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CAV2-expressing Nerves induce Metabolic Switch toward Mitochondrial Oxidative Phosphorylation to Promote Cancer Stemness

ABSTRACT: Cancer cells and the nervous system engage in a dynamic interplay, significantly influencing initiation and progression in head and neck squamous cell carcinoma (HNSCC). Our findings highlight that cancer cells drive an increase in caveolin-2 (Cav2) expression within trigeminal ganglia and associated neural fibers in the tumor milieu, fostering a reciprocal attractant relationship between tumor cells and nerves. Notably, the knockout of Cav2, either globally or specifically in sensory neurons or glial cells, markedly attenuates the growth of orthotopically implanted tongue tumors. Moreover, Cav2-expressing nerves are implicated in shifting cancer cell metabolism towards mitochondrial oxidative phosphorylation, a process involved in maintenance of cancer stem cells (CSCs). Our results also demonstrate that Cav2-expressing nerves confer stemness properties to cancer cells. Disruption of Cav2 expression, both globally and in specific neural cell types, impedes tumorigenesis and progression in a 4-NQO-induced HNSCC mouse model. This interplay between cancer cells, neurons, and glial cells unveils a mechanism through which tumor-associated nerves contribute to cancer stemness via metabolic reprogramming, presenting a novel avenue for anticancer therapy.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Head And Neck Squamous Cell Carcinoma

SUBMITTER: Ze Zhang

LAB HEAD: Zhang ze

PROVIDER: PXD060212 | Pride | 2025-02-04

REPOSITORIES: pride

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CAV2-expressing Nerves induce Metabolic Switch toward Mitochondrial Oxidative Phosphorylation to Promote Cancer Stemness

Project description:Cancer cells and the nervous system engage in a dynamic interplay, significantly influencing initiation and progression in head and neck squamous cell carcinoma (HNSCC). Our findings highlight that cancer cells drive an increase in caveolin-2 (Cav2) expression within trigeminal ganglia and associated neural fibers in the tumor milieu, fostering a reciprocal attractant relationship between tumor cells and nerves. Notably, the knockout of Cav2, either globally or specifically in sensory neurons or glial cells, markedly attenuates the growth of orthotopically implanted tongue tumors. Moreover, Cav2-expressing nerves are implicated in shifting cancer cell metabolism towards mitochondrial oxidative phosphorylation, a process involved in maintenance of cancer stem cells (CSCs). Our results also demonstrate that Cav2-expressing nerves confer stemness properties to cancer cells. Disruption of Cav2 expression, both globally and in specific neural cell types, impedes tumorigenesis and progression in a 4-NQO- induced HNSCC mouse model.This interplay observed between cancer cells, neurons, and glial cells suggests a potential mechanism through which tumor-associated nerves might influence cancer stemness via metabolic reprogramming. This highlights a possible new direction for anticancer therapy that warrants further investigation.

2025-02-04 | GSE288675 | GEO

Dysregulation of splicing proteins in head and neck squamous cell carcinoma

Project description:Aberrant activation of splicing regulators contributes to oncogenic transformation of cells by modulating the alternative splicing events of key oncogenes. Phosphorylation of splicing factors affects subcellular localization and activity of these proteins. Studies have shown a close association between altered phosphorylation of molecules involved in splicing machinery and cancer. We carried out proteomic and phosphoproteomic analysis of head and neck squamous cell carcinoma (HNSCC) cell lines using tandem mass tag (TMT) labeling approach followed by titanium dioxide-based phosphopeptides enrichment method. LC-MS/MS analysis resulted in the identification of 4,920 phosphosites corresponding to 2,288 proteins in six HNSCC cell lines compared to a normal oral cell line; OKF6/TERT1. Among the proteins identified, 23 kinases were found to be hyperphosphorylated in all HNSCC cell lines compared to the normal oral cell line.

2018-10-24 | PXD001862 | Pride

Myelin proteome differences in old and young mice

Project description:Aging of the peripheral nervous system (PNS) is associated with structural and functional changes that lead to a reduction in regenerative capacity and the development of age-related peripheral neuropathy. Myelin is a central component in maintaining physiological peripheral nerve function, and differences in myelin maintenance, degradation, formation and clearance have been suggested to contribute to age-related PNS changes. In addition, recent proteomic studies have elucidated the complex composition of the total myelin proteome in health and its changes in neuropathy models. However, changes in the myelin proteome of peripheral nerves during ageing have not been investigated. Hence, the aim of this proteomics experiment was to define proteome changes in isolated myelin fractions during ageing, by investigating myelin proteome profiles from young (nerves from 2-3 month old mice) and old (nerves from 18 months old mice) nerves.

