|
Malignant neoplasm of breast
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
For clinical relevance, high SOX9 and HDAC5 expression are associated with lower survival rates in breast cancer patients treated with tamoxifen.
|
31690832 |
2019 |
|
Malignant neoplasm of breast
|
0.050 |
Biomarker
|
disease |
BEFREE |
Inhibition of HDAC5-LSD1 axis with sulforaphane blocks breast cancer growth and combined treatment with LSD1 inhibitor improves the therapeutic efficacy of sulforaphane.
|
29633255 |
2018 |
|
Malignant neoplasm of breast
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
Protein expression of HDAC5 and LSD1 was significantly increased in primary breast cancer specimens in comparison with matched-normal adjacent tissues.
|
27212032 |
2017 |
|
Malignant neoplasm of breast
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
HDAC5 was extensively expressed in human BC tissues, and high HDAC5 expression was associated with an inferior prognosis.
|
27177225 |
2016 |
|
Breast Carcinoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
Inhibition of HDAC5-LSD1 axis with sulforaphane blocks breast cancer growth and combined treatment with LSD1 inhibitor improves the therapeutic efficacy of sulforaphane.
|
29633255 |
2018 |
|
Breast Carcinoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
Expression of histone-modifier genes in breast cancer differed significantly from those in normal tissue (HDAC5, HDAC1, lysine (K)-specific demethylase 4A (KDM4A) and lysine (K)-specific demethylase 6A (KDM6A)).
|
22199269 |
2011 |
|
Breast Carcinoma
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
For clinical relevance, high SOX9 and HDAC5 expression are associated with lower survival rates in breast cancer patients treated with tamoxifen.
|
31690832 |
2019 |
|
Breast Carcinoma
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
HDAC5 was extensively expressed in human BC tissues, and high HDAC5 expression was associated with an inferior prognosis.
|
27177225 |
2016 |
|
Breast Carcinoma
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
Protein expression of HDAC5 and LSD1 was significantly increased in primary breast cancer specimens in comparison with matched-normal adjacent tissues.
|
27212032 |
2017 |
|
Neoplasms
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Accordingly, HDAC5 was weakly expressed in UC cell lines suggesting a possible tumor-suppressive function.
|
31052182 |
2019 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Differences in expression profiles were also found to exist between individual breast tumors and, in some cases, were significantly associated with conventional pathological parameters and prognostic indices: tumor grade (K (lysine) acetyltransferase 5 (KAT5), HDAC1, KDM4A, SUV39H1 and KDM6A)); TNM stage (SUV39H1, K (lysine) acetyltransferase 2B (KAT2B), lysine (K)-specific demethylase 1A (KDM1A), KDM4A, lysine (K)-specific demethylase 5C (KDM5C), K (lysine) acetyltransferase 8 (KAT8), HDAC5 and KAT5)); Nottingham Prognostic Index (KDM5C, myeloid/lymphoid or mixed-lineage leukemia (MLL), KAT8 and SET and MYND domain containing 3 (SMYD3)); receptor status (KAT5, SMYD3 and KDM1A); histological type (KAT5, KDM5C, KAT8, KDM4A and MLL); disease-free survival (SUV39H1, SMYD3, HDAC5, KDM6A, HDAC1, KDM1A, KDM4A, KAT8, KDM5C, KAT5 and MLL) and overall survival (KAT8).
|
22199269 |
2011 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Therefore, interference with both glucose and glutamine supply in HDAC5-inhibited cancer cells significantly increases apoptotic cell death and reduces tumour growth in vivo; providing insight into a valuable clinical strategy combining the selective inhibition of HDAC5 with various inhibitors of metabolism as a new therapy to kill cancer cells.
|
28414307 |
2017 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
In the present study, aberrant high levels of HDAC5 were observed in non-small cell lung cancer (NSCLC) and further analysis indicated a negative relationship between HDAC5 and a tumor suppressor, miR‑589‑5p, in NSCLC specimens.
