Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10415)
Regulator Name RNA-binding protein PNO1 (PNO1)
Synonyms
Partner of NOB1
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Gene Name PNO1
Gene ID 56902
Regulator Type Protein coding
Uniprot ID Q9NRX1
Sequence
MESEMETQSARAEEGFTQVTRKGGRRAKKRQAEQLSAAGEGGDAGRMDTEEARPAKRPVF
PPLCGDGLLSGKEETRKIPVPANRYTPLKENWMKIFTPIVEHLGLQIRFNLKSRNVEIRT
CKETKDVSALTKAADFVKAFILGFQVEDALALIRLDDLFLESFEITDVKPLKGDHLSRAI
GRIAGKGGKTKFTIENVTRTRIVLADVKVHILGSFQNIKMARTAICNLILGNPPSKVYGN
IRAVASRSADRF

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Family PNO1 family
Function
Part of the small subunit (SSU) processome, first precursor of the small eukaryotic ribosomal subunit. During the assembly of the SSU processome in the nucleolus, many ribosome biogenesis factors, an RNA chaperone and ribosomal proteins associate with the nascent pre- rRNA and work in concert to generate RNA folding, modifications, rearrangements and cleavage as well as targeted degradation of pre- ribosomal RNA by the RNA exosome. Positively regulates dimethylation of two adjacent adenosines in the loop of a conserved hairpin near the 3'-end of 18S rRNA.

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HGNC ID
HGNC:32790
KEGG ID hsa:56902
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
PNO1 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
Cystine/glutamate transporter (SLC7A11) [Driver; Suppressor]
 Target Info 
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Hepatocellular carcinoma ICD-11: 2C12
 Disease Info 
Pathway Response Autophagy hsa04140
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
Xenograft mouse model experiments were used male BALB/c nude mice (4 weeks old) purchased from SPF Biotechnology (Beijing, China). Each mouse was injected 5 x 106 tumor cells at the volume of 100 uL into the subcutaneous tissue. The tumor volume and weight of the mice was observed every 2 days. Mice were monitored daily and the tumor volume calculated according to the equation volume = length x width2 x 1/2.

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Response regulation PNO1 inhibits autophagy-mediated ferroptosis via GSH metabolic reprogramming as demonstrated above. We also demonstrated that PNO1 inhibition repressed SLC7A11 through p53 to promote ferroptosis. These observations suggested that sh-PNO1 could be a new target in hepatocellular carcinoma therapy.
Experiment 2 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Hepatocellular carcinoma ICD-11: 2C12
 Disease Info 
Pathway Response Autophagy hsa04140
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
Xenograft mouse model experiments were used male BALB/c nude mice (4 weeks old) purchased from SPF Biotechnology (Beijing, China). Each mouse was injected 5 x 106 tumor cells at the volume of 100 uL into the subcutaneous tissue. The tumor volume and weight of the mice was observed every 2 days. Mice were monitored daily and the tumor volume calculated according to the equation volume = length x width2 x 1/2.

    Click to Show/Hide
Response regulation PNO1 inhibits autophagy-mediated ferroptosis via GSH metabolic reprogramming as demonstrated above. We also demonstrated that PNO1 inhibition repressed SLC7A11 through p53 to promote ferroptosis. These observations suggested that sh-PNO1 could be a new target in Hepatocellular carcinoma therapy.
Hepatocellular carcinoma [ICD-11: 2C12]
 Disease Info 
In total 2 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator RNA-binding protein PNO1 (PNO1) Protein coding
 Regulator Info 
Pathway Response Autophagy hsa04140
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
Xenograft mouse model experiments were used male BALB/c nude mice (4 weeks old) purchased from SPF Biotechnology (Beijing, China). Each mouse was injected 5 x 106 tumor cells at the volume of 100 uL into the subcutaneous tissue. The tumor volume and weight of the mice was observed every 2 days. Mice were monitored daily and the tumor volume calculated according to the equation volume = length x width2 x 1/2.

    Click to Show/Hide
Response regulation PNO1 inhibits autophagy-mediated ferroptosis via GSH metabolic reprogramming as demonstrated above. We also demonstrated that PNO1 inhibition repressed SLC7A11 through p53 to promote ferroptosis. These observations suggested that sh-PNO1 could be a new target in hepatocellular carcinoma therapy.
Experiment 2 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator RNA-binding protein PNO1 (PNO1) Protein coding
 Regulator Info 
Pathway Response Autophagy hsa04140
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
Xenograft mouse model experiments were used male BALB/c nude mice (4 weeks old) purchased from SPF Biotechnology (Beijing, China). Each mouse was injected 5 x 106 tumor cells at the volume of 100 uL into the subcutaneous tissue. The tumor volume and weight of the mice was observed every 2 days. Mice were monitored daily and the tumor volume calculated according to the equation volume = length x width2 x 1/2.

    Click to Show/Hide
Response regulation PNO1 inhibits autophagy-mediated ferroptosis via GSH metabolic reprogramming as demonstrated above. We also demonstrated that PNO1 inhibition repressed SLC7A11 through p53 to promote ferroptosis. These observations suggested that sh-PNO1 could be a new target in Hepatocellular carcinoma therapy.
References
Ref 1 PNO1 inhibits autophagy-mediated ferroptosis by GSH metabolic reprogramming in hepatocellular carcinoma. Cell Death Dis. 2022 Nov 29;13(11):1010. doi: 10.1038/s41419-022-05448-7.