of CRC, identifying key microbial differences between LNM and NLNM patients. Our findings implicate Bacteroides plebeius in CRC progression via immune modulation and metabolic alterations. Moreover, machine learning models based on gut microbiota predict LNM status accurately, offering a novel approach for personalized CRC treatment.

microbiology↗
bioRxiv2023

Combinatorial in silico approach for cancer-associated 4Fe-4S protein discovery

Iron-sulfur (Fe-S) proteins play vital roles in multiple cellular processes, including mediating redox balance as well as DNA replication and repair. Given the role of Fe-S cofactors in genome maintenance, mutations in such metalloproteins could be associated with cancer. Nevertheless, only a few cancer-associated Fe-S proteins have been identified. In vitro, Fe-S cluster is susceptible to degradation in oxic environment. It could also be replaced by other metal ions during protein purification, mis-labelled as zinc finger or Zn-containing proteins. In silico, bioinorganic Fe-S cluster lacks unique sequence characteristics that distinguish itself from other metal-coordination sites, making motif prediction based solely on protein sequence difficult. Thus, in this study, three traits have been employed to discover putative cancer-associated 4Fe-4S proteins. Here, we have analyzed the human proteome via a three-pronged approach: (i) the presence of a triamino acid motif, (ii) the geometric arrangements of the cysteines, and (iii) the mutations of cancer-associated cysteines. In addition to MUTYH, a known 4Fe-4S human DNA glycosylase, 21 novel proteins were discovered as potential cancer-associated 4Fe-4S proteins. While 6 receptor proteins and 3 growth factors have been identified as potential targets in this study, 5 histone lysine methyltransferases with SET domains were also predicted to contain 4Fe-4S metallocofactors. This work provides insights for rational adjustments in experimental design and novel cancer biomarker discovery.

bioinformatics↗
bioRxiv2023

An axonemal intron splicing program sustains Plasmodium male development

Differentiation of male gametocyte into flagellated fertile male gamete relies on the axoneme assembly, a major component of male development for mosquito transmission of malaria parasite. RNA-binding protein (RBP)-mediated post-transcription regulation plays important roles in eukaryotic sexual development, including the Plasmodium female development. However, the role of RBP in defining the Plasmodium male transcriptome and its function in the male gametogenesis remain elusive. Here, we screened the gender expression of the genome-wide RBPs and identified an undescribed male-specific RBP gene Rbpm1 in the Plasmodium. RBPm1 is localized in the nucleus of male gametocytes. RBPm1-deficient parasites fail to assemble the axoneme for male gametogenesis and thus mosquito transmission. RBPm1 interacts with spliceosome E complex and regulates splicing initiation of certain introns in a group of 26 axonemal genes. RBPm1 deficiency results in intron retention and protein loss of these axonemal genes. Intron deletion restores axonemal proteins expression and partially rectifies axonemal defects in RBPm1-null gametocytes. Further splicing assays in both reporter and endogenous genes exhibit stringent recognition of the axonemal introns by RBPm1. Therefore, the splicing activator RBPm1 and its target introns constitute an axonemal intron splicing program in the post-transcription regulation essential for Plasmodium male development.

microbiology↗
bioRxiv2023

A multiplexed time-resolved fluorescence resonance energy transfer ultrahigh-throughput screening assay for targeting SMAD4-SMAD3-DNA complex

The signaling pathway of transforming growth factor-beta (TGF{beta}) plays crucial roles in the establishment of an immunosuppressive tumor microenvironment, making anti-TGF{beta} agents a significant area of interest in cancer immunotherapy. However, the clinical translation of current anti-TGF{beta} agents that target upstream cytokines and receptors remains challenging. Therefore, the development of small molecule inhibitors specifically targeting SMAD4, the downstream master regulator of TGF{beta} pathway, would offer an alternative approach with significant therapeutic potential for anti-TGF-{beta} signaling. In this study, we present the development of a cell lysate-based multiplexed time-resolved fluorescence resonance energy transfer (TR-FRET) assay in an ultrahigh-throughput screening (uHTS) 1536-well plate format. This assay enables simultaneous monitoring of the protein-protein interaction (PPI) between SMAD4 and SMAD3, as well as the protein-DNA interaction (PDI) between SMADs and their consensus DNA binding motif. The multiplexed TR-FRET assay exhibits high sensitivity, allowing the dynamic analysis of the SMAD4-SMAD3-DNA complex at single amino acid resolution. Moreover, the multiplexed uHTS assay demonstrates robustness for screening small molecule inhibitors. Through a pilot screening of an FDA-approved and bioactive compound library, we identified gambogic acid and gambogenic acid as potential hit compounds. These proof-of-concept findings underscore the utility of our optimized multiplexed TR-FRET platform for large-scale screening to discover small molecule inhibitors that target the SMAD4-SMAD3-DNA complex as novel anti-TGF{beta} signaling agents.

