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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, and interested parties.
Long press or scan the QR code below to follow us.
iNature hepatocellular carcinoma (HCC) is one of the malignant tumors with the highest mortality rate.
The key regulatory factors and their interaction networks in the pathogenesis of liver cancer are still unclear.
In addition to genetic mutations, abnormal epigenetics include deregulation of miRNAs, which have a profound impact on liver cell transformation and tumor microenvironment remodeling.
However, its underlying mechanism is largely unknown.
On March 3, 2021, Liu Lei and Jia Lintao of the Air Force Military Medical University published an online communication titled "Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated on Molecular Cancer (IF=15.
30)" TAM remodeling" research paper, the study found that the miR-144/miR-451a cluster is down-regulated in liver cancer, and predicts a better prognosis for HCC patients.
These miRNAs promote macrophage M1 polarization and anti-tumor activity by targeting hepatocyte growth factor (HGF) and macrophage migration inhibitory factor (MIF).
The miR-144 / miR-451a cluster and EZH2 form a feedback loop.
miRNA clusters are coordinated and silenced by the hypermethylation of distal enhancers, which disrupts the formation of chromatin loops and the interaction between enhancers and promoters.
Clinical examination showed that the methylation of this chromatin region is a potential HCC biomarker.
In summary, this study reveals a potential new mechanism for the deregulation of miR-144/miR-451a clusters and the crosstalk between malignant cells and tumor-associated macrophages (TAM) in HCC, providing new insights into the pathogenesis and diagnostic strategies of HCC .
In addition, on February 24, 2021, the Air Force Military Medical University Hu Dahai, Jia Lintao and Bai Wendong jointly published a research paper entitled "Glucocorticoid counteracts cellular mechanoresponses by LINC01569-dependent glucocorticoid receptor–mediated mRNA decay" in Science Advances.
Studies have found that glucocorticoids counteract the cellular mechanical response that relies on the new type of long non-coding RNA (lncRNA) LINC01569.
In addition, LINC01569 mediates the effect of glucocorticoids on mechanical conduction by destabilizing the messenger RNA (mRNA) of mechanical sensors including EGR1, CITED2 and BMP7 (mRNA decay (GMD) mode).
In terms of mechanism, LINC01569 directly binds to GMD factor Y-box binding protein 1 (YBX1).
Then, the LINC01569-YBX1 complex is guided to the mRNA of EGR1, CITED2 and BMP7 through the specific LINC01569-mRNA interaction, which helps to successfully assemble the GMD complex and trigger the GMD.
The results of this study reveal the role of glucocorticoids in cell mechanical transduction and new lncRNA-dependent GMD mechanisms, and provide potential strategies for early intervention in mechanical-related diseases (click to read).
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors of the digestive system, with a poor prognosis and high mortality.
A variety of risk factors, including viral infection, fibrosis, alcohol consumption, and metabolic abnormalities, can cause genetic or phenotypic changes and lead to the progression of liver cancer.
The complexity of the etiology makes it difficult to fully understand the molecular mechanisms of liver cancer.
In the past decade, new discoveries have established that the immune microenvironment plays a key role in the HCC process.
Tumor-associated macrophages (TAM), which are widely considered to be the polarized subtype of M2 and inhibit anti-tumor immunity, are involved in the occurrence, development and metastasis of various HCCs.
According to reports, in animal models and clinical trials, therapies targeting TAM can effectively inhibit the development of liver cancer.
Recent strategies have focused on suppressing the production of TAM and re-inducing TAM into M1 polarization.
Interestingly, tumor cells also affect the plasticity of TAM in liver cancer tissues.
Although direct cell contact regulates the development and function of macrophages through cell membrane ligands and integrin signaling, the paracrine factors of HCC cells represent the main factor in the remodeling of the immune microenvironment.
HCC-derived cytokines and growth factors such as CCL2, TGF-β, MIF and HGF are required for macrophage recruitment, differentiation and M2-like stimulation.
In terms of early diagnosis and more effective intervention, it is very important to analyze the molecular mechanism of crosstalk between HCC and TAM.
Epigenetics includes histone modification, DNA methylation and non-coding RNA (ncRNA), which play an important regulatory role in the development of liver cancer.
It has been reported that histone methylation regulates the expression of a subset of genes related to proliferation and metastasis in liver cancer.
EZH2 is highly expressed in liver cancer and is associated with the low survival rate of patients.
Inhibition of EZH2 can significantly inhibit the progression of HCC.
In addition, DNA methylation caused by DNA methyltransferase (DNMT) also plays a vital role in all stages of liver cancer development.
According to reports, the dysregulation of microRNA (miRNA) promotes the occurrence of various malignant tumors including HCC.
However, although most studies have focused on downstream events of miRNAs, how to down-regulate tumor suppressor miRNAs in HCC is still largely elusive.
In this study, it was determined that the miR-144/miR-451a cluster is a key inhibitor of liver cancer development.
Further studies have shown that miR-144/miR-451a promotes the M1 polarization of TAM and enhances anti-tumor immunity by targeting hepatocyte growth factor (HGF) and macrophage migration inhibitory factor (MIF).
The study also found a double negative feedback loop between miRNA cluster transcription and EZH2-mediated histone modification, and revealed that DNA methylation-dependent chromatin remodeling regulates miR-144/miR-451a cluster expression in HCC Detailed mechanism.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021-01343-5
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, and interested parties.
