Identification of an <scp>EMT‐related gene‐based</scp> prognostic signature in osteosarcoma

Gong, Haoli; Tao, Ye; Xiao, Sheng; Li, Xin; Fang, Ke; Wen, Jie; Zeng, Ming; Liu, Yiheng; Chen, Yang

doi:10.1002/cam4.5942

Cited by 6 publications

(3 citation statements)

References 55 publications

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“…Three of the four CpG sites were hypomethylated; one was in a CpG island, and three were associated with a promoter. These CpG sites annotated to genes associated with PFAS related health conditions, including various cancers, − cognition, cardiometabolic − and cardiovascular health (Table S3).…”

Section: Resultsmentioning

confidence: 99%

Lifetime Postnatal Exposure to Perfluoroalkyl Substance Mixture and DNA Methylation at Twelve Years of Age

Liu,

Gairola,

Kuiper

et al. 2023

Environ. Sci. Technol. Lett.

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Per-and polyfluoroalkyl substance (PFAS) exposure has been linked to DNA methylation changes in neonates and adults. We previously reported that prenatal PFAS exposure may have a durable impact on DNA methylation from birth to adolescence. However, few studies have examined the association of postnatal PFAS exposure with alterations in DNA methylation. We examined the associations of lifetime postnatal PFAS mixture exposure with leukocyte DNA methylation in 154 adolescents from the HOME Study (2003Study ( −2006 Cincinnati, Ohio). Lifetime postnatal PFAS mixture exposure was estimated using latent profile analysis of four PFAS concentrations measured at birth, and ages 3, 8, and 12 years. We measured DNA methylation in peripheral leukocytes at 12 years using the Illumina HumanMethylation EPIC BeadChip. We estimated covariate-adjusted associations between postnatal PFAS mixture concentrations and DNA methylation measures using linear regression and used KEGG enrichment analysis to identify molecular pathways. Four significant differentially methylated positions were observed in the higher vs lower PFAS profile (FDR p-value < 0.05). These PFAS-associated CpG sites annotated to gene regions related to various cancers, cognition, and cardiometabolic health. We identified 17 pathways (FDR p-value < 0.05), which indicate possible mechanism linking PFAS exposure to several health effects.

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Section: Resultsmentioning

confidence: 99%

Lifetime Postnatal Exposure to Perfluoroalkyl Substance Mixture and DNA Methylation at Twelve Years of Age

Liu,

Gairola,

Kuiper

et al. 2023

Environ. Sci. Technol. Lett.

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“…Gong et al reported seven novel EMT-related genes for OS outcome prediction, including CDK3, MYC, UHRF2, STC2, COL5A2, MMD, and EHMT2. A high expression of EMT-related genes was associated with poor overall and recurrence-free survival compared to the low-expressing group [156]. The GSVA and GSEA analysis showed a nine-gene set for EMT, including LAMA3, LGALS1, SGCG, VEGFA, WNT5A, MATN3, ANPEP, FUCA1, and FLNA, as independent prognostic markers for OS patient survival [157].…”

Section: Epithelial-to-mesenchymal Transformation and The Osteosarcom...mentioning

confidence: 98%

Decoding the Impact of Tumor Microenvironment in Osteosarcoma Progression and Metastasis

Nirala,

Yamamichi,

Petrescu

et al. 2023

Cancers

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Osteosarcoma (OS) is a heterogeneous, highly metastatic bone malignancy in children and adolescents. Despite advancements in multimodal treatment strategies, the prognosis for patients with metastatic or recurrent disease has not improved significantly in the last four decades. OS is a highly heterogeneous tumor; its genetic background and the mechanism of oncogenesis are not well defined. Unfortunately, no effective molecular targeted therapy is currently available for this disease. Understanding osteosarcoma’s tumor microenvironment (TME) has recently gained much interest among scientists hoping to provide valuable insights into tumor heterogeneity, progression, metastasis, and the identification of novel therapeutic avenues. Here, we review the current understanding of the TME of OS, including different cellular and noncellular components, their crosstalk with OS tumor cells, and their involvement in tumor progression and metastasis. We also highlight past/current clinical trials targeting the TME of OS for effective therapies and potential future therapeutic strategies with negligible adverse effects.

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“…These pathways also aid in cells' epithelial-mesenchymal transition (EMT), encouraging cancer cell migration, invasion, and metastasis. Hinton and colleagues explained the role of these factors in EMT in the pathophysiology of OS [87][88][89] (Figure 3 and Table 5).…”

Section: Signaling Pathwaysmentioning

confidence: 99%

Unveiling the Protective Role of Melatonin in Osteosarcoma: Current Knowledge and Limitations

Al-Ansari,

Samuel,

Büsselberg

2024

Biomolecules

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Melatonin, an endogenous neurohormone produced by the pineal gland, has received increased interest due to its potential anti-cancer properties. Apart from its well-known role in the sleep–wake cycle, extensive scientific evidence has shown its role in various physiological and pathological processes, such as inflammation. Additionally, melatonin has demonstrated promising potential as an anti-cancer agent as its function includes inhibition of tumorigenesis, induction of apoptosis, and regulation of anti-tumor immune response. Although a precise pathophysiological mechanism is yet to be established, several pathways related to the regulation of cell cycle progression, DNA repair mechanisms, and antioxidant activity have been implicated in the anti-neoplastic potential of melatonin. In the current manuscript, we focus on the potential anti-cancer properties of melatonin and its use in treating and managing pediatric osteosarcoma. This aggressive bone tumor primarily affects children and adolescents and is treated mainly by surgical and radio-oncological interventions, which has improved survival rates among affected individuals. Significant disadvantages to these interventions include disease recurrence, therapy-related toxicity, and severe/debilitating side effects that the patients have to endure, significantly affecting their quality of life. Melatonin has therapeutic effects when used for treating osteosarcoma, attributed to its ability to halt cancer cell proliferation and trigger apoptotic cell death, thereby enhancing chemotherapeutic efficacy. Furthermore, the antioxidative function of melatonin alleviates harmful side effects of chemotherapy-induced oxidative damage, aiding in decreasing therapeutic toxicities. The review concisely explains the many mechanisms by which melatonin targets osteosarcoma, as evidenced by significant results from several in vitro and animal models. Nevertheless, if further explored, human trials remain a challenge that could shed light and support its utility as an adjunctive therapeutic modality for treating osteosarcoma.

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Identification of an EMT‐related gene‐based prognostic signature in osteosarcoma

Cited by 6 publications

References 55 publications

Lifetime Postnatal Exposure to Perfluoroalkyl Substance Mixture and DNA Methylation at Twelve Years of Age

Lifetime Postnatal Exposure to Perfluoroalkyl Substance Mixture and DNA Methylation at Twelve Years of Age

Decoding the Impact of Tumor Microenvironment in Osteosarcoma Progression and Metastasis

Unveiling the Protective Role of Melatonin in Osteosarcoma: Current Knowledge and Limitations

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