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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
.
iNatureHACE1 is an E3 ubiquitin protein ligase that is often inactivated and has been shown to be a putative tumor suppressor in different types of cancer
.
However, its role in glioma is still elusive
.
On November 24, 2021, Hou Peng, Yang Jian of Xi’an Jiaotong University, and He Nongyue of Southeast University published an online newsletter titled "HACE1-mediated NRF2 activation causes enhanced malignant phenotypes and decreased in Signal Transduction and Targeted Therapy (IF=18.
19)" Radiosensitivity of glioma cells" research paper, the study observed an increase in the expression of HACE1 in gliomas related to control subjects, and found that the high expression of HACE1 was associated with WHO grade III and IV patients and low-grade glial cells receiving radiotherapy The poor prognosis of LGG patients has a strong correlation
.
HACE1 knockdown significantly inhibits the malignant behavior of glioma cells, while ectopic expression of HACE1 enhances cell growth in vitro and in vivo
.
Further studies have shown that HACE1 enhances the protein stability of nuclear factor red blood cell 2 related factor 2 (NRF2) by competing with another E3 ligase KEAP1 to bind to NRF2
.
In addition, HACE1 also promotes mRNA translation mediated by the internal ribosome entry site (IRES) of NRF2
.
These effects do not depend on its E3 ligase activity
.
Finally, this study proved that HACE1 significantly reduces cellular ROS levels by activating NRF2, thereby reducing the response of glioma cells to radiation
.
In conclusion, the data of this study indicate that HACE1 leads to enhanced malignant phenotype and decreased radiosensitivity of glioma cells by activating NRF2, and suggests that it may act as a prognostic factor and potential therapeutic target in glioma
.
As the most common form of brain tumor, glioma has the characteristics of invasive growth, difficult to be completely removed, easy to relapse, and poor prognosis
.
Although progress has been made in the treatment of glioma, the prognosis is still disappointing
.
Therefore, in order to develop more effective treatment strategies, it has become more urgent to determine the underlying mechanism of the pathogenesis of glioma
.
It is homologous to the E6-AP carboxyl terminal (HECT) domain and ankyrin repeats, including E3 ubiquitin-protein ligase 1 (HACE1), which is involved in cardioprotection and anti-oxidative stress, and has been shown to be frequently found in different types of cancer Down-regulation or mutation, which means that it may act as a putative tumor suppressor
.
Hace1−/− mice will spontaneously develop different tumors
.
Further in vitro and in vivo studies have shown that Hace1 inhibits the cell cycle progression of different cancers by reducing the expression of cyclin D1
.
Schematic model of HACE1 promoting malignant phenotype and reducing radiosensitivity of glioma cells (picture from Signal Transduction and Targeted Therapy) As the substrate of Hace1, lysine 147 of Rho GTPase Rac1 can be ubiquitinated by HACE1
.
Many studies have shown that Rac1 is involved in regulating various biological processes, including cell movement, cell-cell contact, protein translation, and cell growth
.
A previous study demonstrated that HACE1 ubiquitinates optic neuromodulin, thereby inhibiting the growth of lung cancer cells in vitro and in vivo by activating autophagy
.
On the other hand, HACE1 also showed pro-invasive properties in melanoma cells
.
However, its biological characteristics and its function in gliomas remain to be determined
.
This study found that high HACE1 expression is closely related to the poor survival rate of WHO grade III and IV patients
.
Further studies have shown that HACE1 activates nuclear factor red blood cell 2 related factor 2 (NFE2L2, also known as NRF2) through a variety of mechanisms, leading to enhanced malignant phenotype and decreased radiosensitivity of glioma cells
.
Reference message: https://
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
.
iNatureHACE1 is an E3 ubiquitin protein ligase that is often inactivated and has been shown to be a putative tumor suppressor in different types of cancer
.
However, its role in glioma is still elusive
.
On November 24, 2021, Hou Peng, Yang Jian of Xi’an Jiaotong University, and He Nongyue of Southeast University published an online newsletter titled "HACE1-mediated NRF2 activation causes enhanced malignant phenotypes and decreased in Signal Transduction and Targeted Therapy (IF=18.
19)" Radiosensitivity of glioma cells" research paper, the study observed an increase in the expression of HACE1 in gliomas related to control subjects, and found that the high expression of HACE1 was associated with WHO grade III and IV patients and low-grade glial cells receiving radiotherapy The poor prognosis of LGG patients has a strong correlation
.
HACE1 knockdown significantly inhibits the malignant behavior of glioma cells, while ectopic expression of HACE1 enhances cell growth in vitro and in vivo
.
Further studies have shown that HACE1 enhances the protein stability of nuclear factor red blood cell 2 related factor 2 (NRF2) by competing with another E3 ligase KEAP1 to bind to NRF2
.
In addition, HACE1 also promotes mRNA translation mediated by the internal ribosome entry site (IRES) of NRF2
.
These effects do not depend on its E3 ligase activity
.
Finally, this study proved that HACE1 significantly reduces cellular ROS levels by activating NRF2, thereby reducing the response of glioma cells to radiation
.
In conclusion, the data of this study indicate that HACE1 leads to enhanced malignant phenotype and decreased radiosensitivity of glioma cells by activating NRF2, and suggests that it may act as a prognostic factor and potential therapeutic target in glioma
.
As the most common form of brain tumor, glioma has the characteristics of invasive growth, difficult to be completely removed, easy to relapse, and poor prognosis
.
Although progress has been made in the treatment of glioma, the prognosis is still disappointing
.
Therefore, in order to develop more effective treatment strategies, it has become more urgent to determine the underlying mechanism of the pathogenesis of glioma
.
It is homologous to the E6-AP carboxyl terminal (HECT) domain and ankyrin repeats, including E3 ubiquitin-protein ligase 1 (HACE1), which is involved in cardioprotection and anti-oxidative stress, and has been shown to be frequently found in different types of cancer Down-regulation or mutation, which means that it may act as a putative tumor suppressor
.
Hace1−/− mice will spontaneously develop different tumors
.
Further in vitro and in vivo studies have shown that Hace1 inhibits the cell cycle progression of different cancers by reducing the expression of cyclin D1
.
Schematic model of HACE1 promoting malignant phenotype and reducing radiosensitivity of glioma cells (picture from Signal Transduction and Targeted Therapy) As the substrate of Hace1, lysine 147 of Rho GTPase Rac1 can be ubiquitinated by HACE1
.
Many studies have shown that Rac1 is involved in regulating various biological processes, including cell movement, cell-cell contact, protein translation, and cell growth
.
A previous study demonstrated that HACE1 ubiquitinates optic neuromodulin, thereby inhibiting the growth of lung cancer cells in vitro and in vivo by activating autophagy
.
On the other hand, HACE1 also showed pro-invasive properties in melanoma cells
.
However, its biological characteristics and its function in gliomas remain to be determined
.
This study found that high HACE1 expression is closely related to the poor survival rate of WHO grade III and IV patients
.
Further studies have shown that HACE1 activates nuclear factor red blood cell 2 related factor 2 (NFE2L2, also known as NRF2) through a variety of mechanisms, leading to enhanced malignant phenotype and decreased radiosensitivity of glioma cells
.
Reference message: https://
