Cell fusion between tumor cells and macrophages promotes the metastasis of OSCC patient through the activation of the chemokine signaling pathway
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ABSTRACT:
PROVIDER: PRJNA893684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22034373_1.fastq.gz | Fastqsanger.gz | |||
| SRR22034373_2.fastq.gz | Fastqsanger.gz | |||
| SRR22034374_1.fastq.gz | Fastqsanger.gz | |||
| SRR22034374_2.fastq.gz | Fastqsanger.gz | |||
| SRR22034375_1.fastq.gz | Fastqsanger.gz |
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Project description:Tumor metastasis is responsible for the high mortality rate of patients with oral squamous cell carcinoma (OSCC). Although many hypotheses have been proposed to elucidate the mechanism of tumor metastasis, the origin of the metastatic tumor cells remains unclear. In this study, we explored the role of cell fusion in the formation of OSCC metastatic tumor cells. Murine OSCC tumor cells and macrophages were fused in vitro, and the cell proliferation, migration, and phagocytosis abilities of hybrid cells and parental cells were compared. Subsequently, we compared the transcriptome differences between hybrid and parental cells. Finally, we observed an association between the hybrid cells and the prognosis of patients with OSCC. Murine OSCC tumor cells and macrophages were successfully fused in vitro. The cytological and molecular experimental results revealed that OSCC tumor cells obtained a migration-related phenotype after fusion with macrophages, and the migration ability of hybrid cells was related to the activation of the “chemokine signal pathway”. Moreover, we proved that the existence of hybrid cells in OSCC tumor tissues is closely related to lymph node metastasis and poor prognosis. After fusion with macrophages, the chemokine signaling pathway in OSCC tumor cells was activated, leading to metastasis.
2024-03-13 | GSE216480 | GEO
Project description:Lymph node metastasis, a powerful prognostic indicator of oral squamous cell carcinoma (OSCC), is chiefly responsible for cancer death. Long non-coding RNA (lncRNA) is recently addressed to significantly account for modulating OSCC metastasis. Here, we identified a novel alternative splice of Oral Cancer Overexpressed 1 (ORAOV1), ORAOV1-B, which was subsequently validated as an lncRNA and correlated with OSCC lymph node metastasis; significantly increased invasion and migration were observed in ORAOV1-B-overexpressed OSCC cells; In the metastatic model, ORAOV1-B also significantly contributed to OSCC-related lung metastasis. cDNA microarrays was performed to compare up- or down-regulated genes in EV and ORAOV1-B sets of OSCC, which suggested TNFα as a potential downstream of ORAOV1-B and the upregulation of pro-inflammatory genes, indicating the activation of NF-κB pathway. In summary, the novel splice variant ORAOV1-B is an lncRNA, which significantly potentiates OSCC invasion and metastasis by binding to Hsp90 and activating the NF-κB-TNFα loop. Our study implies that ORAOV1-B might serve as an attractive OSCC metastasis intervention target.
2020-03-04 | GSE145599 | GEO
Project description:While altered protein glycosylation is regarded a trait of oral squamous cell carcinoma (OSCC), its heterogeneous glycoproteome and dynamics with disease progression remain unmapped. Employing an integrated multi-omics approach comprising unbiased and quantitative glycomics and glycoproteomics on resected OSCC tissues, we firstly profiled the N-glycome that overall displayed uniform expression in OSCC patients with (N+, n = 19) and without (N0, n = 12) lymph node metastasis, suggesting relatively stable N-glycosylation during metastasis. Notably, glycoproteomics and advanced correlation analysis uncovered altered site-specific N-glycosylation and associations with clinicopathological features. Importantly, targeted analyses of the multi-omics data unveiled two N-glycans and three N-glycopeptides that were closely associated with patient survival. This study provides novel insight into the complex OSCC tissue N-glycoproteome forming an important resource to further explore the underpinning disease mechanisms and uncover new prognostic glyco-markers for OSCC.
2023-06-08 | PXD037134 | Pride
Project description:Background: Cervical lymph node metastasis is a potent prognostic factor in oral squamous cell carcinoma (OSCC). However, lymph nodes resected by sentinel node biopsy or neck dissection are usually diagnosed by examining only one or two sections of the maximal cut surface. Accurate diagnosis of the metastasis in lymph nodes is important but depends on a heavy workload of the pathologist. In this study, we have attempted to identify novel molecular markers to find the harboring cancer cells in the lymph node and establish rapid detection method. Methods: We determined the gene expression profiles of 7 metastatic lymph nodes from patients with OSCC and 1 normal lymph node and 5 salivary glands from non-cancerous patients by microarray analysis. We found the overexpression genes in all metastatic lymph nodes. Subsequently, we examined the expression of these genes in newly 23 metastatic lymph nodes and 9 normal lymph nodes by real-time quantitative RT-PCR (qRT-PCR) assay. Moreover, the rapid detection of lymph node metastasis by these genes was examined using the reverse transcription loop-mediated isothermal amplification (RT-LAMP) method. Result: Among the 4 genes identified by microarray analysis, annexin A8 (ANXA8) and desmoglein 3 (DSG3) were detected in all metastatic lymph nodes at a much higher level but not in normal lymph nodes at all by qRT-PCR. Furthermore, RT-LAMP method targeting ANXA8 rapidly detected almost lymph nodes with metastasis. Conclusions: ANXA8 could be a useful marker for detecting lymph node metastasis in OSCC. Using AB1700 system, we determined the gene expression profiles of lymph nodes with metastasis of OSCC. Normal lymph node and salivary gland tissues were used as control samples.
