HOXA1, a breast cancer oncogene

Belpaire, Magali; Taminiau, Arnaud; Geerts, Dirk; Rezsöhazy, René

doi:10.1016/j.bbcan.2022.188747

Cited by 8 publications

(5 citation statements)

References 232 publications

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“…HOXA1 is a well-reported oncogene that is upregulated in human malignancies including HNSCC, breast cancer, and nonsmall-cell lung cancer (17,32,33). Nevertheless, the mechanism underlying the upregulation of HOXA1 in cancer cells was not completely clear.…”

Section: Discussionmentioning

confidence: 99%

HOXA1 is a radioresistance marker in multiple cancer types

et al. 2022

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Radiotherapy is an important therapeutic method for patients with cancer. However, radioresistance can cause treatment failure. Thus, there is an urgent need to investigate mechanisms of radioresistance and identity markers that could be used to predict radioresistance and prognosis of post-radiotherapy cancer patients. In the present study, we propose HOXA1 as a candidate biomarker of intrinsic radioresistance in multiple cancer types. By analyzing data from The Cancer Genome Atlas (TCGA), we found that HOXA1 was aberrantly upregulated in multiple cancers, and that elevated HOXA1 was significantly associated with poor prognosis of post-radiotherapy head and neck squamous cell carcinoma (HNSCC) and low-grade glioma (LGG) patients. Correlation analysis showed that HOXA1 expression was positively correlated with expression of EGFR, CDK6, and CAV1, which have been reported to enhance radioresistance. In addition, gene set enrichment analysis (GSEA) showed that the oxidative phosphorylation gene set was negatively enriched in HOXA1 high-expression samples in both HNSCC and LGG. Moreover, immunohistochemical assays indicated that high HOXA1 expression was significantly correlated with a high recurrence rate of nasopharyngeal carcinoma (NPC) after radiotherapy. Further in vitro experiments demonstrated that HOXA1 knockdown markedly attenuated the DNA repair capacity of NPC cells and sensibilized NPC cells to irradiation. Taken together, the results of this study demonstrate that HOXA1 has potential to be a predictive marker for radioresistance and post-radiotherapy prognosis that could help to guide individualized treatment in multiple cancer types.

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Section: Discussionmentioning

confidence: 99%

HOXA1 is a radioresistance marker in multiple cancer types

et al. 2022

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“…HOXA11-AS, HOTTIP, HOXA-AS3, and HOXA-AS2 were found to be within the HOXA gene cluster [17]. HOXA1, one of the HOXA gene cluster members, was notably found to be up-regulated in several human cancer, such as hepatocellular carcinoma [18] and breast cancer [19], and function as an oncogene.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HOXA-AS3 promotes glioma progression via miR-542-5p/HOXA1 axis

Cui,

He,

et al. 2024

Preprint

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Aims: Gliomas is one of the brain cancers belongs to the central nervous system(CNS) tumor. We previously showed that administration of natural product pristimerin significantly impaired the U373 cell progression by disturbing the miR-542-5p expression. But the upstream genes of miR-542-5p in glioma is still ill-defined. Methods: We used the RNA 22 v2 to predict the binding sites for lncRNAs and miRNAs. TCGA database was used to analyze the expression of HOXA-AS3, HOXA1 and WNT5A in glioma tissues. Survival curve of HOXA-AS3 in LGG patients was plotted. Glioma cell U373 and U251 were used to transfect with the siRNA to access the apoptosis rate and migration of cells. And tumor model was constructed to access the function of the HOXA-AS3 in vivo. Results: Our results showed the increased HOXA-AS3 and HOXA1 expression in glioma tissues. Cell growth/migration could be effectively suppressed by silencing HOXA-AS3or/and hsa-miR-542-5p in U373 cell, while cell apoptosis rate enhanced, which could be reserved by amplifying hsa-miR-542-5p expression. In addition, we found the decreased HOXA1 and WNT5A expression in HOXA-AS3silenced condition. In vivo experiments showed that silencing HOXA-AS3and hsa-miR-542-5p suppressed U373 tumor growth by inhibiting arginase-1 expression in tumor-associated macrophages. High level of HOXA-AS3, HOXA1, and WNT5A in tumor cell were associated with poor overall survival in patients with low-grade glioma, higher expression of which in tumor-infiltrating lymphocytes also correlated with worse patients’ outcome. Conclusions: Our results showed that HOXA-AS3 might promote glioma progression via regulating hsa-miR-542-5p/HOXA1and WNT5A.

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“…The role of hox genes in cell cycle regulation is of particular importance during cancer formation, where increased hox gene expression induced by oncogenes, growth factors or epigenetic changes drives tumor cell proliferation (reviewed in 6 , 7 , 12 , 13 ). For example, ectopic HOXA1 expression is sufficient to cause the oncogenic transformation of mammary gland cells 58 , over-expression of HOXA9 is required for the proliferation of myeloid leukemia cells 59 , and HOXB13 promotes the growth of ovarian carcinoma 60 .…”

Section: Discussionmentioning

confidence: 99%

“…Different SC populations, such as hematopoietic, colonic and mesenchymal SCs rely on hox gene activity for their maintenance and regenerative capacity 7 – 9 . Besides their function in SC renewal and regeneration, de-regulated hox gene expression has been observed in different types of human cancer, such as acute myeloid lymphoid leukemia 10 , 11 , breast 12 and colorectal carcinoma 7 , 13 . The oncogenic activity of hox genes may in part be due to their ability to directly stimulate cell cycle progression and DNA replication 14 .…”

Section: Introductionmentioning

confidence: 99%

Prolonging somatic cell proliferation through constitutive hox gene expression in C. elegans

Heinze,

Berger,

Engleitner

et al. 2023

Nat Commun

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Abstracthox genes encode a conserved family of homeodomain transcription factors that are essential to determine the identity of body segments during embryogenesis and maintain adult somatic stem cells competent to regenerate organs. In contrast to higher organisms, somatic cells in C. elegans irreversibly exit the cell cycle after completing their cell lineage and the adult soma cannot regenerate. Here, we show that hox gene expression levels in C. elegans determine the temporal competence of somatic cells to proliferate. Down-regulation of the central hox gene lin-39 in dividing vulval cells results in their premature cell cycle exit, whereas constitutive lin-39 expression causes precocious Pn.p cell and sex myoblast divisions and prolongs the proliferative phase of the vulval cells past their normal point of arrest. Furthermore, ectopic expression of hox genes in the quiescent anchor cell re-activates the cell cycle and induces proliferation until young adulthood. Thus, constitutive expression of a single hox transcription factor is sufficient to prolong somatic cell proliferation beyond the restriction imposed by the cell lineage. The down-regulation of hox gene expression in most somatic cells at the end of larval development may be one cause for the absence of cell proliferation in adult C. elegans.

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HOXA1, a breast cancer oncogene

Cited by 8 publications

References 232 publications

HOXA1 is a radioresistance marker in multiple cancer types

HOXA1 is a radioresistance marker in multiple cancer types

Long non-coding RNA HOXA-AS3 promotes glioma progression via miR-542-5p/HOXA1 axis

Prolonging somatic cell proliferation through constitutive hox gene expression in C. elegans

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