Gene expression profiling in the developing secondary palate in the absence of Tbx1 function

Zoupa, Maria; Xavier, Guilherme M.; Bryan, Stephanie; Theologidis, Ioannis; Arno, Matthew; Cobourne, Martyn T.

doi:10.1186/s12864-018-4782-y

Cited by 3 publications

(4 citation statements)

References 77 publications

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“…Complex signaling molecules lead to poor prognosis by affecting the occurrence and development of tumors [ 8 ]. Currently, the application of high-throughput platforms in gene expression analysis is becoming more valuable in many aspects of clinical research [ 9 , 10 , 11 ]. Through second-generation sequencing technology, hundreds of differentially expressed genes (DEGs) have been discovered and are involved in different tumor cell biological processes; the relationships between these genes must be very complicated.…”

Section: Introductionmentioning

confidence: 99%

Identification of the hub genes RUNX2 and FN1 in gastric cancer

Han

Jin

et al. 2020

Open Medicine

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AbstractBackgroundThis study identified key genes in gastric cancer (GC) based on the mRNA microarray GSE19826 from the Gene Expression Omnibus (GEO) database and preliminarily explored the relationships among the key genes.MethodsDifferentially expressed genes (DEGs) were obtained using the GEO2R tool. The functions and pathway enrichment of the DEGs were analyzed using the Enrichr database. Protein–protein interactions (PPIs) were established by STRING. A lentiviral vector was constructed to silence RUNX2 expression in MGC-803 cells. The expression levels of RUNX2 and FN1 were measured. The influences of RUNX2 and FN1 on overall survival (OS) were determined using the Kaplan–Meier plotter online tool.ResultsIn total, 69 upregulated and 65 downregulated genes were identified. Based on the PPI network of the DEGs, 20 genes were considered hub genes. RUNX2 silencing significantly downregulated the FN1 expression in MGC-803 cells. High expression of RUNX2 and low expression of FN1 were associated with long survival time in diffuse, poorly differentiated, and lymph node-positive GC.ConclusionHigh RUNX2 and FN1 expression were associated with poor OS in patients with GC. RUNX2 can negatively regulate the secretion of FN1, and both genes may serve as promising targets for GC treatment.

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Section: Introductionmentioning

confidence: 99%

Identification of the hub genes RUNX2 and FN1 in gastric cancer

Han

Jin

et al. 2020

Open Medicine

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“…Next, we investigated the role and oncogenic function of TBX1 in CML. TBX1 plays a fundamental role in developing muscle cells, regulating their proliferation via CDKN1A [ 40 ]. Downregulation of cell cycle inhibitor CDKN1A is a hallmark of many cancer types [ 41 ].…”

Section: Resultsmentioning

confidence: 99%

“…CDKN1A encodes the cell cycle inhibitor p21 and serves as a tumor suppressor [ 41 ]. CDKN1A is a reported target gene in a mouse TBX1 deletion model of the DiGeorge syndrome [ 40 ], highlighting CDKN1A as a general target of TBX1. Of note, TBX1 may regulate its target genes directly or indirectly via interaction with chromatin factors [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Establishment of the Myeloid TBX-Code Reveals Aberrant Expression of T-Box Gene TBX1 in Chronic Myeloid Leukemia

