Qiao-Li Lv

Table S1: Extra-tumoral fungi in association with various cancer types. Figure S1: Interactions of Candida species with the immune system and their roles in cancer development (a): C. albicans triggers Th17/IL-17 responses, recruiting M2-like TAMs and promoting oral cancer. (b): Candida species translocate to the liver, inducing Th17/Th1 responses, leading to inflammation and liver cancer. (c): Candida spp upregulates MDSCs in the gut, driving immune evasion in CRC. C. albicans interacts with Dectin-3 on macrophages, inducing IL-22 production and contributing to CRC. C. tropicalis interacts with CARD9-expressing macrophages, which recruit MDSCs, influencing CRC. Abbreviations: SCC, squamous cell carcinoma; IL, interleukin; CCL2, C C motif chemokine ligand 2; CD163, Cluster of differentiation 163; AGR-1, arginase 1; GAL9, galentin 9; PD-L1, Programmed death-ligand 1; CD4, Cluster of differentiation 4; MDSC, myeloid-derived suppressor cells; PD1, programmed cell death protein 1; Th, T helper; CLRs, C type lectins; ILC2, innate lymphocyte 2; GM-CSF, granulocyte-macrophage colony-stimulating factor; CTL, Cytotoxic T-lymphocyte. Figure S2: Fungal interactions with the immune system contribute to cancer development in various organs (a): Alternaria species translocate to the pancreas, driving immune suppression and pancreatic cancer. (b): Malassezia species translocate to the pancreas, driving pancreatic cancer development through C3a/C3aR signaling. (c): Aspergillus sydowii activates CARD9 macrophages and recruits MDSCs, driving immune suppression and lung cancer. (d): Highly autoreactive T cells in the esophagus lead to Cladosporium infection and activate EGFR signaling, contributing to esophageal cancer. Abbreviations: Th, T helper; IL, interleukin; CD, Cluster of differentiation; MDSC, myeloid-derived suppressor cells; PD1, programmed cell death protein 1; C3aR, C3a receptor; ILC2, innate lymphocyte 2; EGFR, Epidermal growth factor receptor. Table S2: Overview of clinical strategies targeting specific fungi for the treatment and prevention of cancer.

Fungal dysbiosis is increasingly recognized as a key factor in cancer, influencing tumor initiation, progression, and treatment outcomes. This review explores the role of fungi in carcinogenesis, with a focus on mechanisms such as immunomodulation, inflammation induction, tumor microenvironment remodeling, and interkingdom interactions. Fungal metabolites are involved in oncogenesis, and antifungals can interact with anticancer drugs, including eliciting potential adverse effects and influencing immune responses. Furthermore, mycobiota profiles have potential as diagnostic and prognostic biomarkers, emphasizing their clinical relevance. The interplay between fungi and cancer therapies can affect drug resistance, therapeutic efficacy, and risk of invasive fungal infections associated with targeted therapies. Finally, emerging strategies for modulating mycobiota in cancer care are promising approaches to improve patient outcomes.

To investigate the expression pattern of RBM43 in glioma and evaluate its prognostic significance, with particular attention to its association with the glioma immune microenvironment. RBM43 expression, clinicopathological associations, and prognostic value were analyzed using RNA-seq data from the TCGA and GTEx databases. RBM43 function was evaluated in vitro using proliferation, migration, and apoptosis assays, and was further tested in an in vivo mouse model. To probe RBM43-related biology, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were performed to identify enriched pathways. Immune infiltration and macrophage polarization were assessed using immune-related bioinformatic analyses and flow cytometry with M1/M2 markers. Elevated RBM43 expression in glioma correlated with higher WHO grade, IDH-wildtype status, and reduced overall survival (OS). Kaplan-Meier and univariable Cox analyses indicated that RBM43 was related to unfavorable outcomes. Functionally, RBM43 overexpression promoted glioma cell proliferation and migration and suppressed apoptosis, whereas RBM43 knockdown exerted the opposite effects. Immune analyses revealed that elevated RBM43 expression was closely associated with macrophage M2 polarization, suggesting its involvement in immune evasion. In vivo, RBM43 overexpression accelerated tumor progression, while RBM43 knockdown inhibited tumor growth. RBM43 is associated with glioma aggressiveness and macrophage M2-like polarization. These findings suggest that RBM43 may serve as a prognostic biomarker and a potential therapeutic target in glioma.

