Gene expression profiles and pathway enrichment analysis of human osteosarcoma cells exposed to sorafenib

Dai, Zhehao; Tang, Haoyu; Pan, Yue; Chen, Junquan; Li, Yongping; Jun, Zhu

doi:10.1002/2211-5463.12428

Cited by 14 publications

(13 citation statements)

References 35 publications

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“…CXCL1 pathway might be involved in sorafenib resistance. In sorafenib-treated osteosarcoma and ovarian cancer, expression of CXCL1 increased signi cantly [19,20]. Blockade of CXCR2, receptor of CXCL1, elevated the e cacy of sorafenib and delayed resistance [20].…”

Section: Discussionmentioning

confidence: 99%

Anlotinib in the treatment of advanced hepatocellular carcinoma: an open label phase II study (ALTER-0802 study)

Sun

Zhou

Zhang

et al. 2021

Preprint

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Purpose: This study aimed to assess efficacy and safety of anlotinib as a first- or second-line treatment for advanced or metastatic hepatocellular carcinoma (aHCC) and to identify the predictive plasma cytokines on efficacy of anlotinib.Methods: It was a phase II clinical study. Patients with aHCC were recruited from October 2016 to April 2019 and divided into two cohorts according to previous tyrosine kinase inhibitors (TKIs) therapy. Those without or with prior TKIs were in Cohort 1 or 2, respectively. All patients took anlotinib (12mg/day, Day1–14, three weeks per cycle). The primary endpoint was 12-week progression free survival (PFS) rate. Relationship between series plasma cytokine level and efficacy of anlotinib was analyzed.Results: Enrolled 26 patients in Cohort 1 and 24 in Cohort 2. In Cohort 1, the 12-week PFS rate was 80.8% (95% confidence interval [CI]; 59.8%–91.5%) and median time to progression (TTP) was 5.9 months (95% CI; 4.8–6.9). In Cohort 2, the 12-week PFS rate and median TTP was 72.5% (95% CI; 48.7%–86.6%) and 4.6 months (95% CI; 2.7–10.0), respectively. The median TTP on patients with baseline plasma level of CXCL1 (C-X-C motif chemokine ligand 1) less than 7.6 ng/μl was significant longer in both cohorts. The most common grade 3–5 adverse events were hypertension (8%), diarrhea (8%) and hand-foot syndrome (6%). Conclusion: Anlotinib showed promising efficacy and safety as a first- or second-line treatment with a continuous TKIs treatment strategy in aHCC. The plasma CXCL1 might be a predictor for efficacy of anlotinib.

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Section: Discussionmentioning

confidence: 99%

Anlotinib in the treatment of advanced hepatocellular carcinoma: an open label phase II study (ALTER-0802 study)

Sun

Zhou

Zhang

et al. 2021

Preprint

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“…Similarly, using the GSE53155 data set, PGF was identified as a seed gene in osteosarcoma. 31 Due to the limited availability of osteosarcoma samples, the integration of data from multiple datasets has become a key source of data for studies on this cancer. However, this method is highly influenced by batch effects due to the lack of statistical controls.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential key genes associated with osteosarcoma based on integrated bioinformatics analyses

