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Editor’s note iNature is China’s largest academic public account.
It is jointly created by a team of doctors from Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
Those who are interested can long press/scan the QR code below to follow.
iNature is the first line of defense against viral infections.
Type I interferons (IFN-I, including IFN-α and IFN-β) play a central role by activating the expression of hundreds of IFN-stimulating genes (ISG).
However, the virus is not to be outdone.
In the game with humans for thousands of years, the virus has evolved a variety of strategies to evade the attack of the immune system.
On December 15, 2020, Xuetao Cao’s team published online research results titled Decreased Expression of the Host Long-Noncoding RNA-GM Facilitates Viral Escape by Inhibiting the Kinase activity TBK1 via S-glutathionylation on Immunity.
The screened macrophage virus infection of lncRNAs with decreased expression, identified lncRNA (lncRNA-GM, gene symbol: AK189470.
1), which can promote the production of type I interferon (IFN-I) and inhibit virus replication.
The lack of mouse lncRNA-GM will increase the susceptibility to viral infection and weaken the production of IFN-I.
In terms of mechanism, lncRNA-GM binds to glutathione S-transferase M1 (GSTM1) and prevents GSTM1 from interacting with kinase TBK1, thereby reducing the S-glutathionylation of TBK1 mediated by GSTM1.
The reduction of S-glutathione acylation enhances TBK1 activity and downstream production of antiviral media.
Viral infection will reprogram the glutathione metabolism in the cell.
In addition, oxidized glutathione mimics can inhibit TBK1 activity and promote virus replication.
The findings reveal the regulatory effect of S-glutathione acylation on TBK1 and provide insights into virus-mediated metabolic changes that affect innate immunity and virus escape.
In addition, on October 24, 2020, the Naval Military Medical University Cao Xuetao and Hou Jin jointly published a research paper titled "microRNA-199a-3p inhibits hepatic apoptosis and hepatocarcinogenesis by targeting PDCD4" in the journal Oncogenesis, a journal of Nature.
The research identified and It was verified that miR-199a-3p directly targets programmed cell death 4 (PDCD4), which can promote apoptosis.
In addition, this study confirmed that miR-199a-3p inhibits hepatocyte apoptosis and liver damage by targeting and inhibiting PDCD4.
Therefore, liver miR-199a-3p inhibits liver cell apoptosis and liver cancer, while the reduction of miR-199a-3p in liver cells may aggravate liver damage and the development of HCC (click to read).
On October 21, 2020, Cao Xuetao’s team from Nankai University published an online review paper entitled "The function and regulation of TET2 in innate immunity and inflammation" in Protein Cell.
The review focused on TET2 through epigenetic regulation and signal network triggering and Solve the function of inflammation.
In addition, this review focuses on the regulation of TET2 at various molecular levels and related inflammatory diseases, which will provide insights for intervention in the pathological process caused by TET2 disorders (click to read).
On September 9, 2020, Cao Xuetao and Jiang Minghong of the Peking Union Medical College of the Academy of Medical Sciences published a research paper entitled "LncRNA Malat1 inhibition of TDP43 cleavage suppresses IRF3-initiated antiviral innate immunity" on PNAS.
Differently expressed lncRNAs in phages, and the nuclear-rich lncRNA Malat1 has been identified as a negative regulator of antiviral type I IFN production.
The research findings provide potential targets for the control of viral infections and IFN-I-related inflammatory autoimmune diseases (click to read).
On June 20, 2020, Xuetao Cao’s team published a review article titled "Nuclear innate sensors for nucleic acids in immunity and inflammation" online in Immunological Reviews.
The review summarized the identification of nucleic acid natural innate sensor proteins (such as hnRNPA2B1, IFI16, SAFA).
) And the latest findings on its role in host defense and inflammation (click to read).
On April 9, 2020, Cao Xuetao of Nankai University/Chinese Academy of Medical Sciences published an online opinion article entitled "COVID-19: immunopathology and its implications for therapy" in Nature Reviews Immunology (IF=44), which systematically summarized SARS- The immunological response and potential treatment methods produced by CoV-2 provide a good reference for further understanding the pathogenic mechanism of SARS-CoV-2, and at the same time guide the direction for better control of COVID-19 (click read).
Hepatocellular carcinoma (HCC) is a fatal malignant primary liver cancer.
It ranks fourth in cancer-related deaths and sixth in global emergencies, and its 5-year survival rate is low. Liver diseases, such as chronic hepatitis caused by hepatitis B or C viruses (HBV or HCV), alcoholic liver disease and non-alcoholic fatty liver, increase the risk of hepatocellular carcinoma development.