cancer biology↗
bioRxiv2023

EB1 decoration of microtubule lattice facilitates spindle-kinetochore lateral attachment in Plasmodium male gametogenesis

Faithful chromosome segregation of 8 duplicated haploid genomes into 8 daughter male gametes is essential for male gametogenesis and mosquito transmission of Plasmodium. Plasmodium evolves the endomitosis for this multinucleated cell division. However, the mechanism underlying the spindle-kinetochore attachment remains elusive. End-binding proteins (EBs) are the conserved microtubule (MT) plus-end binding proteins and play an important role in regulating MT plus-end dynamics. Here we report that Plasmodium EB1 is a unique orthologue distinct from the canonical eukaryotic EB1. Both in vitro and in vivo assays revealed that Plasmodium EB1 lost MT plus-end tracking but gained MT-lattice affinity. This MT-binding feature of EB1 is contributed by both the CH domain and the linker region. EB1-deficient parasites produce male gametocytes that develop to the anucleated male gametes, leading to defective mosquito transmission of parasite. EB1 is localized at the nucleoplasm of male gametocytes. Upon gametogenesis, EB1 decorates the full-length of spindle MTs and regulates spindle structure. The kinetochores attach to spindle MTs laterally throughout three rounds of endomitosis and this attachment is EB1-dependent. Consequently, impaired spindle-kinetochore attachment was observed in EB1-deficient parasites. These results indicate that a parasite-specific EB1 with MT-lattice affinity has evolved to fulfill the spindle-kinetochore lateral attachment in male gametogenesis.

microbiology↗
bioRxiv2023

Heat dissipation from photosynthesis contributes to maize thermoregulation under suboptimal temperature conditions

The extent to which plants thermoregulate to maintain relatively stable metabolic function in response to gradual and rapid temperature changes that jeopardize crop production is unclear. Maize thermoregulation was investigated based on leaf temperature (TL) measurements and its relationship with photochemistry and stomatal conductance (gs) under dry and wet soil scenarios. Seasonal climatology was simulated in a growth chamber according to Beijings climatology with extreme "hot days" based on historical maxima. Maize behaved as a limited homeotherm, an adaptive strategy to maintain photosynthesis around optimum temperatures (Topt). Plants on drier soil had lower thermoregulatory capacity, with reduced gs, photosynthesis and transpiration, which impacted final yields, despite acclimation with a higher Topt to sustained stress. On hot days thermoregulation was affected by heat stress and water availability, suggesting that strong and frequent heatwaves will reduce crop activity although increased temperatures could bring photosynthesis closer to Topt in the region. We propose a novel mechanism to explain thermoregulation from the contribution of heat dissipation via non-photochemical quenching (NPQ) to TL, supporting our hypothesis that NPQ acts as a negative feedback mechanism from photosynthesis by increasing TL in suboptimal conditions. These results could help to design adaptation strategies based on deficit irrigation. HighlightMaize was able to maintain leaf temperatures in narrower ranges than air temperatures by dissipating sunlight not used in photosynthesis as heat energy with a key role of transpiration cooling to sustain optimum photosynthesis temperature.

plant biology↗
bioRxiv2022

Ensemble Machine Learning to Boost Ubiquitination-sites Prediction

Ubiquitination-site prediction is an important task because ubiquitination is a critical regulatory function for many biological processes such as proteasome degradation, DNA repair and transcription, signal transduction, endocytoses, and sorting. However, the highly dynamic and reversible nature of ubiquitination makes it difficult to experimentally identify specific ubiquitination sites. In this paper, we explore the possibility of improving the prediction of ubiquitination sites using ensemble machine learning methods including Random Forrest (RF), Adaptive Boosting (ADB), Gradient Boosting (GB), and eXtreme Gradient Boosting (XGB). By doing grid search with the four ensemble methods and six comparison non-ensemble learning methods including Naive Base (NB), Logistic Regression (LR), Decision Trees (DT), Support Vector Machine (SVM), LASSO, and K-Nearest Neighbor (KNN), we find that all the four ensemble methods significantly outperform one or more non-ensemble methods included in this study. XGB outperforms three out of the six non-ensemble methods that we included; ADB and RF both outperform two of the six non-ensemble methods; GB outperforms one non-ensemble method. Comparing the four ensemble methods among themselves. GB performs the worst; XGB and ADB are very comparable in terms of prediction, but ADB beats XGB by far in terms of both the unit model training time and total running time. Both XGB and ADB tend to do better than RF in terms of prediction, but RF has the shortest unit model training time out of the three. In addition, we notice that ADB tends to outperform XGB when dealing with small-scale datasets, and RF can outperform either ADB or XGB when data are less balanced. Interestingly, we find that SVM, LR, and LASSO, three of the six non-ensemble methods included, perform comparably with all the ensemble methods. Based on this study, ensemble learning is a promising approach to ignificantly improving ubiquitination-site prediction using protein segment data.

