OBJECTIVE： This study aims to evaluate the bioactivity of five components of the traditional Chinese medicine complex prescription Jiangzhi granules against hepatocellular steatosis. METHODS： The five major componen...OBJECTIVE： This study aims to evaluate the bioactivity of five components of the traditional Chinese medicine complex prescription Jiangzhi granules against hepatocellular steatosis. METHODS： The five major components, including protopanaxadiol, tanshinone IIA, emodin, chlorogenic acid, and nuciferine, were extracted from Jiangzhi granules. Their cytotoxicity was assessed to determine the safe dose of each component for HepG2 cells. HepG2 cellular steatosis was induced using 1 mmol/L of free fatty acids （FFAs） for 24 h, and then treated with each component at high, intermediate, and low doses （500, 50, and 5 μmol/L）, respectively for another 24 h. The effects on HepG2 steatosis were observed directly under optical phase microscopy, or through oil red O staining and Nile red assays. In addition, the levels of reactive oxygen species （ROS） in the steatotic HepG2 cells with and without high-dose protopanaxadiol treatment were measured using fluorescent dye 2＇,7＇-dichlorodihydrofluorescein diacetate staining. RESULTS： No obvious cytotoxicity was observed in the HepG2 cells incubated with each of the five components at up to 500μmol/L. At 24 h after incubation with FFAs, the HepG2 cells swelled and many lipid droplets accumulated. The lipid content was attenuated after 24 h of incubation with protopanaxadiol, tanshinone IIA, and emodin at 500 or 50 μmol/L （P 〈 0.05）, especially with 500 μmol/L protopanaxadiol （P 〈 0.01）. In addition, the ROS level was elevated in steatotic cells, but decreased after intervention with 500μmol/L protopanaxadiol （P 〈 0.05）. CONCLUSION： Protopanaxadiol, tanshinone IIA, and emodin alleviate hepatocellular steatosis in a dose-dependent manner, and oxidative stress regulation may partially contribute to the effects of protopanaxadiol. ：展开更多
BACKGROUND Stress granules(SGs)could be formed under different stimulation to inhibit cell injury.AIM To investigate whether SGs could protect hepatocytes from hypoxia-induced damage during acute liver failure(ALF)by ...BACKGROUND Stress granules(SGs)could be formed under different stimulation to inhibit cell injury.AIM To investigate whether SGs could protect hepatocytes from hypoxia-induced damage during acute liver failure(ALF)by reducing endoplasmic reticulum stress(ERS)mediated apoptosis.METHODS The agonist of SGs,arsenite(Ars)was used to intervene hypoxia-induced hepatocyte injury cellular model and ALF mice models.Further,the siRNA of activating transcription factor 4(ATF4)and SGs inhibitor anisomycin was then used to intervene in cell models.RESULTS With the increase of hypoxia time from 4 h to 12 h,the levels of HIF-1α,ERS and apoptosis gradually increased,and the expression of SGs marker G3BP1 and TIA-1 was increased and then decreased.Compared with the hypoxia cell model group and ALF mice model,the levels of HIF-1α,apoptosis and ERS were increased in the Ars intervention group.After siRNA-ATF4 intervention,the level of SGs in cells increased,and the levels of HIF-1α,ERS and apoptosis decreased.Compared with the siRNA-ATF4 group,the levels of G3BP1 in the siRNAATF4+anisomycin group were decreased,and the levels of HIF-1α,ERS and apoptosis were increased.Moreover,compared with the ALF group,the degree of liver injury and liver function,the levels of HIF-1α,ERS and apoptosis in the Ars intervention group were decreased,the level of SGs was increased.CONCLUSION SGs could protect hepatocytes from hypoxia-induced damage during ALF by reducing ERSmediated apoptosis.展开更多
Over the past decades,tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others,holding more than half of all modifications occurring in RNA molecules....Over the past decades,tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others,holding more than half of all modifications occurring in RNA molecules.Moreover,tRNA was discovered to be a source of various small noncoding RNA species,such as the stress induced angiogenin cleaved tRNA halves(tiRNA)or the miRNA like tRNA derived fragments.tRNA cleavage under stress was fist discovered in bacteria and later was found to be conserved across different species,including mammals.Under cellular stress conditions,tRNA undergoes conformational changes and angiogenin cleaves it into 3′and 5′halves.5′tiRNA halves were shown to repress protein translations.tRNA cleavage is thought of to be a cytoprotective mechanism by which cells evade apoptosis,however some data hints to the opposite;that tiRNA are cytotoxic or at least related to apoptosis initiation.tRNA cleavage also was shown to be affected by tRNA modifications via different enzymes in the cytosol and mitochondria.In this review,we will highlight the biology of tRNA cleavage,show the evidence of it being cytoprotective or a marker of cell death and shed a light on its role in disease models and human diseases as well as possible future directions in this field of RNA research.展开更多