Generally, HCC carcinogenesis is caused by repeated cycles of liver injury, induced liver inflammation and compensatory hepatocyte proliferation.
Liver injury plays a key role in this vicious cycle.
The death of liver cells can release damage-related pattern molecules (DAMPs), which activate immune cells in the liver, recruit circulating inflammatory cells and trigger liver inflammation.
Induced hepatitis stimulates compensatory hepatocyte proliferation, and the hepatitis response also worsens liver damage and aggravates hepatitis.
Persistent liver damage can cause chronic hepatitis and repetitive compensatory hepatocellular hyperplasia, which ultimately leads to the occurrence of liver cancer.
The potential regulatory mechanism of liver cancer has attracted widespread attention, but it is still largely unknown and needs further research.
Cell death plays a key role in the initiation of liver cancer.
Apoptosis, necroptosis, pyrolysis, and iron death are the types of cell death that are deeply studied during tissue damage.
Different types of liver cell death ultimately lead to different types of liver cancer.
For example, necroptosis of liver cells hatches an environment that determines the growth of intrahepatic cholangiocarcinoma (ICC).
However, if hepatocytes are in an environment produced by apoptotic hepatocytes, they tend to become HCC.
Hepatocyte-specific deletion of IκB kinase (IKK) subunit NEMO/IKKγ sensitizes hepatocyte apoptosis through NF-κB inhibition, and spontaneously forms mouse HCC within 12 months.
Similarly, mice lacking anti-apoptotic myeloid leukemia 1 (Mcl-1) in liver cells have severe liver damage caused by spontaneous apoptosis, and more than 50% of mice tumor formation was observed within 8 months .
In addition, mice in which the receptor-interacting serine/threonine protein kinase 1 (RIPK1) and Rel-like domain-containing protein A (RelA) were knocked out in mice hepatocytes showed increased hepatocyte apoptosis.
And the formation of spontaneous HCC. In addition, other proteins that regulate liver cell apoptosis, such as TGF-β activated kinase 1 (TAK1), TNF receptor related factor 2 (TRAF2) and IκB kinase subunit β (IKKβ), are also involved in the occurrence of liver cancer.
Therefore, liver cell apoptosis is very important in the initiation of liver cancer, and the molecular regulation mechanism of liver cell apoptosis and its role in liver cancer have attracted widespread attention.
MicroRNA (miRNA) is a type of single-stranded RNA with a length of approximately 22 nucleotides.
The function of miRNA has been extensively studied and it has been determined to play a key role in cancer progression, especially in HCC.
It has been proposed that a group of miRNAs, such as miR-330-5p, miR-520a and miR-483-3p, participate in cancer progression by regulating proliferation, apoptosis, migration and invasion.
However, the role of miRNA in the occurrence of liver cancer, especially the established role in vivo, is still lacking in research.
Mice bearing the miR-122 gene knockout spontaneously develop steatohepatitis, fibrosis, and eventually HCC within 11 months.
However, until now, it is still unknown whether miRNAs can regulate hepatocyte apoptosis and related liver cancer in vivo.
Previously, using high-throughput sequencing to analyze the dysregulated miRNA in liver cancer, it was found that miR-199a/b-3p was expressed in large amounts in normal human liver, but was significantly reduced in liver cancer, thus promoting the progression of liver cancer.
So far, it is unclear whether miR-199a/b-3p is involved in HCC carcinogenesis.
Therefore, in this study, we focused on the role and mechanism of miR-199a/b-3p in the occurrence of liver cancer.
It is determined that liver miR-199a/b-3p is expressed by miR-199a-2 gene in mice.
This study constructed miR-199a-2 gene knockout mice and hepatocyte-specific miR-199a-2 gene knockout mice mouse. Hepatocyte-specific miR-199a-3p knockout significantly increased the occurrence of liver cancer induced by diethylnitrosamine (DEN), which was mediated by the enhanced hepatocyte apoptosis and liver injury induced by DEN administration.
In the acute liver injury model induced by acetaminophen (APAP), hepatocyte-specific miR-199a-3p knockout also aggravated hepatocyte apoptosis.
Through proteomics screening and reporter gene verification, the study identified and verified that miR-199a-3p directly targets programmed cell death 4 (PDCD4), which can promote apoptosis.
In addition, this study confirmed that miR-199a-3p inhibits hepatocyte apoptosis and liver damage by targeting and inhibiting PDCD4.
Therefore, liver miR-199a-3p inhibits liver cell apoptosis and liver cancer, while the decrease of miR-199a-3p in liver cells may aggravate liver damage and the development of HCC.