2023-10-19 | PXD040719 | Pride

LC-MS characterization of anti-PD-L1 and CXCR4 bispecific nanobodies

Project description:Antibodies and derivative drugs targeting immune checkpoints have been approved for the treatment of several malignancies, but there are fewer responses in patients with pancreatic cancer. Here, we designed a nanobody molecule with bi-targeting on PD-L1 and CXCR4, as both targets are overexpressed in many cancer cells and play important roles in tumorigenesis. The nanobody sequences targeting PD-L1 and CXCR4 were linked by the (G4S)3 flexible peptide to construct the anti-PD-L1/CXCR4 bispecific nanobody. The bispecific nanobody was expressed in E. coli cells and purified by affinity chromatography. The purified nanobody was biochemically characterized by mass spectrometry, Western blotting and flow cytometry to confirm the molecule and its association with both PD-L1 and CXCR4. The biological function of the nanobody and its anti-tumour effects were examined.

2023-03-11 | PXD037102 | Pride

DYRK1A, a potential therapeutic target for head and neck squamous cell carcinoma

Project description:To identify the activated tyrosine kinase signaling pathways in HNSCC, we carried out phosphotyrosine profiling using a panel of HNSCC cell lines compared to a normal oral keratinocyte. A total of 61 unique phosphosites were identified across these cell lines. Dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A) was one of the kinases hyperphosphorylated at Y321 in all the HNSCC cell lines compared to the normal oral cell line OKF6/TERT1. Inhibition of DYRK1A using its specific siRNA and inhibitor resulted in a decrease in the invasion and colony formation ability of the HNSCC cell lines. Further, the treatment of mice bearing HNSCC xenograft tumors with DYRK1A inhibitor (harmine) showed regression of tumor growth. Our results demonstrate that DYRK1A could be a novel therapeutic target in HNSCC.

2018-10-24 | PXD002132 | Pride

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2024-12-02 | PXD046582 | Pride

Expression analysis of radio-resistant and -sensitive head and neck cancer cells

Project description:Head and Neck Squamous Cell Carcinoma (HNSCC) is a common cause of cancer death. Despite enormous technical advances in surgery and radiotherapy in the recent decade, survival of HNSCC patients has not markedly improved, with only 30% of patients diagnosed with advanced HNSCC that will survive for 5 years. This highlights the need to look into molecular processes leading to mechanisms of HNSCC radioresistance in HNSCC and identify novel radiosensitizers. To identify the lncRNAs associated with radiotherapy resistance in HNSCC, we performed RNA-seq analysis of radiation resistant and sensitive HNSCC cells.

2024-11-01 | GSE217645 | GEO

Effect of SNHG6 depletion on gene expression in radioresistant RTR61 cells

Project description:Head and Neck Squamous Cell Carcinoma (HNSCC) is a common cause of cancer death. Despite enormous technical advances in surgery and radiotherapy in the recent decade, survival of HNSCC patients has not markedly improved, with only 30% of patients diagnosed with advanced HNSCC that will survive for 5 years. This highlights the need to look into molecular processes leading to mechanisms of HNSCC radioresistance in HNSCC and identify novel radiosensitizers. Up-regulation of the SNHG6 micropeptide is associated with radioresistance of HNSCC cells. To assess the mechanism SNHG6-mediated radioresistance, we performed transcriptome analyses of RTR61 cells expressing either siScramble, or siSNHG6.

2024-11-01 | GSE217642 | GEO

Gene expression profiles of rat tissues surrounding Vcap xenograft tumors with chemical or physical denervation.

Project description:We propose that nerves play a trophic function for epithelium, not only during development, but also in adult homeostasis. Hence, nerves are likely key in cancer progression. Furthermore nerves are a functional regulator of prostate cancer genesis and progression to malignancy. A further understanding of the role of nerves in prostate cancer progression and a dissection of specific mechanisms would aid in identifying potential therapeutic targets that are centered on cancer-nerve interactions. To address this in detail, we have examined the effects of nerve function in the VCaP prostate cancer xenograft model and have elucidated differential gene expression profiles in this model.

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SILAC-based proteomic approach to delineate molecular alterations associated with erlotinib resistance in head and neck squamous cell carcinoma

Project description:Although Epidermal growth factor receptor (EGFR) is overexpressed in 90% of Head and neck squamous cell carcinoma (HNSCC) patients. Clinical trials with EGFR-targeted small molecule inhibitors such as erlotinib have shown a modest activity in recurrent or advanced HNSCC. To investigate the acquired mechanisms of erlotinib resistance we employed SILAC-based total proteomic analysis of an isogenic pair of erlotinib sensitive (SCC-S) and resistant (SCC-R) HNSCC cell line. This resulted in the identification of 5,427 proteins of which 532 proteins were overexpressed and 527 proteins were downregulated in SCC-R cells as compared to SCC-S cells (≥2 fold). Several proteins known to mediate erlotinib resistance in HNSCC and lung cancer were found to be dysregulated. Bioinformatics analysis of differentially expressed proteins showed enrichment of proteins involved in focal adhesion kinase (FAK) pathway downstream of EGFR. We identified CUB-domain containing protein 1 (CDCP1) and integrin β1 as upstream regulators of FAK signalling pathway to be overexpressed. We further demonstrated that CDCP1 and FAK can be targeted in combination as an alternative to erlotinib in HNSCC.

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