miR-23b-3p suppressing PGC1α promotes proliferation through reprogramming metabolism in osteosarcoma

Zhu, Rixiang; Li, Xinpan; Ma, Yue

doi:10.1038/s41419-019-1614-1

Cited by 41 publications

(31 citation statements)

References 31 publications

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“…Moreover, MSCs/CAFs regulate tumor growth and metastasis through PDGFRα/β and MIF‐CXCR4/7 signaling, enhancing sarcoma aggressiveness via the secretion of inflammatory cytokines, exosomes (Miller et al , 2013; Cortini et al , 2016; Avnet et al , 2017; Baglio et al , 2017; preprint: Evdokimova et al , 2019), or metabolites that can fuel the oxidative metabolism of tumor cells (Bonuccelli et al , 2014). Metabolic fueling of sarcoma cells by stromal cells may be particularly relevant to sustain the energy demand of uncontrolled tumor growth and progression (Zhang et al , 2010; Ren et al , 2017; Gaude et al , 2018; Zhu et al , 2019). Consequently, the composition of the local TME has direct influence on the histological response to chemotherapy (Crenn et al , 2017).…”

Section: Epidemiology Of Sarcomamentioning

confidence: 99%

Sarcoma treatment in the era of molecular medicine

et al. 2020

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Sarcomas are heterogeneous and clinically challenging soft tissue and bone cancers. Although constituting only 1% of all human malignancies, sarcomas represent the second most common type of solid tumors in children and adolescents and comprise an important group of secondary malignancies. More than 100 histological subtypes have been characterized to date, and many more are being discovered due to molecular profiling. Owing to their mostly aggressive biological behavior, relative rarity, and occurrence at virtually every anatomical site, many sarcoma subtypes are in particular difficult‐to‐treat categories. Current multimodal treatment concepts combine surgery, polychemotherapy (with/without local hyperthermia), irradiation, immunotherapy, and/or targeted therapeutics. Recent scientific advancements have enabled a more precise molecular characterization of sarcoma subtypes and revealed novel therapeutic targets and prognostic/predictive biomarkers. This review aims at providing a comprehensive overview of the latest advances in the molecular biology of sarcomas and their effects on clinical oncology; it is meant for a broad readership ranging from novices to experts in the field of sarcoma.

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Section: Epidemiology Of Sarcomamentioning

confidence: 99%

Sarcoma treatment in the era of molecular medicine

et al. 2020

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“…The results of GSEA with c2.cp.kegg.v7.0.symbols.gmt as the reference gene set showed that the enrichment pathways were mainly involved in the circadian rhythm, oxidative phosphorylation, DNA replication and ECM-receptor interaction pathway. Previous reports have shown that oxidative phosphorylation [39,40], circadian rhythm [41], and DNA replication [42] were closely related to the occurrence and progress of OS. Another study has reported that ECM-receptor interaction pathway plays an important role in the occurrence, development, invasion and metastasis of malignant tumors [43].…”

Section: Discussionmentioning

confidence: 95%

“…Compared to the control group, myogenesis, adipogenesis, oxidative phosphorylation, PI3K-AKT-mTOR signaling, p53 pathway was signi cantly activated in OS samples, while E2F targets, WNT beta-catenin signaling, TGF beta signaling and glycolysis signal pathways were signi cantly inhibited. Previous studies have shown that PI3K-AKT-mTOR signaling [44,45], adipogenesis [46], WNT beta-catenin signaling [47,48], TGF beta signaling [49], glycolysis [40], and p53 pathway [50] play an important role in the development and occurrence of OS. Therefore, our analysis results are consistent with previous ndings and have high credibility, indicating that these DEGs and signaling pathways may be involved in the occurrence and progression of OS.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Immune Infiltration Pattern in Osteosarcoma and Its Clinical Significance

