The most potent and selective compound, 3d (IC<sub>50</sub>, 4 nM, HDAC6; IC<sub>50</sub> > 10 μM, HDAC1), substantially increased acetylation of α-tubulin instead of histones in the lung cancer cell line, LL2.
SUMOylation could enhance the transcriptional repression activity of Slug via recruiting more HDAC1, resulting in reduced expression of downstream Slug target genes and enhanced lung cancer metastasis.
The expression of HDAC1 and uPAR shows the minimal expression pattern in control and initial stages of lung cancer, but its expression increased in advanced stage of cancer.
Finally, HDAC1 mRNA or protein expression was negatively correlated with the overall survival rate of patients with lung cancer (HR = 2.40, 95% CI = 1.48-3.88, P = .0004).
The down expression of miR-449a/b might be one mechanism for over-expression of HDAC1 in lung cancer. miR-449a/b inhibited cell growth and anchorage-independent growth.
17beta-Estradiol decreased DNMT1 and HDAC1 protein expressions and their binding activity on MGMT promoter, and this may partially contribute to the gender difference of MGMT hypermethylation in lung cancer.
The HDAC1/GAPDH mRNA levels were significantly higher in stage III or IV lung cancer (50.929 +/- 120.433) than in stage I lung cancer (11.430 +/- 25.611, P = 0.0472).