Aspergillosis is a serious public health concern worldwide; however, its epidemiology and clinical predictors remain poorly characterized among cancer patients in China, particularly in regions such as Jiangxi, where regional data are limited. This study aimed to evaluate the epidemiology, risk factors, and potential utility of routine inflammatory biomarkers in distinguishing Aspergillus colonization from infection in this population. In the current retrospective study, the epidemiology, risk factors, and blood biomarkers of Aspergillus cases among cancer patients at Jiangxi Cancer Hospital in Nanchang, China, were investigated from 2021 to 2025. There were 354 cases in all, with 14.1% colonization, 43.5% possible infections, and 42.4% probable infections. Almost half of the patients had underlying lung cancer (n = 161, 45.48%), and Aspergillus fumigatus (n = 313, 88.42%) was the most frequently detected species. The use of steroids (OR 18.16, p < 0.001), chemotherapy (OR 5.41, p = 0.003), and high glucose levels (OR 1.68, p = 0.02) were shown to be independent risk factors for infection in all cancer populations. In lung cancer patients, smoking (OR 4.11, p < 0.001), chronic obstructive pulmonary disease (COPD) (OR 3.83, p = 0.02), and steroid usage (OR 3.06, p = 0.03) were independently related to higher infection risk. Biomarker analysis revealed that probable infection was associated with higher neutrophil and white blood cell (WBC) counts, a higher neutrophil-to-lymphocyte ratio (NLR), and metabolic markers, including glucose and creatinine. Principal component analysis (PCA) demonstrated distinct clustering driven by inflammatory signatures. This study provides comprehensive epidemiological data on aspergillosis in a large cohort of cancer patients in Jiangxi, China, and highlights the potential value of routinely available inflammatory markers in differentiating colonization from infection. These findings may support early risk stratification and improve clinical decision-making, particularly in resource-limited settings where advanced fungal diagnostics are not readily available.

Glioblastoma (GBM) is a highly aggressive and lethal brain tumor, and despite conventional treatments, patient prognosis remains poor. Understanding the molecular mechanisms driving GBM and identifying potential therapeutic targets is critical. MOV10, an RNA helicase, is overexpressed in multiple cancers and is considered an oncogene. Our analysis of datasets from TCGA, GEO, and CGGA showed that MOV10 expression is elevated in GBM and strongly negatively correlated with overall survival (OS). Cox regression confirmed MOV10 as an independent prognostic risk factor for GBM.Functional enrichment analysis revealed that MOV10 is involved in immune regulation and tumor progression pathways. We found that MOV10 expression is closely linked to immune infiltration, immune checkpoint expression, and responses to immunotherapy. Immunofluorescence and Transwell assays confirmed that MOV10 knockdown reduced M2 macrophage migration and invasion in GBM cells. Clinical analysis further validated MOV10 overexpression in GBM tissues.In vitro, MOV10 silencing suppressed GBM cell proliferation, inhibited EMT-like processes, and promoted apoptosis through autophagy modulation. Our findings suggest that MOV10 plays a crucial role in GBM progression and could be a promising molecular target for therapy.

Tumor immunity and metabolism are interconnected through the tumor microenvironment (TME), with RNA modifications playing pivotal epigenetic regulatory rol

Background: Paclitaxel (PTX) serves as a first-line chemotherapeutic agent for the treatment of advanced non-small cell lung cancer (NSCLC). However, the emergence of drug resistance poses a significant threat to patient survival. The serine synthetic pathway (SSP) has been implicated in drug resistance across various cancers and is notably activated in NSCLC. Nevertheless, its role in PTX resistance remains poorly understood. Methods: In this study, we investigated the influence of the SSP on PTX resistance in NSCLC and explored a novel combination therapeutic strategy involving PTX and anlotinib to reverse NSCLC drug resistance. Specifically, using integrated transcriptomic and metabolomic analyses along with in vitro and in vivo experimental approaches, we aimed to elucidate the regulatory role of activated SSP in PTX resistance and to determine whether the combination of anlotinib and PTX can overcome PTX resistance in NSCLC through modulation of the SSP. Results: We found that SSP activation drives PTX resistance by promoting the proliferation of PTX-resistant NSCLC cells, increasing the expression and transport function of P-glycoprotein (P-gp), inducing epithelial-to-mesenchymal transition (EMT), and maintaining redox homeostasis. Anlotinib synergizes with PTX by suppressing SSP. This leads to attenuated glycolysis, disruption of the AKT/ERK proliferative signaling pathway, inhibition of P-gp expression and function, reversal of EMT, and redox imbalance, which subsequently elevates reactive oxygen species (ROS) levels and activates the mitochondrial apoptosis pathway, ultimately inducing apoptosis. Conclusion: Collectively, our study demonstrates that anlotinib combined with PTX, via SSP inhibition, is a promising strategy for overcoming PTX resistance in NSCLC. Graphical