|
28440397 |
2017 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
Class I histone deacetylases (HDACs) generally promote cell proliferation and tumorigenesis, whereas class IIA HDACs like HDAC4 and HDAC5 may promote or impede cancer development in a tissue-dependent manner.
|
31052182 |
2019 |
|
Primary malignant neoplasm
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Hypermethylation of miRNA-589 promoter leads to upregulation of HDAC5 which promotes malignancy in non-small cell lung cancer.
|
28440397 |
2017 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
Our study suggested that knockdown of HDAC5 could inhibit cancer cell proliferation by the induction of cell cycle arrest and apoptosis; thus, suppression of HDAC5 may be a viable option for treating HCC patients.
|
25129440 |
2014 |
|
Primary malignant neoplasm
|
0.040 |
AlteredExpression
|
group |
BEFREE |
A comparative microarray analysis demonstrated a genome wide cooperative effect of HDAC5 and LSD1 on cancer-related gene expression. shRNA knockdown and sulforaphane inhibition of HDAC5/LSD1 exhibited similar effects on expression of HDAC5/LSD1 target genes.
|
29633255 |
2018 |
|
Neoplasm Metastasis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
MYCN and HDAC5 transcriptionally repress CD9 to trigger invasion and metastasis in neuroblastoma.
|
27572323 |
2016 |
|
Neoplasm Metastasis
|
0.030 |
AlteredExpression
|
phenotype |
BEFREE |
Novel HDAC5-interacting motifs of Tbx3 are essential for the suppression of E-cadherin expression and for the promotion of metastasis in hepatocellular carcinoma.
|
30151243 |
2018 |
|
Neoplasm Metastasis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Phenotype experiments showed that the migration and invasion of hepatocellular carcinoma cells were impaired by knockdown of histone deacetylase 5 or hypoxia-inducible factor-1α but rescued when eliminating homeodomain-interacting protein kinase-2 in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2-hypoxia-inducible factor-1α pathway in hypoxia-induced metastasis.
|
28653891 |
2017 |
|
Mammary Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Differences in expression profiles were also found to exist between individual breast tumors and, in some cases, were significantly associated with conventional pathological parameters and prognostic indices: tumor grade (K (lysine) acetyltransferase 5 (KAT5), HDAC1, KDM4A, SUV39H1 and KDM6A)); TNM stage (SUV39H1, K (lysine) acetyltransferase 2B (KAT2B), lysine (K)-specific demethylase 1A (KDM1A), KDM4A, lysine (K)-specific demethylase 5C (KDM5C), K (lysine) acetyltransferase 8 (KAT8), HDAC5 and KAT5)); Nottingham Prognostic Index (KDM5C, myeloid/lymphoid or mixed-lineage leukemia (MLL), KAT8 and SET and MYND domain containing 3 (SMYD3)); receptor status (KAT5, SMYD3 and KDM1A); histological type (KAT5, KDM5C, KAT8, KDM4A and MLL); disease-free survival (SUV39H1, SMYD3, HDAC5, KDM6A, HDAC1, KDM1A, KDM4A, KAT8, KDM5C, KAT5 and MLL) and overall survival (KAT8).
|
22199269 |
2011 |
|
Mammary Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
We aimed to evaluate HDAC5 expression in human breast tumors and to determine the effects of the inhibition of HDAC5 expression in BC cells.
|
27177225 |
2016 |
|
Mammary Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Here, we report that expression of HDAC5 and LSD1 proteins were positively correlated in human breast cancer cell lines and tissue specimens of primary breast tumors.
|
27212032 |
2017 |
|
Arteriosclerosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
Histone deacetylases (HDACs) regulate gene transcription by deacetylating lysine residues in histone and nonhistone proteins and a heightened HDAC activation, notably of HDAC5, is associated with vascular disorders, such as atherosclerosis.
|
30793765 |
2019 |
|
Arteriosclerosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
Taken together, our results reveal that phosphorylation-dependent derepression of HDAC5 mediates flow-induced KLF2 and eNOS expression as well as flow anti-inflammation, and suggest that HDAC5 could be a potential therapeutic target for the prevention of atherosclerosis.
|
20042720 |
2010 |