Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10449)
Regulator Name Histone deacetylase 1 (HDAC1)
Synonyms
Protein deacetylase HDAC1; Protein decrotonylase HDAC1
    Click to Show/Hide
Gene Name HDAC1
Gene ID 3065
Regulator Type Protein coding
Uniprot ID Q13547
Sequence
MAQTQGTRRKVCYYYDGDVGNYYYGQGHPMKPHRIRMTHNLLLNYGLYRKMEIYRPHKAN
AEEMTKYHSDDYIKFLRSIRPDNMSEYSKQMQRFNVGEDCPVFDGLFEFCQLSTGGSVAS
AVKLNKQQTDIAVNWAGGLHHAKKSEASGFCYVNDIVLAILELLKYHQRVLYIDIDIHHG
DGVEEAFYTTDRVMTVSFHKYGEYFPGTGDLRDIGAGKGKYYAVNYPLRDGIDDESYEAI
FKPVMSKVMEMFQPSAVVLQCGSDSLSGDRLGCFNLTIKGHAKCVEFVKSFNLPMLMLGG
GGYTIRNVARCWTYETAVALDTEIPNELPYNDYFEYFGPDFKLHISPSNMTNQNTNEYLE
KIKQRLFENLRMLPHAPGVQMQAIPEDAIPEESGDEDEDDPDKRISICSSDKRIACEEEF
SDSEEEGEGGRKNSSNFKKAKRVKTEDEKEKDPEEKKEVTEEEKTKEEKPEAKGVKEEVK
LA

    Click to Show/Hide
Family Histone deacetylase family
Function
Histone deacetylase that catalyzes the deacetylation of lysine residues on the N-terminal part of the core histones (H2A, H2B, H3 and H4). Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression and developmental events. Histone deacetylases act via the formation of large multiprotein complexes. Acts as a component of the histone deacetylase NuRD complex which participates in the remodeling of chromatin. Also functions as deacetylase for non-histone targets, such as NR1D2, RELA, SP1, SP3 and TSHZ3. Deacetylates SP proteins, SP1 and SP3, and regulates their function. Component of the BRG1-RB1-HDAC1 complex, which negatively regulates the CREST-mediated transcription in resting neurons. Upon calcium stimulation, HDAC1 is released from the complex and CREBBP is recruited, which facilitates transcriptional activation. Deacetylates TSHZ3 and regulates its transcriptional repressor activity. Deacetylates 'Lys-310' in RELA and thereby inhibits the transcriptional activity of NF-kappa-B. Deacetylates NR1D2 and abrogates the effect of KAT5- mediated relieving of NR1D2 transcription repression activity. Component of a RCOR/GFI/KDM1A/HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development (By similarity). Involved in CIART-mediated transcriptional repression of the circadian transcriptional activator: CLOCK-BMAL1 heterodimer (By similarity). Required for the transcriptional repression of circadian target genes, such as PER1, mediated by the large PER complex or CRY1 through histone deacetylation (By similarity). In addition to protein deacetylase activity, also has protein-lysine deacylase activity: acts as a protein decrotonylase by mediating decrotonylation ((2E)-butenoyl) of histones.

    Click to Show/Hide
HGNC ID
HGNC:4852
KEGG ID hsa:3065
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
HDAC1 can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
Browse Disease
Browse Drug
Unspecific Target [Unspecific Target]
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Drug BEBT-908 Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
PI3K-Akt signaling pathway hsa04151
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 MC-38 cells Colon adenocarcinoma Homo sapiens CVCL_B288
In Vivo Model
About 2 x 105 MC38 tumor cells were inoculated subcutaneously into C57BL/6 mice. A total of 100 mg/kg BEBT-908 was intravenously injected every other day for four times initiating from day 4 after tumor cell inoculation. Tumors were harvested on day 12 after inoculation, weighted, mechanically minced and incubated with 50 ug/mL DNase I (Sigma) and 2 mg/mL collagenase P (Sigma) for 20 minutes at 37.