Nagel,

Haake,

Pommerenke

et al. 2023

IJMS

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T-box genes encode transcription factors, which control developmental processes and promote cancer if deregulated. Recently, we described the lymphoid TBX-code, which collates T-box gene activities in normal lymphopoiesis, enabling identification of members deregulated in lymphoid malignancies. Here, we have extended this analysis to cover myelopoiesis, compiling the myeloid TBX-code and, thus, highlighting which of these genes might be deregulated in myeloid tumor types. We analyzed public T-box gene expression datasets bioinformatically for normal and malignant cells. Candidate T-box-gene-expressing model cell lines were identified and examined by RQ-PCR, Western Blotting, genomic profiling, and siRNA-mediated knockdown combined with RNA-seq analysis and live-cell imaging. The established myeloid TBX-code comprised 10 T-box genes, including progenitor-cell-restricted TBX1. Accordingly, we detected aberrant expression of TBX1 in 10% of stem/progenitor-cell-derived chronic myeloid leukemia (CML) patients. The classic CML cell line K-562 expressed TBX1 at high levels and served as a model to identify TBX1 activators, including transcription factor GATA1 and genomic amplification of the TBX1 locus at 22q11; inhibitors, including BCR::ABL1 fusion and downregulated GNAI2, as well as BMP, FGF2, and WNT signaling; and the target genes CDKN1A, MIR17HG, NAV1, and TMEM38A. The establishment of the myeloid TBX-code permitted identification of aberrant TBX1 expression in subsets of CML patients and cell lines. TBX1 forms an integral part of an oncogenic regulatory network impacting proliferation, survival, and differentiation. Thus, the data spotlight novel diagnostic markers and potential therapeutic targets for this malignancy.

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“…Recent research demonstrated that Tbx1 mutants displayed a significantly reduced palatal mesenchymal cell proliferation, which might be the cause of slightly downregulated Pax9 expression (Funato et al 2012; Zoupa et al 2018). With the discoveries that Tbx1 mutants exhibited downregulation of Fgf8 expression and FGF8 increased Pax9 expression in the explants of the posterior palatal mesenchyme, TBX1 might indirectly mediate Pax9 expression via regulating Fgf8 .…”

Section: Regulatory Network Of Pax9 In Palatal Growthmentioning

confidence: 99%

The Function and Regulatory Network ofPax9Gene in Palate Development

Weng

et al. 2018

J Dent Res

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Cleft palate, a common congenital deformity, can arise from disruptions in any stage of palatogenesis, including palatal shelf growth, elevation, adhesion, and fusion. Paired box gene 9 (Pax9) is recognized as a vital regulator of palatogenesis with great relevance to cleft palate in humans and mice. Pax9-deficient murine palatal shelves displayed deficient elongation, postponed elevation, failed contact, and fusion. Pax9 is expressed in epithelium and mesenchyme, exhibiting a dynamic expression pattern that changes according to the proceeding of palatogenesis. Recent studies highlighted the Pax9-related genetic interactions and their critical roles during palatogenesis. During palate growth, PAX9 interacts with numerous molecules and members of pathways (e.g., OSR2, FGF10, SHOS2, MSX1, BARX1, TGFβ3, LDB1, BMP, WNT β-catenin dependent, and EDA) in the mesenchyme and functions as a key mediator in epithelial-mesenchymal communications with FGF8, TBX1, and the SHH pathway. During palate elevation, PAX9 is hypothesized to mediate the time point of the elevation event in the anterior and posterior parts of the palatal shelves. The delayed elevation of Pax9 mutant palatal shelves probably results from abnormal expressions of a series of genes ( Osr2 and Bmpr1a) leading to deficient palate growth, abnormal tongue morphology, and altered hyaluronic acid distribution. The interactions between PAX9 and genes encoding the OSR2, TGFβ3, and WNT β-catenin-dependent pathways provide evidence that PAX9 might participate in the regulation of palate fusion. This review summarizes the current understanding of PAX9’s functions and emphasizes the interactions between PAX9 and vital genes during palatogenesis. We hope to provide some clues for further exploration of the function and mechanism of PAX9, especially during palate elevation and fusion events.

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Gene expression profiling in the developing secondary palate in the absence of Tbx1 function

Cited by 3 publications

References 77 publications

Identification of the hub genes RUNX2 and FN1 in gastric cancer

Identification of the hub genes RUNX2 and FN1 in gastric cancer

Establishment of the Myeloid TBX-Code Reveals Aberrant Expression of T-Box Gene TBX1 in Chronic Myeloid Leukemia

The Function and Regulatory Network ofPax9Gene in Palate Development

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