The onset of amyotrophic lateral sclerosis is usually characterized by focal death of both upper and/or lower motor neurons occurring in the motor cortex,basal ganglia,brainstem,and spinal cord,and commonly involves t...The onset of amyotrophic lateral sclerosis is usually characterized by focal death of both upper and/or lower motor neurons occurring in the motor cortex,basal ganglia,brainstem,and spinal cord,and commonly involves the muscles of the upper and/or lower extremities,and the muscles of the bulbar and/or respiratory regions.However,as the disease progresses,it affects the adjacent body regions,leading to generalized muscle weakness,occasionally along with memory,cognitive,behavioral,and language impairments;respiratory dysfunction occurs at the final stage of the disease.The disease has a complicated pathophysiology and currently,only riluzole,edaravone,and phenylbutyrate/taurursodiol are licensed to treat amyotrophic lateral sclerosis in many industrialized countries.The TAR DNA-binding protein 43 inclusions are observed in 97%of those diagnosed with amyotrophic lateral sclerosis.This review provides a preliminary overview of the potential effects of TAR DNAbinding protein 43 in the pathogenesis of amyotrophic lateral sclerosis,including the abnormalities in nucleoplasmic transport,RNA function,post-translational modification,liquid-liquid phase separation,stress granules,mitochondrial dysfunction,oxidative stress,axonal transport,protein quality control system,and non-cellular autonomous functions(e.g.,glial cell functions and prion-like propagation).展开更多
A key to tackling the coronavirus disease 2019(COVID-19)pandemic is to understand how severe acute respiratory syndrome coronavirus 2(SARS-Co V-2)manages to outsmart host antiviral defense mechanisms.Stress granules(S...A key to tackling the coronavirus disease 2019(COVID-19)pandemic is to understand how severe acute respiratory syndrome coronavirus 2(SARS-Co V-2)manages to outsmart host antiviral defense mechanisms.Stress granules(SGs),which are assembled during viral infection and function to sequester host and viral m RNAs and proteins,are part of the antiviral responses.Here,we show that the SARS-Co V-2 nucleocapsid(N)protein,an RNA binding protein essential for viral production,interacted with RasGTPase-activating protein SH3-domain-binding protein(G3 BP)and disrupted SG assembly,both of which require intrinsically disordered region1(IDR1)in N protein.The N protein partitioned into SGs through liquid-liquid phase separation with G3 BP,and blocked the interaction of G3 BP1 with other SG-related proteins.Moreover,the N protein domains important for phase separation with G3 BP and SG disassembly were required for SARS-Co V-2 viral production.We propose that N protein-mediated SG disassembly is crucial for SARS-Co V-2 production.展开更多
骨关节炎(osteoarthritis,OA)是以软骨磨损和无菌性炎症为主要表现的复杂的病理生理过程。根据国际骨关节炎研究学会(Osteoarthritis Research Society International,OARSI)的定义,该疾病首先表现为分子紊乱,即关节组织代谢异常,然后...骨关节炎(osteoarthritis,OA)是以软骨磨损和无菌性炎症为主要表现的复杂的病理生理过程。根据国际骨关节炎研究学会(Osteoarthritis Research Society International,OARSI)的定义,该疾病首先表现为分子紊乱,即关节组织代谢异常,然后发生解剖和(或)生理紊乱,包括软骨退变、骨重塑、骨赘形成、关节炎症和正常关节功能丧失等。中华医学会运动医疗分会发布的临床专家共识也指出,OA病因尚不完全明确,其发生与年龄、肥胖、炎症、创伤及遗传因素等有关[1]。由此可见,机械应力、生物应激和衰老都参与了OA的病理过程,考虑单一因素不能准确地阐释其机制。展开更多
Stress granules(SGs)represent important non-membrane cytoplasmic compartments,involved in cellular adaptation to various stressful conditions(e.g.,hypoxia,nutrient deprivation,oxidative stress).These granules contain ...Stress granules(SGs)represent important non-membrane cytoplasmic compartments,involved in cellular adaptation to various stressful conditions(e.g.,hypoxia,nutrient deprivation,oxidative stress).These granules contain several scaffold proteins and RNA-binding proteins,which bind to mRNAs and keep them translationally silent while protecting them from harmful conditions.Although the role of SGs in cancer development is still poorly known and vary between cancer types,increasing evidence indicate that the expression and/or the activity of several key SGs components are deregulated in colorectal tumors but also in pre-neoplastic conditions(e.g.,inflammatory bowel disease),thus suggesting a potential role in the onset of colorectal cancer(CRC).It is therefore believed that SGs formation importantly contributes to various steps of colorectal tumorigenesis but also in chemoresistance.As CRC is the third most frequent cancer and one of the leading causes of cancer mortality worldwide,development of new therapeutic targets is needed to offset the development of chemoresistance and formation of metastasis.Abolishing SGs assembly may therefore represent an appealing therapeutic strategy to re-sensitize colon cancer cells to anti-cancer chemotherapies.In this review,we summarize the current knowledge on SGs in colorectal cancer and the potential therapeutic strategies that could be employed to target them.