Reference message: https://
It is jointly created by a team of doctors from Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
Those who are interested can long press/scan the QR code below to follow.
iNature is the first line of defense against viral infections.
Type I interferons (IFN-I, including IFN-α and IFN-β) play a central role by activating the expression of hundreds of IFN-stimulating genes (ISG).
However, the virus is not to be outdone.
In the game with humans for thousands of years, the virus has evolved a variety of strategies to evade the attack of the immune system.
On December 15, 2020, Xuetao Cao’s team published online research results titled Decreased Expression of the Host Long-Noncoding RNA-GM Facilitates Viral Escape by Inhibiting the Kinase activity TBK1 via S-glutathionylation on Immunity.
The screened macrophage virus infection of lncRNAs with decreased expression, identified lncRNA (lncRNA-GM, gene symbol: AK189470.
1), which can promote the production of type I interferon (IFN-I) and inhibit virus replication.
The lack of mouse lncRNA-GM will increase the susceptibility to viral infection and weaken the production of IFN-I.
In terms of mechanism, lncRNA-GM binds to glutathione S-transferase M1 (GSTM1) and prevents GSTM1 from interacting with kinase TBK1, thereby reducing the S-glutathionylation of TBK1 mediated by GSTM1.
The reduction of S-glutathione acylation enhances TBK1 activity and downstream production of antiviral media.
Viral infection will reprogram the glutathione metabolism in the cell.
In addition, oxidized glutathione mimics can inhibit TBK1 activity and promote virus replication.
The findings reveal the regulatory effect of S-glutathione acylation on TBK1 and provide insights into virus-mediated metabolic changes that affect innate immunity and virus escape.
In addition, on October 24, 2020, the Naval Military Medical University Cao Xuetao and Hou Jin jointly published a research paper titled "microRNA-199a-3p inhibits hepatic apoptosis and hepatocarcinogenesis by targeting PDCD4" in the journal Oncogenesis, a journal of Nature.
The research identified and It was verified that miR-199a-3p directly targets programmed cell death 4 (PDCD4), which can promote apoptosis.
In addition, this study confirmed that miR-199a-3p inhibits hepatocyte apoptosis and liver damage by targeting and inhibiting PDCD4.
Therefore, liver miR-199a-3p inhibits liver cell apoptosis and liver cancer, while the reduction of miR-199a-3p in liver cells may aggravate liver damage and the development of HCC (click to read).
On October 21, 2020, Cao Xuetao’s team from Nankai University published an online review paper entitled "The function and regulation of TET2 in innate immunity and inflammation" in Protein Cell.
The review focused on TET2 through epigenetic regulation and signal network triggering and Solve the function of inflammation.
In addition, this review focuses on the regulation of TET2 at various molecular levels and related inflammatory diseases, which will provide insights for intervention in the pathological process caused by TET2 disorders (click to read).
On September 9, 2020, Cao Xuetao and Jiang Minghong of the Peking Union Medical College of the Academy of Medical Sciences published a research paper entitled "LncRNA Malat1 inhibition of TDP43 cleavage suppresses IRF3-initiated antiviral innate immunity" on PNAS.
Differently expressed lncRNAs in phages, and the nuclear-rich lncRNA Malat1 has been identified as a negative regulator of antiviral type I IFN production.
The research findings provide potential targets for the control of viral infections and IFN-I-related inflammatory autoimmune diseases (click to read).
On June 20, 2020, Xuetao Cao’s team published a review article titled "Nuclear innate sensors for nucleic acids in immunity and inflammation" online in Immunological Reviews.
The review summarized the identification of nucleic acid natural innate sensor proteins (such as hnRNPA2B1, IFI16, SAFA).
) And the latest findings on its role in host defense and inflammation (click to read).
On April 9, 2020, Cao Xuetao of Nankai University/Chinese Academy of Medical Sciences published an online opinion article entitled "COVID-19: immunopathology and its implications for therapy" in Nature Reviews Immunology (IF=44), which systematically summarized SARS- The immunological response and potential treatment methods produced by CoV-2 provide a good reference for further understanding the pathogenic mechanism of SARS-CoV-2, and at the same time guide the direction for better control of COVID-19 (click read).
Hepatocellular carcinoma (HCC) is a fatal malignant primary liver cancer.
It ranks fourth in cancer-related deaths and sixth in global emergencies, and its 5-year survival rate is low. Liver diseases, such as chronic hepatitis caused by hepatitis B or C viruses (HBV or HCV), alcoholic liver disease and non-alcoholic fatty liver, increase the risk of hepatocellular carcinoma development.