2015-12-21 | E-GEOD-70604 | biostudies-arrayexpress
Project description:Mitochondrial fusion limits breast cancer metastasis
| PRJNA1027379 | ENA
Project description:Background: Cervical lymph node metastasis is a potent prognostic factor in oral squamous cell carcinoma (OSCC). However, lymph nodes resected by sentinel node biopsy or neck dissection are usually diagnosed by examining only one or two sections of the maximal cut surface. Accurate diagnosis of the metastasis in lymph nodes is important but depends on a heavy workload of the pathologist. In this study, we have attempted to identify novel molecular markers to find the harboring cancer cells in the lymph node and establish rapid detection method. Methods: We determined the gene expression profiles of 7 metastatic lymph nodes from patients with OSCC and 1 normal lymph node and 5 salivary glands from non-cancerous patients by microarray analysis. We found the overexpression genes in all metastatic lymph nodes. Subsequently, we examined the expression of these genes in newly 23 metastatic lymph nodes and 9 normal lymph nodes by real-time quantitative RT-PCR (qRT-PCR) assay. Moreover, the rapid detection of lymph node metastasis by these genes was examined using the reverse transcription loop-mediated isothermal amplification (RT-LAMP) method. Result: Among the 4 genes identified by microarray analysis, annexin A8 (ANXA8) and desmoglein 3 (DSG3) were detected in all metastatic lymph nodes at a much higher level but not in normal lymph nodes at all by qRT-PCR. Furthermore, RT-LAMP method targeting ANXA8 rapidly detected almost lymph nodes with metastasis. Conclusions: ANXA8 could be a useful marker for detecting lymph node metastasis in OSCC.
2015-12-21 | GSE70604 | GEO
Project description:Mitochondrial metabolism plays a central role in promoting cancer growth and metastatic progression. The transition between a hyperfused and fragmented mitochondrial network is termed mitochondrial dynamics and is important for many mitochondria-associated functions; however, little is known regarding how this process influences metastasis. Here, we show that breast cancer cells with low metastatic potential exhibit a more fused mitochondrial network compared to highly metastatic breast cancer cells. To examine whether a fused mitochondrial network could impair metastasis, we inhibited mitochondrial fission in metastatic breast cancer cells by individual genetic deletion of three key regulators of mitochondrial fission (Drp1, Fis1 and Mff) or pharmacological intervention using leflunomide, an anti-rheumatic drug. These cells displayed a fused mitochondrial network and limited survival under anoikis conditions, consistent with mitochondrial fusion limiting metastasis. Transcriptomics and metabolomics analyses revealed that mitochondrial fusion causes significant alterations in metabolic pathways and processes related to cell adhesion. Functional bioenergetics assays demonstrated that mitochondrial fusion limited the mitochondrial capacity of cancer cells. Mitochondrial fusion in breast cancer cells had no significant effect on primary tumor growth but almost completely ablated lung metastasis in vivo. Furthermore, the transcriptomics signature associated with enhanced mitochondrial fusion correlated with improved survival in patients with breast cancer. Overall, our findings highlight mitochondrial fusion as a therapeutic opportunity for breast cancer.
2024-09-25 | GSE245216 | GEO
Project description:We have utilized our custom array GPL11054 to screen a set of sarcoma patient samples for fusion genes One negative control was included in the study. We wanted to investigate the power of our fusion-gene array GPL11054 as a means for fusion gene detection in a series of sarcoma patient samples from two diagnostic laboratories with expertise in fusion gene detection.
2013-10-23 | E-GEOD-43632 | biostudies-arrayexpress
Project description:Gene expression profiling of 66 HPV-negative OSCC primary tumor was performed to identify gene expression that is related to lymph node metastasis and poor prognosis. These gene expression profiles were combined in silico with gene expression profiles of 84 OSCC primary tumors retrieved from GSE30788.
2017-08-10 | GSE85446 | GEO
Project description:The function and mechanism about how ORAOV1-B potentiates the OSCC metastasis.
| PRJNA609923 | ENA