bioinformatics↗
bioRxiv2022

Mechanistic basis for targeting homologous recombination defective liver cancer via synthetic lethality

Many cancers harbour homologous recombination defects (HRD). The identification of PARP inhibitors as synthetic lethal with HRD has led to new therapeutic strategies for HRD cancers. Here we report a subtype of HRD that is caused by the perturbation of a previously uncharacterised proteasome variant, CDW19S, in hepatitis virus B (HBV) positive hepatocellular carcinoma (HBVHCC). CDW19S contains the 19S complex decorated with a Cullin 4 ubiquitin ligase (CRL4WDR70) that is assembled at broken chromatin and regulates end processing nucleases. The HBV oncoprotein, HBx, prevents integration of the CRL4 backbone into CDW19S. We show that CDW19S directly ubiquitinates ADRM1Rpn13, targeting it for degradation, and that HBx interferes with this, leading to the imposition of a novel ADRM1Rpn13-dependent resection barrier that results in HRD and promotes carcinogenesis with concurrent TP53 loss. Using cellular and patient-derived xenograft models we demonstrate that HRD in HBVHCC can be exploited to restrict tumour progression. Our work clarifies the mechanism of a virally-induced HRD and suggests a new route for targeted HBVHCC therapy.

cancer biology↗
bioRxiv2022

Tyrosine phosphorylation tunes chemical and thermal sensitivity of TRPV2 ion channel

Transient receptor potential vanilloid 2 (TRPV2) is a multimodal ion channel widely regulating central and peripheral functions. Its important involvement in immune responses has been suggested such as in the macrophages phagocytosis process. However, the endogenous signaling cascades controlling the gating of TRPV2 remain to be understood. Here, we report that enhancing tyrosine phosphorylation remarkably alters the chemical and thermal sensitivities of TRPV2 endogenously expressed in rat bone marrow-derived macrophages. We identify that the protein tyrosine kinase JAK1 mediates TRPV2 phosphorylation at the molecular sites Tyr(335), Tyr(471), and Tyr(525). JAK1 phosphorylation is required for maintaining TRPV2 activity and the phagocytic ability of macrophages. We further show that TRPV2 phosphorylation is dynamically balanced by protein tyrosine phosphatase non-receptor type 1 (PTPN1). PTPN1 inhibition increases TRPV2 phosphorylation, further reducing the activation temperature threshold to [~]40 {degrees}C. Our data thus unveil an intrinsic mechanism where the phosphorylation/dephosphorylation dynamic balance sets the basal chemical and thermal sensitivity of TRPV2. Targeting this pathway will aid therapeutic interventions in physiopathological contexts.

physiology↗
bioRxiv2021

Interferon-Gamma Signaling Promotes Melanoma Progression and Metastasis

Interferon-gamma (IFNG) has long been regarded as the flag-bearer for the anti-cancer immunosurveillance mechanisms. However, relatively recent studies have suggested a dual role of IFNG, albeit there is no direct experimental evidence for its potential pro-tumor functions. Here we provide in vivo evidence that treatment of mouse melanoma cell lines with physiological levels of Ifng enhances their tumorigenicity and metastasis in lung colonization allograft assays performed in immunocompetent syngeneic host mice, but not in immunocompromised host mice. We also show that this enhancement is dependent on downstream signaling via Stat1 but not Stat3, providing evidence of an oncogenic function of Stat1 in melanoma. The experimental results suggest that melanoma cell-specific Ifng signaling modulates the tumor microenvironment and its pro-tumorigenic effects are dependent on the {gamma}{delta} T cells, as Ifng-enhanced tumorigenesis was inhibited in the TCR-{delta} knockout mice. Overall, these results show that Ifng signaling may have tumor-promoting effects in melanoma by modulating the immune cell composition of the tumor microenvironment.

cancer biology↗