Generally, HCC carcinogenesis is caused by repeated cycles of liver injury, induced liver inflammation and compensatory hepatocyte proliferation.
Liver injury plays a key role in this vicious cycle.
The death of liver cells can release damage-related pattern molecules (DAMPs), which activate immune cells in the liver, recruit circulating inflammatory cells and trigger liver inflammation.
Induced hepatitis stimulates compensatory hepatocyte proliferation, and the hepatitis response also worsens liver damage and aggravates hepatitis.
Persistent liver damage can cause chronic hepatitis and repetitive compensatory hepatocellular hyperplasia, which ultimately leads to the occurrence of liver cancer.
The potential regulatory mechanism of liver cancer has attracted widespread attention, but it is still largely unknown and needs further research.
Cell death plays a key role in the initiation of liver cancer.
Apoptosis, necroptosis, pyrolysis, and iron death are the types of cell death that are deeply studied during tissue damage.
Different types of liver cell death ultimately lead to different types of liver cancer.
For example, necroptosis of liver cells hatches an environment that determines the growth of intrahepatic cholangiocarcinoma (ICC).
However, if hepatocytes are in an environment produced by apoptotic hepatocytes, they tend to become HCC.
Hepatocyte-specific deletion of IκB kinase (IKK) subunit NEMO/IKKγ sensitizes hepatocyte apoptosis through NF-κB inhibition, and spontaneously forms mouse HCC within 12 months.
Similarly, mice lacking anti-apoptotic myeloid leukemia 1 (Mcl-1) in liver cells have severe liver damage caused by spontaneous apoptosis, and more than 50% of mice tumor formation was observed within 8 months .
In addition, mice in which the receptor-interacting serine/threonine protein kinase 1 (RIPK1) and Rel-like domain-containing protein A (RelA) were knocked out in mice hepatocytes showed increased hepatocyte apoptosis.
And the formation of spontaneous HCC. In addition, other proteins that regulate liver cell apoptosis, such as TGF-β activated kinase 1 (TAK1), TNF receptor related factor 2 (TRAF2) and IκB kinase subunit β (IKKβ), are also involved in the occurrence of liver cancer.
Therefore, liver cell apoptosis is very important in the initiation of liver cancer, and the molecular regulation mechanism of liver cell apoptosis and its role in liver cancer have attracted widespread attention.
MicroRNA (miRNA) is a type of single-stranded RNA with a length of approximately 22 nucleotides.
The function of miRNA has been extensively studied and it has been determined to play a key role in cancer progression, especially in HCC.
It has been proposed that a group of miRNAs, such as miR-330-5p, miR-520a and miR-483-3p, participate in cancer progression by regulating proliferation, apoptosis, migration and invasion.
However, the role of miRNA in the occurrence of liver cancer, especially the established role in vivo, is still lacking in research.
Mice bearing the miR-122 gene knockout spontaneously develop steatohepatitis, fibrosis, and eventually HCC within 11 months.
However, until now, it is still unknown whether miRNAs can regulate hepatocyte apoptosis and related liver cancer in vivo.
Previously, using high-throughput sequencing to analyze the dysregulated miRNA in liver cancer, it was found that miR-199a/b-3p was expressed in large amounts in normal human liver, but was significantly reduced in liver cancer, thus promoting the progression of liver cancer.
So far, it is unclear whether miR-199a/b-3p is involved in HCC carcinogenesis.
Therefore, in this study, we focused on the role and mechanism of miR-199a/b-3p in the occurrence of liver cancer.
It is determined that liver miR-199a/b-3p is expressed by miR-199a-2 gene in mice.
This study constructed miR-199a-2 gene knockout mice and hepatocyte-specific miR-199a-2 gene knockout mice mouse. Hepatocyte-specific miR-199a-3p knockout significantly increased the occurrence of liver cancer induced by diethylnitrosamine (DEN), which was mediated by the enhanced hepatocyte apoptosis and liver injury induced by DEN administration.
In the acute liver injury model induced by acetaminophen (APAP), hepatocyte-specific miR-199a-3p knockout also aggravated hepatocyte apoptosis.
Through proteomics screening and reporter gene verification, the study identified and verified that miR-199a-3p directly targets programmed cell death 4 (PDCD4), which can promote apoptosis.
In addition, this study confirmed that miR-199a-3p inhibits hepatocyte apoptosis and liver damage by targeting and inhibiting PDCD4.
Therefore, liver miR-199a-3p inhibits liver cell apoptosis and liver cancer, while the decrease of miR-199a-3p in liver cells may aggravate liver damage and the development of HCC.
Reference message: https://
