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| Enzymes involved in regulating gene expression by removing acetyl groups from histones, the proteins around which DNA is wrapped. -Many cancers exhibit altered expression levels of HDACs, which can contribute to the dysregulation of genes involved in cell growth, survival, and differentiation. -HDACs can repress the expression of tumor suppressor genes, leading to uncontrolled cell proliferation and survival. This repression can be a key factor in the development and progression of cancer. -HDAC inhibitors (HDACi) have been developed and are being investigated for their ability to reactivate silenced genes, induce cell cycle arrest, and promote apoptosis in cancer cells. -HDAC1, HDAC2): Often overexpressed in various cancers, including breast, prostate, and colorectal cancers. Their overexpression is associated with poor prognosis. -HDAC4, HDAC5): These may have both oncogenic and tumor-suppressive roles depending on the context and cancer type. -While HDACs are not classified as traditional oncogenes, their overexpression and activity can contribute to oncogenic processes. -HDAC inhibitor works by preventing the removal of acetyl groups from histones, thereby modulating gene expression, influencing cell behavior, and potentially reversing aberrant gene silencing seen in various diseases. -HDAC inhibitors can help reactivate these genes, thereby inhibiting growth and inducing apoptosis in cancer cells. |
| Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression. TP53 is the most commonly mutated gene in human cancer. HH↑, GLI-1↑, SHH↑ P53↓ The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca. It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma. Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer. It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress. Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC. |
| 1151- | Api, | Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: In vitro and in vivo study |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | 22Rv1 | - | in-vivo, | NA, | NA |
| 163- | CUR, | Epigenetic CpG Demethylation of the Promoter and Reactivation of the Expression of Neurog1 by Curcumin in Prostate LNCaP Cells |
| - | in-vitro, | Pca, | LNCaP |
| 2064- | PB, | Rad, | Phenylbutyrate Attenuates the Expression of Bcl-XL, DNA-PK, Caveolin-1, and VEGF in Prostate Cancer Cells |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | LNCaP |
| 2040- | SAHA, | The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | CRC, | T24/HTB-9 | - | in-vitro, | BC, | MCF-7 |
| 3192- | SFN, | Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention |
| - | in-vitro, | Pca, | PC3 |
| - | in-vitro, | Pca, | NA |
| 1453- | SFN, | Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7 |
| - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | PC3 |
| 1497- | SFN, | Differential effects of sulforaphane on histone deacetylases, cell cycle arrest and apoptosis in normal prostate cells versus hyperplastic and cancerous prostate cells |
| - | in-vitro, | Nor, | PrEC | - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:22 Cells:% prod#:% Target#:140 State#:% Dir#:1
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