展开更多
Post-transcriptional methylation of N6-adenine and Nl-adenine can affect transcriptome turnover and translation.Furthermore,the regulatory function of N6-methyladenine(m6A)during heat shock has been uncovered,includin...Post-transcriptional methylation of N6-adenine and Nl-adenine can affect transcriptome turnover and translation.Furthermore,the regulatory function of N6-methyladenine(m6A)during heat shock has been uncovered,including the enhancement of the phase separation potential of RNAs.In response to acute stress,e.g.heat shock,the orderly sequestration of mRNAs in stress granules(SGs)is considered important to protect transcripts from the irreversible aggregation.Until recently,the role of N1-methyladenine(m^(1)A)on mRNAs during acute stress response remains largely unknown.Here we show that the methyltransferase complex TRMT6/61A,which generates the tag,is involved in transcriptome protection during heat shock.Our bioinformatics analysis indicates that occurrence of the motif is increased in mRNAs known to be enriched in SGs.Accordingly,the m^(1)A-generating methyltransferase TRMT6/61A accumulated in SGs and mass spectrometry confirmed enrichment of in the SG RNAs.The insertion of a single methylation motif in the untranslated region of a reporter RNA leads to more efficient recovery of protein synthesis from that transcript after the return to normal temperature.Our results demonstrate far-reaching functional consequences of a minimal RNA modification on N1-adenine during acute proteostasis stress.展开更多
microRNAs (miRNAs) are identified as a class of non-protein regulators and a new source for broad control of gene expression in eukaryotes. The past years have witnessed substantial progress in understanding miRNA fun...microRNAs (miRNAs) are identified as a class of non-protein regulators and a new source for broad control of gene expression in eukaryotes. The past years have witnessed substantial progress in understanding miRNA functions and mechanisms, although a few controversies remain. Various hypotheses and models have been suggested for the mechanisms of miRNA repression, including translational inhibition at the level of initiation or elongation, rapid degradation of the nascent peptide, mRNA degradation, and mRNA sequestration into P bodies (processing bodies) and SGs (stress granules) for degradation or/and storage. Recently, some noncanonical miRNA regulation, such as miRNA activation and de-repression of miRNA inhibition, have been uncovered. This review discusses some recent advances about how miRNAs regulate their targets and various modes of miRNA function.展开更多
Stress granules are non-membranous cytoplasmic foci induced by various stress conditions.It is a protective strategy used by cells to suppress overall translation during stress.In cancer cells,it was thought that the ...Stress granules are non-membranous cytoplasmic foci induced by various stress conditions.It is a protective strategy used by cells to suppress overall translation during stress.In cancer cells,it was thought that the formation of stress granules could protect them from apoptosis and induces resistance towards anti-cancer drugs or radiation treatment which makes the stress granules a potential target for cancer treatment.However,most of our understanding of stress granules are still in the stage of molecular and cell biology,and a transitional gap for its actual effect on clinical settings remains.In this review,we summarize the mechanism and effect of stress granules formation in cancer and try to illuminate its potential applications in cancer therapy,using breast cancer as an example.展开更多
基金supported by Natural Science Foundation of Shanghai (No. 11ZR1436900)Leading Academic Discipline Project, Shanghai Municipal Education Commission (No. J50305 & E03008)+1 种基金Innovation Program of Shanghai Municipal Education Commission(No. 12ZZ119)Budget Research Program of Shanghai Municipal Education Commission (No. 2010JW35)