Yuan¹,

Deng²,

Ren³

et al. 2020

Preprint

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ObjectiveOsteosarcoma (OS), the most common malignant bone tumor, is prone to early metastasis and recurrence, resulting in poor prognosis. The purpose of this study was to investigate gene expression in OS samples, and to study the relationship between tumor infiltrating immune cells (TIICS) in the tumor microenvironment and the occurrence, development, and prognosis of OS. MethodsIntegrated analysis was performed on the gene expression profile of OS samples in the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database, and normal muscle tissue samples in the Genotype-Tissue Expression (GTEx) database. Screening of differentially expressed genes in OS samples and healthy muscle tissue samples was performed using R software. Functional annotation and pathway enrichment analyses were performed, a protein-protein interaction network was constructed, and the Hub genes were screened. The infiltration differences of 22 TIICs in OS samples and normal muscle tissue samples were analyzed using CIBERSORT. ROC curve, and OS survival analyses were performed on the Hub genes and 22 TIICs. The correlation between Hub genes with prognostic value and the 22 TIICs was discussed. ResultsTen Hub genes were screened. OS and normal muscle tissue samples were compared. Significant differences were observed in the infiltration of follicular helper T cells, resting NK cells, plasma cells, activated CD4 memory T cells, gamma delta T cells, monocytes, M0 macrophages and resting dendritic cells (P<0.05). ROC curve analysis showed that the area under the curve (AUC) for the 10 hub genes was 0.9 ~ 1.0, and for naive B cells (AUC=0.942), plasma cells (AUC=0.999), follicular T helper cells (AUC=0.814), resting NK cells (AUC=0.864), monocytes (AUC=0.987), and M0 macrophages (AUC=0.995). Kaplan-Meier curves revealed positive correlation between the expression levels of TNNI2, TTN, ACTN3, TNNC2, MYL3, and survival of OS patients. Correlation analysis revealed close association between ACTN3, TNNI2, TNNC2, MYL3, TTN, and the infiltration of M0 macrophages and plasma cells. ConclusionOur findings provide a theoretical basis for further study of the molecular mechanisms underlying OS development and occurrence. It serves as a reference for the development of new diagnostics, identification of prognostic biomarkers, and targeted drug therapy for OS.

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“…It has been reported that, on the one hand, the tissue levels of miR-23b-3p are decreased and act as a predictor in hepatocellular carcinoma 23 and GC and miR-23b-3p reverses chemotherapy resistance in GC by targeting ATG12 and HMGB2 24 . On the other hand, the serum or tissue levels of miR-23b-3p are increased in non-small cell lung cancer 25 , osteosarcoma 26 , and esophageal squamous cell carcinomas 27 , and miR-23b-3p promotes tumor proliferation and metastasis by targeting PGC1a or EBF3 26,27 . In the present study, low expression of miR-23b-3p indicated a poor survival in GC and ectopic miR-23b-3p repressed GC cell growth and invasion by targeting RAI14.…”

Section: Discussionmentioning

confidence: 99%

RAI14 Regulated by circNFATC3/miR-23b-3p axis Facilitates Cell Growth and Invasion in Gastric Cancer

Yan

Zhang

et al. 2021

Cell Transplant

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Circular RNAs (circRNAs) have been proved to act crucial roles in multiple malignancies including gastric cancer (GC). Retinoic acid induced 14 (RAI14) acts as an oncogene in human cancers, but the underlying mechanisms by which RAI14 is regulated by circRNA/miRNA axis remain elusive. The clinical value of RAI14, miR-23b-3p and circNFATC3 was estimated by The Cancer Genome Atlas and fluorescence in situ hybridization. The interplay between miR-23b-3p and RAI14 or circNFATC3 was determined by qRT-PCR, Western blot, luciferase gene report and RIP assays. Biological function assays and a subcutaneous xenograft model were executed to unveil the role of circNFATC3/miR-23b-3p/RAI14 axis in GC cells. As a consequence, upregulation of RAI14 and circNFATC3 or downregulation of miR-23b-3p was associated with poor prognosis in patients with GC. Restored miR-23b-3p depressed cell proliferation, colony formation, and cell invasion by targeting RAI14, whereas RAI14 facilitated cell progression and reversed the anti-tumor effects of miR-23b-3p in GC cells. Then, circNFATC3 had a co-localization with miR-23b-3p in the cytoplasm in GC tissue cells and could act as a sponge of miR-23b-3p in GC cell line. Silencing of circNFATC3 inhibited cell growth and in vivo tumorigenesis by upregulating miR-23b-3p and downregulating RAI14. In conclusion, our findings indicated that RAI14 facilitated cell growth and invasion and was regulated by circNFATC3/miR-23b-3p axis in GC.

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miR-23b-3p suppressing PGC1α promotes proliferation through reprogramming metabolism in osteosarcoma

Cited by 41 publications

References 31 publications

Sarcoma treatment in the era of molecular medicine

Sarcoma treatment in the era of molecular medicine

Analysis of Immune Infiltration Pattern in Osteosarcoma and Its Clinical Significance

RAI14 Regulated by circNFATC3/miR-23b-3p axis Facilitates Cell Growth and Invasion in Gastric Cancer

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