The overexpression and clinical significance of TBX15 in human gliomas

Yan, Dongming; Yu, Yaping; Ni, Qiongwei; Meng, Qingwen; Wu, Haolin; Ding, Shun; Liu, Xiaoqian; Tang, Caiying; Liu, Qibing; Yang, Kun

doi:10.1038/s41598-023-36410-y

Cited by 6 publications

(4 citation statements)

References 27 publications

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“… 24 There is a study showed that TBX15 was upregulated in glioma tissues and indicated poor prognosis of glioma patients. 25 Results of our study on gliomas was consistent with these studies. In addition, knocking down TBX15 in glioma cells repressed their proliferation, migration and invasion rates, along with their ability to polarize macrophages to the M2 phenotype.…”

Section: Discussionsupporting

confidence: 90%

TBX15 facilitates malignant progression of glioma by transcriptional activation of TXDNC5

Ge,

Jia,

Zhang

et al. 2024

iScience

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Section: Discussionsupporting

confidence: 90%

TBX15 facilitates malignant progression of glioma by transcriptional activation of TXDNC5

Ge,

Jia,

Zhang

et al. 2024

iScience

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“…In addition, it is known that recurrent GBMs are highly immunosuppressive [ 68 ]. TBX15 was suggested to be associated with immune cell infiltration and immunosuppression and exhibit poor clinicopathological characteristics and survival prognosis in glioma patients [ 69 ]. For the remaining signatures ( TAS2R1 , CDKL1 , and CD101 ), the relevance of them to GBM recurrence is still greatly unknown.…”

Section: Discussionmentioning

confidence: 99%

A longer time to relapse is associated with a larger increase in differences between paired primary and recurrent IDH wild-type glioblastomas at both the transcriptomic and genomic levels

Ho,

Chen,

Chiang

et al. 2024

acta neuropathol commun

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Glioblastoma (GBM) is the most common malignant brain tumor in adults, which remains incurable and often recurs rapidly after initial therapy. While large efforts have been dedicated to uncover genomic/transcriptomic alternations associated with the recurrence of GBMs, the evolutionary trajectories of matched pairs of primary and recurrent (P-R) GBMs remain largely elusive. It remains challenging to identify genes associated with time to relapse (TTR) and construct a stable and effective prognostic model for predicting TTR of primary GBM patients. By integrating RNA-sequencing and genomic data from multiple datasets of patient-matched longitudinal GBMs of isocitrate dehydrogenase wild-type (IDH-wt), here we examined the associations of TTR with heterogeneities between paired P-R GBMs in gene expression profiles, tumor mutation burden (TMB), and microenvironment. Our results revealed a positive correlation between TTR and transcriptomic/genomic differences between paired P-R GBMs, higher percentages of non-mesenchymal-to-mesenchymal transition and mesenchymal subtype for patients with a short TTR than for those with a long TTR, a high correlation between paired P-R GBMs in gene expression profiles and TMB, and a negative correlation between the fitting level of such a paired P-R GBM correlation and TTR. According to these observations, we identified 55 TTR-associated genes and thereby constructed a seven-gene (ZSCAN10, SIGLEC14, GHRHR, TBX15, TAS2R1, CDKL1, and CD101) prognostic model for predicting TTR of primary IDH-wt GBM patients using univariate/multivariate Cox regression analyses. The risk scores estimated by the model were significantly negatively correlated with TTR in the training set and two independent testing sets. The model also segregated IDH-wt GBM patients into two groups with significantly divergent progression-free survival outcomes and showed promising performance for predicting 1-, 2-, and 3-year progression-free survival rates in all training and testing sets. Our findings provide new insights into the molecular understanding of GBM progression at recurrence and potential targets for therapeutic treatments.

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“…Ген TBX15 принадлежит к семейству генов T-box. Фактор транскрипции TBX15 активируется в различных опухолях и способствует неконтролируемой пролиферации опухолевых клеток, помогая избегать апоптоз [38]. Экспрессия TBX15 увеличена в глиомах человека и ассоциируется с ухудшением выживаемости пациентов с данной патологией.…”

Section: матричная рнкunclassified

“…Экспрессия TBX15 увеличена в глиомах человека и ассоциируется с ухудшением выживаемости пациентов с данной патологией. Кроме того, повышенная экспрессия TBX15 связана с генами, участвующими в иммуносупрессии при глиоме [38].…”

Section: матричная рнкunclassified

Transcriptomic analysis of neural stem and progenitor cells in comparison with glioblastoma stem cells

Shevchenko,

Arnotskaya,

Kushnir

et al. 2023

Usp. mol. onkol

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Introduction. There is currently no effective therapy for the treatment of glioblastoma. This is partly explained by the high degree of intra- and intertumor heterogeneity of GB, the source of which is believed to be glioblastoma stem cells (GSC). The question of the origin of GSC, which is important for improving clinical outcomes, still remains open. It is believed that GSCs can be formed as a result of oncogenic transformation of neural stem and progenitor cells (NSPcs), which have morphological and functional properties similar to them. Despite significant progress in elucidating the nature of GSCs, little is yet known about the specifically expressed genes and transcripts in these cells in comparison with NSPcs. In this regard, it becomes relevant to study the molecular mechanisms of gliomagenesis using model cell systems based on various clones of GSC.Aim. To conduct a comparative transcriptomic analysis of CD133+-NSPCs and CD133+-GSCs to study the molecular genetic differences between the phenotypes of these cells and identify potential targets for therapeutic effects on GSCs.Materials and methods. Used: highly sensitive transcriptomic analysis on high-density microarrays, cellular technologies, modern bioinformatics analysis.Results. Transcriptomic analysis of CD133+-GSCs and CD133+-NSPCs identified 1825 differentially expressed genes. The biological processes and signaling cascades activated in CD133+-GSCs have been established. It was shown that significant transcriptomic aberrations in CD133+-GSC compared to CD133+-NSPC are primarily due to a group of transcripts regulated by the Shh (Sonic hedgehog), mTOR (mammalian target of rapamycin), ALK (anaplastic lymphoma kinase) signaling cascades, transcription factors E2F1, PRC2, HOXA9, MYC, as well as oncogenes ERBB2 and KRAS. Six transcripts (AQP9, TOX15, HOXB2, STEAP3, TREM1, RFC2) highly expressed in CD133+-GSC and closely associated with the survival of patients with glioblastoma, which may be potential targets for therapeutic effects on CD133+-GSC associated with gliomagenesis, which may be potential targets for therapeutic effects on CD133+-GSC, have been identified and annotated.Conclusion. The data obtained indicate a number of significant molecular genetic differences between the two cell phenotypes, which can be used in the development of new therapeutic approaches for the treatment of glioblastoma.

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The overexpression and clinical significance of TBX15 in human gliomas

Cited by 6 publications

References 27 publications

TBX15 facilitates malignant progression of glioma by transcriptional activation of TXDNC5

TBX15 facilitates malignant progression of glioma by transcriptional activation of TXDNC5

A longer time to relapse is associated with a larger increase in differences between paired primary and recurrent IDH wild-type glioblastomas at both the transcriptomic and genomic levels

Transcriptomic analysis of neural stem and progenitor cells in comparison with glioblastoma stem cells

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