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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNature metabolic reprogramming maintains tumorigenesis and aggressiveness of neuroblastoma (NB).
Neuroblastoma is the most common extracranial malignant tumor in childhood, but the underlying mechanism and treatment methods are still elusive
.
On September 27, 2021, Tong Qiangsong and Zheng Liduan of Huazhong University of Science and Technology jointly published a research paper entitled "p113 isoform encoded by CUX1 circular RNA drives tumor progression via facilitating ZRF1/BRD4 transactivation" in Molecular Cancer (IF=27.
40).
The study found a new 113 amino acid CUT-like homeobox 1 (CUX1) protein (p113) in NB cells treated with serum deprivation
.
Further validation studies have shown that nuclear p113 is encoded by the circRNA of CUX1 and promotes lipid metabolism reprogramming, mitochondrial activity, proliferation, invasion and metastasis of NB cells
.
In mechanism, p113 interacts with Zuotin-related factor 1 (ZRF1) and bromodomain protein 4 (BRD4) to form a transcriptional regulatory complex, and mediates the transactivation of ZRF1/BRD4 to upregulate the conversion of fatty aldehydes into fatty acids and fatty acid β-oxidation and mitochondrial complex I activity necessary ALDH3A1, NDUFA1 and NDUFAF5
.
Administration of inhibitory peptides that block the interaction of p113-ZRF1 can inhibit tumorigenesis and invasiveness of NB cells
.
In clinical NB cases, the high expression of p113, ZRF1 or BRD4 is related to the poor survival rate of patients
.
In summary, this study shows that the p113 isoform encoded by the CUX1 circular RNA drives tumor progression by promoting ZRF1/BRD4 transactivation
.
Neuroblastoma (NB) is a solid malignant tumor with rapid progression and high mortality, accounting for more than 15% of tumor-related deaths in the pediatric population
.
For high-risk NB patients, despite the multimodal treatment, the clinical results are still unfavorable
.
In addition to aerobic glycolysis and glutamine breakdown, tumor cells also obtain energy from lipid metabolism in order to thrive in challenging environments, including fatty acid uptake, lipid de novo synthesis, and fatty acid β-oxidation (FAO)
.
FAO allows mitochondria to convert long-chain fatty acids into acetyl-CoA, and then through the tricarboxylic acid cycle and electron transfer chain (ETC) oxidation to produce ATP
.
The FAO pathway is dysregulated in a variety of human malignancies, and tumor cells rely on FAO for proliferation, survival, dryness, drug resistance or metastasis
.
However, the transcriptional regulators of lipid metabolism reprogramming in NB are still largely elusive
.
Circular RNA (circRNA) is a subclass of non-coding RNA (ncRNA) with a closed continuous loop.
By acting as a miRNA (microRNA) sponge or RNA binding protein chaperone, it serves as a key regulator of cancer gene expression
.
For example, CDR1as exerts miRNA sponge activity as a competitive endogenous RNA
.
Eukaryotic translation elongation factor 3 J (EIF3J)-derived circRNA (circ-EIF3J) interacts with U1 snRNP and RNA polymerase II to promote the transcription of parental genes
.
Circ-AMOTL1 derived from angiomotin-like protein 1 (AMOTL1) promotes tumorigenesis by increasing the nuclear retention of c-Myc
.
The article pattern (picture from Molecular Cancer) At the same time, some circRNAs have the ability to encode peptides or proteins
.
For example, the circRNA-encoded protein FBXW7-185aa inhibits the proliferation of glioblastoma by reducing the stability of c-Myc
.
A novel protein encoded by the circular RNA of AKT serine/threonine kinase 3 (circAKT3) inhibits the occurrence of glioblastoma by competing with active phosphoinositide-dependent kinase 1
.
At the same time, β-catenin cyclic RNA (circβ-catenin)-derived protein promotes the growth of liver cancer cells by activating the Wnt pathway
.
The circular RNA of protein phosphatase 1 regulatory subunit 12A (circPPP1R12A) encodes a protein that drives colon cancer metastasis through the Hippo-YAP signaling pathway
.
However, the role and potential mechanism of circRNA-encoded protein in NB remain to be determined
.
In this study, the 113 amino acid protein (p113) encoded by the circRNA of CUT-like homeobox 1 (CUX1) was identified as a driving factor for the progress of NB
.
In mechanism, p113 interacts with Zuotin-related factor 1 (ZRF1) and bromodomain protein 4 (BRD4) to form a transcriptional regulatory complex, and mediates the transactivation of ZRF1/BRD4 to upregulate the conversion of fatty aldehydes into fatty acids and fatty acid β-oxidation and mitochondrial complex I activity necessary ALDH3A1, NDUFA1 and NDUFAF5
.
Administration of inhibitory peptides that block the interaction of p113-ZRF1 inhibits FAO, mitochondrial complex I activity, tumorigenesis and invasiveness of NB cells, indicating the carcinogenic effects of p113 and ZRF1 in lipid metabolism reprogramming and NB progression
.
In summary, this study shows that the p113 isoform encoded by CUX1 circular RNA drives tumor progression by promoting ZRF1/BRD4 transactivation.