Long press or scan the QR code below to follow us.
iNature hepatocellular carcinoma (HCC) is one of the malignant tumors with the highest mortality rate.
The key regulatory factors and their interaction networks in the pathogenesis of liver cancer are still unclear.
In addition to genetic mutations, abnormal epigenetics include deregulation of miRNAs, which have a profound impact on liver cell transformation and tumor microenvironment remodeling.
However, its underlying mechanism is largely unknown.
On March 3, 2021, Liu Lei and Jia Lintao of the Air Force Military Medical University published an online communication titled "Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated on Molecular Cancer (IF=15.
30)" TAM remodeling" research paper, the study found that the miR-144/miR-451a cluster is down-regulated in liver cancer, and predicts a better prognosis for HCC patients.
These miRNAs promote macrophage M1 polarization and anti-tumor activity by targeting hepatocyte growth factor (HGF) and macrophage migration inhibitory factor (MIF).
The miR-144 / miR-451a cluster and EZH2 form a feedback loop.
miRNA clusters are coordinated and silenced by the hypermethylation of distal enhancers, which disrupts the formation of chromatin loops and the interaction between enhancers and promoters.
Clinical examination showed that the methylation of this chromatin region is a potential HCC biomarker.
In summary, this study reveals a potential new mechanism for the deregulation of miR-144/miR-451a clusters and the crosstalk between malignant cells and tumor-associated macrophages (TAM) in HCC, providing new insights into the pathogenesis and diagnostic strategies of HCC .
In addition, on February 24, 2021, the Air Force Military Medical University Hu Dahai, Jia Lintao and Bai Wendong jointly published a research paper entitled "Glucocorticoid counteracts cellular mechanoresponses by LINC01569-dependent glucocorticoid receptor–mediated mRNA decay" in Science Advances.
Studies have found that glucocorticoids counteract the cellular mechanical response that relies on the new type of long non-coding RNA (lncRNA) LINC01569.
In addition, LINC01569 mediates the effect of glucocorticoids on mechanical conduction by destabilizing the messenger RNA (mRNA) of mechanical sensors including EGR1, CITED2 and BMP7 (mRNA decay (GMD) mode).
In terms of mechanism, LINC01569 directly binds to GMD factor Y-box binding protein 1 (YBX1).
Then, the LINC01569-YBX1 complex is guided to the mRNA of EGR1, CITED2 and BMP7 through the specific LINC01569-mRNA interaction, which helps to successfully assemble the GMD complex and trigger the GMD.
The results of this study reveal the role of glucocorticoids in cell mechanical transduction and new lncRNA-dependent GMD mechanisms, and provide potential strategies for early intervention in mechanical-related diseases (click to read).
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors of the digestive system, with a poor prognosis and high mortality.
A variety of risk factors, including viral infection, fibrosis, alcohol consumption, and metabolic abnormalities, can cause genetic or phenotypic changes and lead to the progression of liver cancer.
The complexity of the etiology makes it difficult to fully understand the molecular mechanisms of liver cancer.
In the past decade, new discoveries have established that the immune microenvironment plays a key role in the HCC process.
Tumor-associated macrophages (TAM), which are widely considered to be the polarized subtype of M2 and inhibit anti-tumor immunity, are involved in the occurrence, development and metastasis of various HCCs.
According to reports, in animal models and clinical trials, therapies targeting TAM can effectively inhibit the development of liver cancer.
Recent strategies have focused on suppressing the production of TAM and re-inducing TAM into M1 polarization.
Interestingly, tumor cells also affect the plasticity of TAM in liver cancer tissues.
Although direct cell contact regulates the development and function of macrophages through cell membrane ligands and integrin signaling, the paracrine factors of HCC cells represent the main factor in the remodeling of the immune microenvironment.
HCC-derived cytokines and growth factors such as CCL2, TGF-β, MIF and HGF are required for macrophage recruitment, differentiation and M2-like stimulation.
In terms of early diagnosis and more effective intervention, it is very important to analyze the molecular mechanism of crosstalk between HCC and TAM.
Epigenetics includes histone modification, DNA methylation and non-coding RNA (ncRNA), which play an important regulatory role in the development of liver cancer.
It has been reported that histone methylation regulates the expression of a subset of genes related to proliferation and metastasis in liver cancer.
EZH2 is highly expressed in liver cancer and is associated with the low survival rate of patients.
Inhibition of EZH2 can significantly inhibit the progression of HCC.
In addition, DNA methylation caused by DNA methyltransferase (DNMT) also plays a vital role in all stages of liver cancer development.
According to reports, the dysregulation of microRNA (miRNA) promotes the occurrence of various malignant tumors including HCC.
However, although most studies have focused on downstream events of miRNAs, how to down-regulate tumor suppressor miRNAs in HCC is still largely elusive.
In this study, it was determined that the miR-144/miR-451a cluster is a key inhibitor of liver cancer development.
Further studies have shown that miR-144/miR-451a promotes the M1 polarization of TAM and enhances anti-tumor immunity by targeting hepatocyte growth factor (HGF) and macrophage migration inhibitory factor (MIF).
The study also found a double negative feedback loop between miRNA cluster transcription and EZH2-mediated histone modification, and revealed that DNA methylation-dependent chromatin remodeling regulates miR-144/miR-451a cluster expression in HCC Detailed mechanism.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021-01343-5