文摘OBJECTIVE： This study aims to evaluate the bioactivity of five components of the traditional Chinese medicine complex prescription Jiangzhi granules against hepatocellular steatosis. METHODS： The five major components, including protopanaxadiol, tanshinone IIA, emodin, chlorogenic acid, and nuciferine, were extracted from Jiangzhi granules. Their cytotoxicity was assessed to determine the safe dose of each component for HepG2 cells. HepG2 cellular steatosis was induced using 1 mmol/L of free fatty acids （FFAs） for 24 h, and then treated with each component at high, intermediate, and low doses （500, 50, and 5 μmol/L）, respectively for another 24 h. The effects on HepG2 steatosis were observed directly under optical phase microscopy, or through oil red O staining and Nile red assays. In addition, the levels of reactive oxygen species （ROS） in the steatotic HepG2 cells with and without high-dose protopanaxadiol treatment were measured using fluorescent dye 2＇,7＇-dichlorodihydrofluorescein diacetate staining. RESULTS： No obvious cytotoxicity was observed in the HepG2 cells incubated with each of the five components at up to 500μmol/L. At 24 h after incubation with FFAs, the HepG2 cells swelled and many lipid droplets accumulated. The lipid content was attenuated after 24 h of incubation with protopanaxadiol, tanshinone IIA, and emodin at 500 or 50 μmol/L （P 〈 0.05）, especially with 500 μmol/L protopanaxadiol （P 〈 0.01）. In addition, the ROS level was elevated in steatotic cells, but decreased after intervention with 500μmol/L protopanaxadiol （P 〈 0.05）. CONCLUSION： Protopanaxadiol, tanshinone IIA, and emodin alleviate hepatocellular steatosis in a dose-dependent manner, and oxidative stress regulation may partially contribute to the effects of protopanaxadiol. ：
基金the National Natural Science Foundation of China,No.82100630 and No.82100894the Fundamental Research Funds for the Central Universities,No.2042021kf0080.
文摘BACKGROUND Stress granules(SGs)could be formed under different stimulation to inhibit cell injury.AIM To investigate whether SGs could protect hepatocytes from hypoxia-induced damage during acute liver failure(ALF)by reducing endoplasmic reticulum stress(ERS)mediated apoptosis.METHODS The agonist of SGs,arsenite(Ars)was used to intervene hypoxia-induced hepatocyte injury cellular model and ALF mice models.Further,the siRNA of activating transcription factor 4(ATF4)and SGs inhibitor anisomycin was then used to intervene in cell models.RESULTS With the increase of hypoxia time from 4 h to 12 h,the levels of HIF-1α,ERS and apoptosis gradually increased,and the expression of SGs marker G3BP1 and TIA-1 was increased and then decreased.Compared with the hypoxia cell model group and ALF mice model,the levels of HIF-1α,apoptosis and ERS were increased in the Ars intervention group.After siRNA-ATF4 intervention,the level of SGs in cells increased,and the levels of HIF-1α,ERS and apoptosis decreased.Compared with the siRNA-ATF4 group,the levels of G3BP1 in the siRNAATF4+anisomycin group were decreased,and the levels of HIF-1α,ERS and apoptosis were increased.Moreover,compared with the ALF group,the degree of liver injury and liver function,the levels of HIF-1α,ERS and apoptosis in the Ars intervention group were decreased,the level of SGs was increased.CONCLUSION SGs could protect hepatocytes from hypoxia-induced damage during ALF by reducing ERSmediated apoptosis.
文摘Over the past decades,tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others,holding more than half of all modifications occurring in RNA molecules.Moreover,tRNA was discovered to be a source of various small noncoding RNA species,such as the stress induced angiogenin cleaved tRNA halves(tiRNA)or the miRNA like tRNA derived fragments.tRNA cleavage under stress was fist discovered in bacteria and later was found to be conserved across different species,including mammals.Under cellular stress conditions,tRNA undergoes conformational changes and angiogenin cleaves it into 3′and 5′halves.5′tiRNA halves were shown to repress protein translations.tRNA cleavage is thought of to be a cytoprotective mechanism by which cells evade apoptosis,however some data hints to the opposite;that tiRNA are cytotoxic or at least related to apoptosis initiation.tRNA cleavage also was shown to be affected by tRNA modifications via different enzymes in the cytosol and mitochondria.In this review,we will highlight the biology of tRNA cleavage,show the evidence of it being cytoprotective or a marker of cell death and shed a light on its role in disease models and human diseases as well as possible future directions in this field of RNA research.
