Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.07.30.741861

Exploratory Network Analysis of Oral Bacteria Taste Signaling Autophagy Crosstalk in Oral Squamous Cell Carcinoma and Multi-Target Ligand Design for the MAPK1 STAT3 mTOR Axis

Abstract

G protein-coupled receptor (GPCR) signaling represents a critical interface between oral bacteria and host cellular regulation in oral squamous cell carcinoma (OSCC). Here, we integrated systems biology, exploratory machine learning, and structure-based drug design to characterize potential associations between bacteria-related signaling and autophagy and to identify candidate therapeutic targets. Taste-associated signaling genes belonging to the GPCR superfamily were curated from KEGG, while OSCC- and autophagy-associated proteins were obtained from STRING, Reactome, UniProt, KEGG, and HMDB. Ten bacteria-associated host-interaction datasets were integrated using NetworkAnalyst to construct protein- protein interaction networks, and key hub nodes were identified through degree and betweenness centrality. Feature matrices derived from network topology were analyzed using exploratory dimensionality reduction (PCA), hierarchical clustering, and supervised models (SVM and Gradient Boosting) to assess whether network-derived features showed separability according to literature-informed bacterial reference categories; a Dysbiosis Index was additionally calculated. Results suggested that bacterial sensing through taste-associated GPCR signaling may converge on a MAPK1-centered axis linking calcium signaling, autophagy, and oncogenic pathways. Pathobiont-associated networks showed greater representation of inflammatory and terminal-autophagy-related signaling through MAPK1-STAT3, whereas commensal-associated networks were more closely aligned with cytoprotective autophagy through balanced MAPK1-TP53/PTEN networks. Exploratory machine learning analyses highlighted MDM2 and AKT3 as high-contribution, network-associated candidate features linked to group separability within the current dataset. A dual-target MTDL (SG101) was designed to target downstream nodes (MDM2 and JAK2), showing favorable predicted docking interactions and computationally predicted ADMET properties. In conclusion, bacteria-associated host taste signaling may be linked to differing autophagy-related network states in OSCC, and targeting downstream regulatory hubs with multi-target ligands represents a hypothesis-generating strategy that warrants experimental validation for pathway-oriented therapy.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Akhavan, M., Latifi-Navid, S. G., Barzegar Behrooz, A., Vakili, S., Vitorino, R., Aftabi, S., Peela, S., Ponamgi, S., Schroth, R. J., Berumen, M., Yuan, C., Akbari Azirani, T., Pecic, S., Chelikani, P., Ghavami, S.. 2026-07-31. Exploratory Network Analysis of Oral Bacteria Taste Signaling Autophagy Crosstalk in Oral Squamous Cell Carcinoma and Multi-Target Ligand Design for the MAPK1 STAT3 mTOR Axis. https://doi.org/10.64898/2026.07.30.741861

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Tet2-Clonal Hematopoiesis Promotes Whereas Dnmt3a-CH Inhibits Breast Cancer Progression During Aging

Clonal hematopoiesis of indeterminate potential (CHIP) driven by somatic mutations in blood cells increases with age and is associated with adverse outcomes in cancer patients. How CHIP mutations influence solid tumor progression remains unclear. Using inducible murine models of Dnmt3a- or Tet2-mutant CHIP combined with orthotopic syngeneic breast cancer models, we demonstrate that upon aging Dnmt3a-mutant CHIP prevents whereas Tet2-mutant CHIP drives breast cancer progression. Dnmt3a-mutant immune infiltrates established interferon-mediated MHCIIhigh tumor-associated macrophages (TAMs) that supported cytotoxic CD8+ T cell-mediated tumor rejection. In contrast, Tet2-mutant TAMs exhibited an inflammatory, immunosuppressive phenotype characterized by increased IL-1 and CXCL2 production, reduced MHCII expression, and impaired T cell recruitment and activation. Therapeutic blockade of IL-1R1 or CXCR2 reduced tumor progression in aged Tet2-mutant CHIP mice and partially restored anti-tumor immunity. These findings establish that the effects of CHIP on cancer are mutation- and age-dependent and identify IL-1/CXCL2-driven inflammation as a therapeutic vulnerability of tumor-promoting Tet2-mutant CHIP.

cancer biology↗

Single Nucleus Profiling Reveals Rewired Tumor-Immune-Stromal Cell Communication in Plasmacytoid Urothelial Carcinoma

Plasmacytoid urothelial carcinoma (PUC) is an aggressive histologic subtype of bladder cancer associated with worse patient outcomes and therapeutic response compared to conventional urothelial carcinoma (CUC). While recent work has demonstrated metastatic lymph nodes from PUC tumors have an inflamed phenotype, how the tumor microenvironment (TME) and crosstalk between tumor, stromal, and immune cells in primary PUC bladder tumors differs from those in CUC remains poorly understood. The impact of these differences on response to immunotherapy is also unknown. To understand TME differences between CUC and PUC and their impact on cell signaling, we performed single nucleus RNA sequencing on PUC and CUC tumors, as well as Xenium spatial transcriptomics on a mixed CUC / PUC tumor. We identified increased signaling between PUC-enriched, CDH1-low urothelial cells, immunosuppressive lipid-associated macrophages, and SFRP2+/CTHRC1+ fibroblasts in PUC tumors compared to CUC. Spatial transcriptomics identified increased macrophage infiltration in PUC histology and colocalization of PUC tumor cells, immunosuppressive macrophages, and SFRP2+ fibroblasts. Taken together, this study delineates PUC architecture and demonstrates interplay CDH1-low tumor cells, EMT, and immunosuppressive macrophages, identifying possible therapeutic vulnerabilities in PUC.

cancer biology↗

The Phospholipase A2 Activity of Peroxiredoxin 6 Protects Hepatocarcinoma Cells Against Ferroptosis and Mitophagy Impairment

Peroxiredoxin 6 (PRDX6) is a moonlighting protein that plays a key role in regulating redox homeostasis and lipid metabolism through its unique dual peroxidase and calcium-independent phospholipase A2 (iPLA2) activities. Here, we generated a stable HepG2 cell line harboring a D140A mutation to selectively ablate iPLA2 activity, and we compared its phenotype with that of wild-type (WT) and PRDX6-knockout (KO) cells. D140A exhibited low ROS leves, similar to WT cells, confirming that oxidative stress is due to peroxidase deficiency. In contrast, D140A cells displayed higher lipid peroxidation than WT cells, though significantly lower than that of KO cells. Furthermore, the D140A mutant mirrored the KO phenotype regarding intracellular ferrous iron accumulation, impaired lipid droplet biogenesis, and the downregulation of the key ferroptosis regulator GPX4. Mechanistically, integrated proteomic, lipidomic, and enzymatic analyses revealed that a deficiency in iPLA2 activity of PRDX6 disrupted the release of key lipid species necessary for cell structure and signaling. Consequently, organelles involved in lipid synthesis and trafficking, such as peroxisomes, endoplasmic reticulum, mitochondria and lipid droplet, were affected. Specifically, we found that mitochondria exhibited a reduction in cristae and a diminished capacity for mitophagy and autophagy, which ultimately makes cells much more susceptible to erastin-induced ferroptotic cell death. Taken together, our findings demonstrate that PRDX6 iPLA2 activity uniquely coordinates organelle lipid homeostasis and mitophagy to protect cancer cells from ferroptotic cell death. Consequently, the use of iPLA2 inhibitors such as MJ33, which decreased PRDX6 iPLA2 activity to a level comparable to the mutant D140A, could represent a promising therapeutic strategy for inducing ferroptotic cell death in hepatocellular carcinoma.

cancer biology↗