    Click to Show/Hide
Response regulation Treatment with BEBT-908 promoted ferroptotic cell death of cancer cells by hyperacetylating p53 and facilitating the expression of ferroptotic signaling. The dual PI3K/HDAC inhibitor BEBT-908 elicits potent antitumor responses, effectively inducing immunogenic ferroptosis of colorectal cancer cells and potentiating cancer immunotherapy.
Experiment 2 Reporting the Ferroptosis Target of This Regulator [2]
Responsed Disease Adrenocortical carcinoma ICD-11: 2D11
 Disease Info 
Responsed Drug Romidepsin Investigative
 Drug Info 
Pathway Response Cell adhesion molecules hsa04514
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 SW13 cells Adrenal cortex carcinoma Homo sapiens CVCL_0542
Response regulation HDAC inhibitor Romidepsin converted SW13+ cells also had reduced mRNA expression of the mitochondrial ROS detoxifier superoxide dismutase 2 (SOD2), and the tumor suppressor p53. HDAC inhibitor treatment synergistically increased adrenocortical carcinoma cell death following induction of ferroptosis.
Colorectal cancer [ICD-11: 2B91]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Histone deacetylase 1 (HDAC1) Protein coding
 Regulator Info 
Responsed Drug BEBT-908 Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
PI3K-Akt signaling pathway hsa04151
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 MC-38 cells Colon adenocarcinoma Homo sapiens CVCL_B288
In Vivo Model
About 2 x 105 MC38 tumor cells were inoculated subcutaneously into C57BL/6 mice. A total of 100 mg/kg BEBT-908 was intravenously injected every other day for four times initiating from day 4 after tumor cell inoculation. Tumors were harvested on day 12 after inoculation, weighted, mechanically minced and incubated with 50 ug/mL DNase I (Sigma) and 2 mg/mL collagenase P (Sigma) for 20 minutes at 37.

    Click to Show/Hide
Response regulation Treatment with BEBT-908 promoted ferroptotic cell death of cancer cells by hyperacetylating p53 and facilitating the expression of ferroptotic signaling. The dual PI3K/HDAC inhibitor BEBT-908 elicits potent antitumor responses, effectively inducing immunogenic ferroptosis of colorectal cancer cells and potentiating cancer immunotherapy.
Adrenocortical carcinoma [ICD-11: 2D11]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator Histone deacetylase 1 (HDAC1) Protein coding
 Regulator Info 
Responsed Drug Romidepsin Investigative
 Drug Info 
Pathway Response Cell adhesion molecules hsa04514
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 SW13 cells Adrenal cortex carcinoma Homo sapiens CVCL_0542
Response regulation HDAC inhibitor Romidepsin converted SW13+ cells also had reduced mRNA expression of the mitochondrial ROS detoxifier superoxide dismutase 2 (SOD2), and the tumor suppressor p53. HDAC inhibitor treatment synergistically increased adrenocortical carcinoma cell death following induction of ferroptosis.
BEBT-908 [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Inducer
Response Target Unspecific Target
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
PI3K-Akt signaling pathway hsa04151
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 MC-38 cells Colon adenocarcinoma Homo sapiens CVCL_B288
In Vivo Model
About 2 x 105 MC38 tumor cells were inoculated subcutaneously into C57BL/6 mice. A total of 100 mg/kg BEBT-908 was intravenously injected every other day for four times initiating from day 4 after tumor cell inoculation. Tumors were harvested on day 12 after inoculation, weighted, mechanically minced and incubated with 50 ug/mL DNase I (Sigma) and 2 mg/mL collagenase P (Sigma) for 20 minutes at 37.

    Click to Show/Hide
Response regulation Treatment with BEBT-908 promoted ferroptotic cell death of cancer cells by hyperacetylating p53 and facilitating the expression of ferroptotic signaling. The dual PI3K/HDAC inhibitor BEBT-908 elicits potent antitumor responses, effectively inducing immunogenic ferroptosis of colorectal cancer cells and potentiating cancer immunotherapy.
Romidepsin [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [2]
Drug for Ferroptosis Inducer
Response Target Unspecific Target
Responsed Disease Adrenocortical carcinoma ICD-11: 2D11
 Disease Info 
Pathway Response Cell adhesion molecules hsa04514
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 SW13 cells Adrenal cortex carcinoma Homo sapiens CVCL_0542
Response regulation HDAC inhibitor Romidepsin converted SW13+ cells also had reduced mRNA expression of the mitochondrial ROS detoxifier superoxide dismutase 2 (SOD2), and the tumor suppressor p53. HDAC inhibitor treatment synergistically increased adrenocortical carcinoma cell death following induction of ferroptosis.
References
Ref 1 A Dual PI3K/HDAC Inhibitor Induces Immunogenic Ferroptosis to Potentiate Cancer Immune Checkpoint Therapy. Cancer Res. 2021 Dec 15;81(24):6233-6245. doi: 10.1158/0008-5472.CAN-21-1547. Epub 2021 Oct 28.
Ref 2 HDAC inhibition induces EMT and alterations in cellular iron homeostasis to augment ferroptosis sensitivity in SW13 cells. Redox Biol. 2021 Nov;47:102149. doi: 10.1016/j.redox.2021.102149. Epub 2021 Sep 25.