HOXA5 and p53 cooperate to suppress lung cancer cell invasion and serve as good prognostic factors in non-small cell lung cancer

Chang, Chi Jen; Chen, Yen‐Lin; Hsieh, Chi-Hsun; Liu, Ya Jung; Yu, Sung-Liang; Chen, Jeremy J.W.; Wang, Chi Chung

doi:10.7150/jca.17295

Cited by 37 publications

(26 citation statements)

References 41 publications

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“…In solid malignancies such as breast carcinoma, HOXA5 functions as a positive regulator of TP53, and loss of HOXA5 expression results in failure to block malignant transformation of epithelial cells (Raman et al 2000;Chen et al 2004). Similar findings of HOXA5 inducing apoptosis and a better clinical outcome have been observed in lung carcinoma (Chang et al 2017) and liposarcoma (Lee et al 2015). This previously described cooperative axis of HOXA5 and TP53 suppressing cellular proliferation in human carcinoma and liposarcoma is the inverse effect of what we observed in glioblastomas, where HOXA5 promotes cellular proliferation and inhibits TP53 expression.…”

Section: Discussionmentioning

confidence: 55%

Increased HOXA5 expression provides a selective advantage for gain of whole chromosome 7 in IDH wild-type glioblastoma

Cimino

Kim

et al. 2018

Genes Dev.

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Glioblastoma is the most frequently occurring and invariably fatal primary brain tumor in adults. The vast majority of glioblastomas is characterized by chromosomal copy number alterations, including gain of whole chromosome 7 and loss of whole chromosome 10. Gain of whole chromosome 7 is an early event in gliomagenesis that occurs in proneural-like precursor cells, which give rise to all isocitrate dehydrogenase (IDH) wild-type glioblastoma transcriptional subtypes. () is one gene on chromosome 7 known to drive gliomagenesis, but, given its location near the end of 7p, there are likely several other genes located along chromosome 7 that select for its increased whole-chromosome copy number within glioblastoma cells. To identify other potential genes that could select for gain of whole chromosome 7, we developed an unbiased bioinformatics approach that identified () as a gene whose expression correlated with gain of chromosome 7 and a more aggressive phenotype of the resulting glioma. High expression of in glioblastoma was associated with a proneural gene expression pattern and decreased overall survival in both human proneural and PDGF-driven mouse glioblastoma. Furthermore, overexpression promoted cellular proliferation and potentiated radioresistance. We also found enrichment of expression in recurrent human and mouse glioblastoma at first recurrence after radiotherapy. Overall, this study implicates as a chromosome 7-associated gene-level locus that promotes selection for gain of whole chromosome 7 and an aggressive phenotype in glioblastoma.

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Section: Discussionmentioning

confidence: 55%

Increased HOXA5 expression provides a selective advantage for gain of whole chromosome 7 in IDH wild-type glioblastoma

Cimino

Kim

et al. 2018

Genes Dev.

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“…Here, we revealed that Hoxa5 was direct target of miR-19a-3p and contribute to miR-19a-3p-induced BMSC osteogenic differentiation. Hoxa5 was served as tumor suppressor in a number of cancers including non-small cell lung cancer [28], osteosarcoma [29], gastric cancer [30] and gastric cancer [31]. Hoxa5 was also reported to alleviate inflammation and induce adipose tissue browning [32].…”

Section: Discussionmentioning

confidence: 99%

lncRNA Xist Regulates Osteoblast Differentiation by Sponging miR-19a-3p in Aging-induced Osteoporosis

Chen¹,

Li²,

Zhi³

et al. 2020

Aging and disease

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The switch between osteogenic and adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) plays a key role in aging-induced osteoporosis. In this study, miR-19a-3p was obviously downregulated in BMSCs from aged humans and mice. Overexpressed miR-19a-3p evidently reduced aginginduced bone loss in mice and promoted osteogenic differentiation of BMSCs, while silenced miR-19a-3p manifestly increased aging-induced bone loss in mice and repressed osteogenic differentiation of BMSCs. Hoxa5 was significantly downregulated in the BMSCs from aged mice and contribute to miR-19a-3p-induced osteoblast differentiation as a direct target gene of miR-19a-3p. Furthermore, lncRNA Xist was found as a sponge of miR-19a-3p to repress BMSCs osteogenic differentiation. In conclusion, our study reveals the critical role of the lncRNA Xist/miR-19a-3p/Hoxa5 pathway in aging-induced osteogenic differentiation of BMSCs, indicating the potential therapeutic target for osteoporosis.

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“…Furthermore, the cooperation between HOXA5 and p53 is found to be able to inhibit the invasion of tumor cells, at least partially owing to the decrease of MMP2 activity in NSCLC. [56]. Low expression of HOXA5 is associated with high levels of nuclear β-catenin, which is the hallmark of the Wnt signaling pathway in colorectal carcinoma [57].…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Hub Genes Through Expression Profiles Analysis in Adrenocortical Carcinoma

Yao¹,

Zhao²,

Shang³

et al. 2020

Preprint

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Abstract Background: Adrenocortical carcinoma (ACC) is a heterogeneous and rare malignant tumor associated with a poor prognosis. The molecular mechanisms of ACC remain elusive and more accurate biomarkers for the prediction of prognosis are needed.Methods: In this study, integrative profiling analyses were performed to identify novel hub genes in ACC to provide promising targets for future investigation. Three gene expression profiling datasets in the GEO database were used for the identification of overlapped differentially expressed genes (DEGs) following the criteria of adj.P.Value<0.05 and |log2 FC|>0.5 in ACC. Novel hub genes were screened out following a series of processes: the retrieval of DEGs with no known associations with ACC on Pubmed, then the cross-validation of expression values and significant associations with overall survival in the GEPIA2 and starBase databases, and finally the prediction of gene-tumor association in the GeneCards database.Results: Four novel hub genes were identified and two of them, TPX2 and RACGAP1, were positively correlated with the staging. Interestingly, co-expression analysis revealed that the association between TPX2 and RACGAP1 was the strongest and that the expression of HOXA5 was almost completely independent of that of RACGAP1 and TPX2. Furthermore, the PPI network consisting of four novel genes and seed genes in ACC revealed that HOXA5, TPX2, and RACGAP1 were all associated with TP53. Conclusions: This study identified four novel hub genes (TPX2, RACHAP1, HXOA5 and FMO2) that may play crucial roles in the tumorigenesis and the prediction of prognosis of ACC.

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HOXA5 and p53 cooperate to suppress lung cancer cell invasion and serve as good prognostic factors in non-small cell lung cancer

Cited by 37 publications

References 41 publications

Increased HOXA5 expression provides a selective advantage for gain of whole chromosome 7 in IDH wild-type glioblastoma

Increased HOXA5 expression provides a selective advantage for gain of whole chromosome 7 in IDH wild-type glioblastoma

lncRNA Xist Regulates Osteoblast Differentiation by Sponging miR-19a-3p in Aging-induced Osteoporosis

Identification of Novel Hub Genes Through Expression Profiles Analysis in Adrenocortical Carcinoma

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