Cheng

et al. 2019

J of Cellular Biochemistry

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Due to high rates of metastasis and poor clinical outcomes for patients, it is important to study the pathomechanisms of osteosarcoma. However, due to the fact that osteosarcoma shows significant interindividual variation and high heterogeneity, the identification of differentially expressed genes (DEGs) at the population level cannot answer many important questions related to osteosarcoma tumorigenesis. Therefore, a new strategy to identify dysregulated genes in osteosarcoma samples is required. The aim of this study was to improve our understanding of osteosarcoma pathogenesis by identifying genes with universal aberrant expression in osteosarcoma samples. Because the relative expression ordering of genes is stable in normal bone tissues but is disrupted in osteosarcoma tissues, we used the RankComp algorithm to identify DEGs in normal and osteosarcoma tissue samples. We then calculated the dysregulation frequency for each gene. Genes with deregulation frequencies above 80% were deemed to be universal DEGs. Next, coexpression, pathway enrichment, and protein-protein interaction network analyses were performed to characterize the functions of these genes. From 188 samples of osteosarcoma obtained from four datasets measured on different platforms, 51 universal DEGs were identified, including 4 universally upregulated genes and 47 universally downregulated genes. Genes that were differentially coexpressed with these universal DEGs were found to be enriched in 46 cancer-related pathways. In addition, functional and network analyses showed that genes with high dysregulation frequencies were involved in cancer-related functions. Thus, the commonly aberrant genes identified in osteosarcoma tissues may be important targets for osteosarcoma diagnosis and therapy. K E Y W O R D S differentially expressed gene (DEGs), individualized analysis, osteosarcoma, relative expression ordering J Cell Biochem. 2019;120:13554-13561. wileyonlinelibrary.com/journal/jcb 13554 |Abbreviations: DEGs, differentially expressed genes; GEO, the Gene Expression Omnibus; GO, gene ontology; KEGG, kyoto encyclopedia of genes and genomes; PPI, protein-protein interaction; REO, relative expression ordering; STRING, search tool for the retrieval of interacting genes.Hu and Cheng have contributed equally to this study.

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“…KEGG pathway analysis (50) revealed that adipogenesis-related pathways were highly enriched upon TEAD4 knockdown, including the brown fat differentiation pathway, lipid metabolism pathway, PPAR signaling pathway, triglyceride metabolism process, acylglycerol metabolism process, neutral lipid metabolism process, and glycerol ether metabolism process ( Fig. 2A).…”

Section: Tead4 Modulates Adipogenesis-related Pathwaysmentioning

confidence: 99%

The TEA domain family transcription factor TEAD4 represses murine adipogenesis by recruiting the cofactors VGLL4 and CtBP2 into a transcriptional complex

Zhang

et al. 2018

Journal of Biological Chemistry

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The Hippo signaling pathway is known to play an important role in multiple physiological processes, including adipogenesis. However, whether the downstream components of the Hippo pathway are involved in adipogenesis remains unknown. Here we demonstrate that the TEA domain family (TEAD) transcription factors are essential for adipogenesis in murine 3T3-L1 preadipocytes. Knockdown of TEAD1-4 stimulated adipogenesis and increased the expression of adipocyte markers in these cells. Interestingly, we found that the TEAD4 knockdown-mediated adipogenesis proceeded in a Yes-associated protein (YAP)/TAZ (Wwtr1)-independent manner and that adipogenesis suppression in WT cells involved formation of a ternary complex comprising TEAD4 and the transcriptional cofactors C-terminal binding protein 2 (CtBP2) and vestigial-like family member 4 (VGLL4). VGLL4 acted as an adaptor protein that enhanced the interaction between TEAD4 and CtBP2, and this TEAD4-VGLL4-CtBP2 ternary complex dynamically existed at the early stage of adipogenesis. Finally, we verified that TEAD4 directly targets the promoters of major adipogenesis transcription factors such as peroxisome proliferator-activated receptor γ (PPARγ) and adiponectin, C1Q, and collagen domain-containing (Adipoq) during adipogenesis. These findings reveal critical insights into the role of the TEAD4-VGLL4-CtBP2 transcriptional repressor complex in suppression of adipogenesis in murine preadipocytes.

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Gene expression profiles and pathway enrichment analysis of human osteosarcoma cells exposed to sorafenib

Cited by 14 publications

References 35 publications

Anlotinib in the treatment of advanced hepatocellular carcinoma: an open label phase II study (ALTER-0802 study)

Anlotinib in the treatment of advanced hepatocellular carcinoma: an open label phase II study (ALTER-0802 study)

Identification of potential key genes associated with osteosarcoma based on integrated bioinformatics analyses

The TEA domain family transcription factor TEAD4 represses murine adipogenesis by recruiting the cofactors VGLL4 and CtBP2 into a transcriptional complex

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