基金in part supported by the National Natural Science Foundation of China,Nos.30560042,81160161,81360198,and 82160255Education Department of Jiangxi Province,Nos.GJJ13198 and GJJ170021+1 种基金Jiangxi Provincial Department of Science and Technology,No.20192BAB205043Health and Family Planning Commission of Jiangxi Province,Nos.20181019 and 202210002(all to RX)。
文摘The onset of amyotrophic lateral sclerosis is usually characterized by focal death of both upper and/or lower motor neurons occurring in the motor cortex,basal ganglia,brainstem,and spinal cord,and commonly involves the muscles of the upper and/or lower extremities,and the muscles of the bulbar and/or respiratory regions.However,as the disease progresses,it affects the adjacent body regions,leading to generalized muscle weakness,occasionally along with memory,cognitive,behavioral,and language impairments;respiratory dysfunction occurs at the final stage of the disease.The disease has a complicated pathophysiology and currently,only riluzole,edaravone,and phenylbutyrate/taurursodiol are licensed to treat amyotrophic lateral sclerosis in many industrialized countries.The TAR DNA-binding protein 43 inclusions are observed in 97%of those diagnosed with amyotrophic lateral sclerosis.This review provides a preliminary overview of the potential effects of TAR DNAbinding protein 43 in the pathogenesis of amyotrophic lateral sclerosis,including the abnormalities in nucleoplasmic transport,RNA function,post-translational modification,liquid-liquid phase separation,stress granules,mitochondrial dysfunction,oxidative stress,axonal transport,protein quality control system,and non-cellular autonomous functions(e.g.,glial cell functions and prion-like propagation).
基金supported by the National Natural Science Foundation of China(81830004,31970755,and 31970173)the Local Grant(608285568031)。
文摘A key to tackling the coronavirus disease 2019(COVID-19)pandemic is to understand how severe acute respiratory syndrome coronavirus 2(SARS-Co V-2)manages to outsmart host antiviral defense mechanisms.Stress granules(SGs),which are assembled during viral infection and function to sequester host and viral m RNAs and proteins,are part of the antiviral responses.Here,we show that the SARS-Co V-2 nucleocapsid(N)protein,an RNA binding protein essential for viral production,interacted with RasGTPase-activating protein SH3-domain-binding protein(G3 BP)and disrupted SG assembly,both of which require intrinsically disordered region1(IDR1)in N protein.The N protein partitioned into SGs through liquid-liquid phase separation with G3 BP,and blocked the interaction of G3 BP1 with other SG-related proteins.Moreover,the N protein domains important for phase separation with G3 BP and SG disassembly were required for SARS-Co V-2 viral production.We propose that N protein-mediated SG disassembly is crucial for SARS-Co V-2 production.
文摘骨关节炎(osteoarthritis,OA)是以软骨磨损和无菌性炎症为主要表现的复杂的病理生理过程。根据国际骨关节炎研究学会(Osteoarthritis Research Society International,OARSI)的定义,该疾病首先表现为分子紊乱,即关节组织代谢异常,然后发生解剖和(或)生理紊乱,包括软骨退变、骨重塑、骨赘形成、关节炎症和正常关节功能丧失等。中华医学会运动医疗分会发布的临床专家共识也指出,OA病因尚不完全明确,其发生与年龄、肥胖、炎症、创伤及遗传因素等有关[1]。由此可见,机械应力、生物应激和衰老都参与了OA的病理过程,考虑单一因素不能准确地阐释其机制。
基金Supported by Geneva Cancer League,No.1711National Institutes of Health,No.R01 CA243445and National Cancer Institute Cancer Center Support Grant,No.P30 CA168524.
