COL6A3 promotes cellular malignancy of osteosarcoma by activating the PI3K/AKT pathway

Guo, Hongli; Chen, Gang; Song, Zelong; Sun, Jia; Gao, Xihai; Han, Yuxia

doi:10.1590/1806-9282.66.6.740

Cited by 7 publications

(6 citation statements)

References 15 publications

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“…Among the 13 hub genes (MVP, WISP1, LCP1, FTL, FCN1, PAPSS1, KRT14, SULT1C2, RARRES1, DIRAS3, AMPD3, F2RL1, COL6A3) identi ed in this study, MVP [20,21], RARRES1 [22], DIRAS [23], F2RL1 [24], and COL6A3 [25] have been previously reported as hub genes associated with tumorigenesis and progression in multiple tumor types. AMPD3 belongs to the AMPD proteins family, and a recent study has shown that AMPD3 is associated with malignant features of gastrointestinal mesenchymal tumors and may be a potential target for cancer therapy [26].…”

Section: Discussionsupporting

confidence: 50%

Identifying Immune Cell Infiltration and Effective Diagnostic Biomarkers in DCM by Bioinformatics Analysis

Cao,

Ji,

Zhang

et al. 2024

Preprint

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Background Dilated cardiomyopathy (DCM) is a primary cardiomyopathy of unknown etiology that is common in children and older adults. Nevertheless, the absence of noticeable symptoms and suitable biomarkers pose obstacles to the timely detection and management of DCM. Results By comparing samples from dilated cardiomyopathy and controls, 629 differentially expressed genes were identified. Combined with WGCAN results, a total of 13 hub genes were identified by finding the intersection of DEGs and OS-related modular genes. The ROC curve correction results showed that these hub genes had a good predictive ability for DCM, and the GO and KEGG results showed that the hub genes and related genes were mainly enriched in the transmembrane transport of transporters and nucleotide metabolism, suggesting that hub genes induced the occurrence of DCM by affecting normal transmembrane transport and metabolism of genetic materials. The results of immune cell infiltration also showed five types of immune cells (activated B cells, natural killer cells, CD56dim natural killer cells, macrophages, and monocytes) were significantly more infiltrated in the DCM group than in the control group, suggesting that DCM patients have a different immune microenvironment from ordinary people. Conclusion In this study, we used transcriptome technology to study DCM and identified 13 hub genes between the experimental and control groups, and subsequent validation demonstrated the potential of these hub genes as potential biomarkers for DCM. These findings may provide new insights into the clinical diagnosis of DCM.

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Section: Discussionsupporting

confidence: 50%

Identifying Immune Cell Infiltration and Effective Diagnostic Biomarkers in DCM by Bioinformatics Analysis

Cao,

Ji,

Zhang

et al. 2024

Preprint

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“… 33 COL6A3 increased the proliferation and colony formation of OS cells in vitro via activating PI3K/AKT pathway. 34 COL1A1 polymorphism at rs1061970 was associated with death cases in patients with OS. 35 COL9A3 was involved in the immune regulation and OS progression.…”

Section: Discussionmentioning

confidence: 92%

“…COL6A1 was highly expressed in OS tissues and promoted OS lung metastasis 33 . COL6A3 increased the proliferation and colony formation of OS cells in vitro via activating PI3K/AKT pathway 34 . COL1A1 polymorphism at rs1061970 was associated with death cases in patients with OS 35 .…”

Section: Discussionmentioning

confidence: 94%

Analysis of the effects of M2 macrophage‐derived PDE4C on the prognosis, metastasis and immunotherapy benefit of osteosarcoma