Reference news: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021 -01421-8
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNature metabolic reprogramming maintains tumorigenesis and aggressiveness of neuroblastoma (NB).
Neuroblastoma is the most common extracranial malignant tumor in childhood, but the underlying mechanism and treatment methods are still elusive
.
On September 27, 2021, Tong Qiangsong and Zheng Liduan of Huazhong University of Science and Technology jointly published a research paper entitled "p113 isoform encoded by CUX1 circular RNA drives tumor progression via facilitating ZRF1/BRD4 transactivation" in Molecular Cancer (IF=27.
40).
The study found a new 113 amino acid CUT-like homeobox 1 (CUX1) protein (p113) in NB cells treated with serum deprivation
.
Further validation studies have shown that nuclear p113 is encoded by the circRNA of CUX1 and promotes lipid metabolism reprogramming, mitochondrial activity, proliferation, invasion and metastasis of NB cells
.
In mechanism, p113 interacts with Zuotin-related factor 1 (ZRF1) and bromodomain protein 4 (BRD4) to form a transcriptional regulatory complex, and mediates the transactivation of ZRF1/BRD4 to upregulate the conversion of fatty aldehydes into fatty acids and fatty acid β-oxidation and mitochondrial complex I activity necessary ALDH3A1, NDUFA1 and NDUFAF5
.
Administration of inhibitory peptides that block the interaction of p113-ZRF1 can inhibit tumorigenesis and invasiveness of NB cells
.
In clinical NB cases, the high expression of p113, ZRF1 or BRD4 is related to the poor survival rate of patients
.
In summary, this study shows that the p113 isoform encoded by the CUX1 circular RNA drives tumor progression by promoting ZRF1/BRD4 transactivation
.
Neuroblastoma (NB) is a solid malignant tumor with rapid progression and high mortality, accounting for more than 15% of tumor-related deaths in the pediatric population
.
For high-risk NB patients, despite the multimodal treatment, the clinical results are still unfavorable
.
In addition to aerobic glycolysis and glutamine breakdown, tumor cells also obtain energy from lipid metabolism in order to thrive in challenging environments, including fatty acid uptake, lipid de novo synthesis, and fatty acid β-oxidation (FAO)
.
FAO allows mitochondria to convert long-chain fatty acids into acetyl-CoA, and then through the tricarboxylic acid cycle and electron transfer chain (ETC) oxidation to produce ATP
.
The FAO pathway is dysregulated in a variety of human malignancies, and tumor cells rely on FAO for proliferation, survival, dryness, drug resistance or metastasis
.
However, the transcriptional regulators of lipid metabolism reprogramming in NB are still largely elusive
.
Circular RNA (circRNA) is a subclass of non-coding RNA (ncRNA) with a closed continuous loop.
By acting as a miRNA (microRNA) sponge or RNA binding protein chaperone, it serves as a key regulator of cancer gene expression
.
For example, CDR1as exerts miRNA sponge activity as a competitive endogenous RNA
.
Eukaryotic translation elongation factor 3 J (EIF3J)-derived circRNA (circ-EIF3J) interacts with U1 snRNP and RNA polymerase II to promote the transcription of parental genes
.
Circ-AMOTL1 derived from angiomotin-like protein 1 (AMOTL1) promotes tumorigenesis by increasing the nuclear retention of c-Myc
.
The article pattern (picture from Molecular Cancer) At the same time, some circRNAs have the ability to encode peptides or proteins
.
For example, the circRNA-encoded protein FBXW7-185aa inhibits the proliferation of glioblastoma by reducing the stability of c-Myc
.
A novel protein encoded by the circular RNA of AKT serine/threonine kinase 3 (circAKT3) inhibits the occurrence of glioblastoma by competing with active phosphoinositide-dependent kinase 1
.
At the same time, β-catenin cyclic RNA (circβ-catenin)-derived protein promotes the growth of liver cancer cells by activating the Wnt pathway
.
The circular RNA of protein phosphatase 1 regulatory subunit 12A (circPPP1R12A) encodes a protein that drives colon cancer metastasis through the Hippo-YAP signaling pathway
.
However, the role and potential mechanism of circRNA-encoded protein in NB remain to be determined
.
In this study, the 113 amino acid protein (p113) encoded by the circRNA of CUT-like homeobox 1 (CUX1) was identified as a driving factor for the progress of NB
.
In mechanism, p113 interacts with Zuotin-related factor 1 (ZRF1) and bromodomain protein 4 (BRD4) to form a transcriptional regulatory complex, and mediates the transactivation of ZRF1/BRD4 to upregulate the conversion of fatty aldehydes into fatty acids and fatty acid β-oxidation and mitochondrial complex I activity necessary ALDH3A1, NDUFA1 and NDUFAF5
.
Administration of inhibitory peptides that block the interaction of p113-ZRF1 inhibits FAO, mitochondrial complex I activity, tumorigenesis and invasiveness of NB cells, indicating the carcinogenic effects of p113 and ZRF1 in lipid metabolism reprogramming and NB progression
.
In summary, this study shows that the p113 isoform encoded by CUX1 circular RNA drives tumor progression by promoting ZRF1/BRD4 transactivation.
Reference news: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021 -01421-8