文摘Stress granules(SGs)represent important non-membrane cytoplasmic compartments,involved in cellular adaptation to various stressful conditions(e.g.,hypoxia,nutrient deprivation,oxidative stress).These granules contain several scaffold proteins and RNA-binding proteins,which bind to mRNAs and keep them translationally silent while protecting them from harmful conditions.Although the role of SGs in cancer development is still poorly known and vary between cancer types,increasing evidence indicate that the expression and/or the activity of several key SGs components are deregulated in colorectal tumors but also in pre-neoplastic conditions(e.g.,inflammatory bowel disease),thus suggesting a potential role in the onset of colorectal cancer(CRC).It is therefore believed that SGs formation importantly contributes to various steps of colorectal tumorigenesis but also in chemoresistance.As CRC is the third most frequent cancer and one of the leading causes of cancer mortality worldwide,development of new therapeutic targets is needed to offset the development of chemoresistance and formation of metastasis.Abolishing SGs assembly may therefore represent an appealing therapeutic strategy to re-sensitize colon cancer cells to anti-cancer chemotherapies.In this review,we summarize the current knowledge on SGs in colorectal cancer and the potential therapeutic strategies that could be employed to target them.
基金This work was funded by the European Research Council grants MetaMeta_311522(R.M.V.)RIBOMYLOME_309545(G.G.T.)+5 种基金ASTRA_855923(G.G.T)G.G.T.acknowledges support of the H2020 projects IASIS_727658 and INFORE_825080the Spanish Ministry of Economy and Competitiveness BFU2017-86970-Pas well as the collaboration with Peter St.George-Hyslop financed by the Wellcome TrustR.M.V.acknowledges support by the Deutsche Forschungsgemeinschaft(DFG)grant EXC115M.H.is funded by DFG CRC902‘Molecular Principles of RNA-based Regulation’。
文摘Post-transcriptional methylation of N6-adenine and Nl-adenine can affect transcriptome turnover and translation.Furthermore,the regulatory function of N6-methyladenine(m6A)during heat shock has been uncovered,including the enhancement of the phase separation potential of RNAs.In response to acute stress,e.g.heat shock,the orderly sequestration of mRNAs in stress granules(SGs)is considered important to protect transcripts from the irreversible aggregation.Until recently,the role of N1-methyladenine(m^(1)A)on mRNAs during acute stress response remains largely unknown.Here we show that the methyltransferase complex TRMT6/61A,which generates the tag,is involved in transcriptome protection during heat shock.Our bioinformatics analysis indicates that occurrence of the motif is increased in mRNAs known to be enriched in SGs.Accordingly,the m^(1)A-generating methyltransferase TRMT6/61A accumulated in SGs and mass spectrometry confirmed enrichment of in the SG RNAs.The insertion of a single methylation motif in the untranslated region of a reporter RNA leads to more efficient recovery of protein synthesis from that transcript after the return to normal temperature.Our results demonstrate far-reaching functional consequences of a minimal RNA modification on N1-adenine during acute proteostasis stress.
基金Supported by the National Basic Research Program of China (Grant No. 2005 CB 724603)the National Natural Science Foundation of China (Grant No. 30770474)
文摘microRNAs (miRNAs) are identified as a class of non-protein regulators and a new source for broad control of gene expression in eukaryotes. The past years have witnessed substantial progress in understanding miRNA functions and mechanisms, although a few controversies remain. Various hypotheses and models have been suggested for the mechanisms of miRNA repression, including translational inhibition at the level of initiation or elongation, rapid degradation of the nascent peptide, mRNA degradation, and mRNA sequestration into P bodies (processing bodies) and SGs (stress granules) for degradation or/and storage. Recently, some noncanonical miRNA regulation, such as miRNA activation and de-repression of miRNA inhibition, have been uncovered. This review discusses some recent advances about how miRNAs regulate their targets and various modes of miRNA function.
基金This work was supported by the National Natural Science Foundation of China(No.82002979 and 81702839)the Scientific Research and Development Funds of Peking Uni・versity People's Hospital,China(No.RDY2020-16).
文摘Stress granules are non-membranous cytoplasmic foci induced by various stress conditions.It is a protective strategy used by cells to suppress overall translation during stress.In cancer cells,it was thought that the formation of stress granules could protect them from apoptosis and induces resistance towards anti-cancer drugs or radiation treatment which makes the stress granules a potential target for cancer treatment.However,most of our understanding of stress granules are still in the stage of molecular and cell biology,and a transitional gap for its actual effect on clinical settings remains.In this review,we summarize the mechanism and effect of stress granules formation in cancer and try to illuminate its potential applications in cancer therapy,using breast cancer as an example.