Pan,

et al. 2024

J Cellular Molecular Medi

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Tumour‐associated macrophages (TAMs), encompassing M1 and M2 subtypes, exert significant effects on osteosarcoma (OS) progression and immunosuppression. However, the impacts of TAM‐derived biomarkers on the progression of OS remains limited. The GSE162454 profile was subjected to single‐cell RNA (scRNA) sequencing analysis to identify crucial mediators between TAMs and OS cells. The clinical features, effects and mechanisms of these mediators on OS cells and tumour microenvironment were evaluated via biological function experiments and molecular biology experiments. Phosphodiesterase 4C (PDE4C) was identified as a pivotal mediator in the communication between M2 macrophages and OS cells. Elevated levels of PDE4C were detected in OS tissues, concomitant with M2 macrophage level, unfavourable prognosis and metastasis. The expression of PDE4C was observed to increase during the conversion process of THP‐1 cells to M2 macrophages, which transferred the PDE4C mRNA to OS cells through exosome approach. PDE4C increased OS cell proliferation and mobility via upregulating the expression of collagens. Furthermore, a positive correlation was observed between elevated levels of PDE4C and increased TIDE score, decreased response rate following immune checkpoint therapy, reduced TMB and diminished PDL1 expression. Collectively, PDE4C derived from M2 macrophages has the potential to enhance the proliferation and mobility of OS cells by augmenting collagen expression. PDE4C may serve as a valuable biomarker for prognosticating patient outcomes and response rates following immunotherapy.

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“…Of note, a previous work demonstrated that COL6 is able to activate AKT signaling through the NG2/CPSG2 receptor expressed on the plasma membrane of breast cancer cells, in turn promoting tumor growth [ 65 ]. Interestingly, AKT phosphorylation was shown to be similarly affected upon COL6A3 siRNA-mediated silencing in osteosarcoma cells [ 75 ], also displaying a marked deregulation upon COL6A1 and COL6A2 modulation in bladder cancer cells [ 76 ]. Beside COL6 ability to modulate the PI3K/AKT pathway in cancer, in vivo and in vitro studies demonstrated an impact of COL6 on such axis in other districts, with also deregulation of MAPK/ERK kinases and upregulation of mTOR in the COL6 knockout context [ 21 , 77 ].…”

Section: Discussionmentioning

confidence: 99%

Collagen VI sustains cell stemness and chemotherapy resistance in glioblastoma

Cescon

Rampazzo

Bresolin

et al. 2023

Cell. Mol. Life Sci.

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Microenvironmental factors are known fundamental regulators of the phenotype and aggressiveness of glioblastoma (GBM), the most lethal brain tumor, characterized by fast progression and marked resistance to treatments. In this context, the extracellular matrix (ECM) is known to heavily influence the behavior of cancer cells from several origins, contributing to stem cell niches, influencing tumor invasiveness and response to chemotherapy, mediating survival signaling cascades, and modulating inflammatory cell recruitment. Here, we show that collagen VI (COL6), an ECM protein widely expressed in both normal and pathological tissues, has a distinctive distribution within the GBM mass, strongly correlated with the most aggressive and phenotypically immature cells. Our data demonstrate that COL6 sustains the stem-like properties of GBM cells and supports the maintenance of an aggressive transcriptional program promoting cancer cell proliferation and survival. In particular, we identified a specific subset of COL6-transcriptionally co-regulated genes, required for the response of cells to replicative stress and DNA damage, supporting the concept that COL6 is an essential stimulus for the activation of GBM cell response and resistance to chemotherapy, through the ATM/ATR axis. Altogether, these findings indicate that COL6 plays a pivotal role in GBM tumor biology, exerting a pleiotropic action across different GBM hallmarks, including phenotypic identity and gene transcription, as well as response to treatments, thus providing valuable information for the understanding of the complex microenvironmental cues underlying GBM malignancy.

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COL6A3 promotes cellular malignancy of osteosarcoma by activating the PI3K/AKT pathway

Cited by 7 publications

References 15 publications

Identifying Immune Cell Infiltration and Effective Diagnostic Biomarkers in DCM by Bioinformatics Analysis

Identifying Immune Cell Infiltration and Effective Diagnostic Biomarkers in DCM by Bioinformatics Analysis

Analysis of the effects of M2 macrophage‐derived PDE4C on the prognosis, metastasis and immunotherapy benefit of osteosarcoma

Collagen VI sustains cell stemness and chemotherapy resistance in glioblastoma

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