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stress granules inhibit endoplasmic reticulum stress-mediated apoptosis during hypoxia-induced injury in acute liver failure

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World Journal of Gastroenterology 2023年第8期29卷 1315-1329页

作者： Wen-Yuan Li Fan Yang Xun Li Lu-Wen Wang Yao Wang Department of Anesthesiology Renmin Hospital of Wuhan UniversityWuhan 430060Hubei ProvinceChina Department of Infectious Diseases Renmin Hospital of Wuhan UniversityWuhan 430060Hubei ProvinceChina

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.

关键词： Acute liver failure stress granules Hypoxia Endoplasmic reticulum stress Apoptosis

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The pathogenic mechanism of TAR DNA-binding protein 43(TDP-43)in amyotrophic lateral sclerosis

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Neural Regeneration Research 2024年第4期19卷 800-806页

作者： Xinxin Wang Yushu Hu Renshi Xu Medical College of Nanchang University Department of Neurology Jiangxi Provincial People's HospitalThe First Affiliated Hospital of Nanchang Medical CollegeThe Clinical College of Nanchang Medical College

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).

关键词： amyotrophic lateral sclerosis axonal transport liquid-liquid phase separation noncellular autonomous functions oxidative stress pathogenesis post-translational modification protein quality control system stress granules TAR DNA-binding protein 43(TDP-43)

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Paclitaxel-induced stress granules increase LINE-1 mRNA stability to promote drug resistance in breast cancer cells

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The Journal of Biomedical Research 2021年第6期35卷 411-424页

作者： Xiao Shi Xinxin Si Ershao Zhang Ruochen Zang Nan Yang He Cheng Zhihong Zhang Beijing Pan Yujie Sun Key Laboratory of Human Functional Genomics of Jiangsu Province Nanjing Medical UniversityNanjingJiangsu 211166China Department of Cell Biology School of Basic Medical SciencesNanjing Medical UniversityNanjingJiangsu 211166China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjingJiangsu 211166China Department of Pathology the First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu 210036China.

Abnormal expression of long interspersed element-1(LINE-1)has been implicated in drug resistance,while our previous study showed that chemotherapy drug paclitaxel(PTX)increased LINE-1 level with unknown mechanism.Bioinformatics analysis suggested the regulation of LINE-1 mRNA by drug-induced stress granules(SGs).This study aimed to explore whether and how SGs are involved in drug-induced LINE-1 increase and thereby promotes drug resistance of triple negative breast cancer(TNBC)cells.We demonstrated that SGs increased LINE-1 expression by recruiting and stabilizing LINE-1 mRNA under drug stress,thereby adapting TNBC cells to chemotherapy drugs.Moreover,LINE-1 inhibitor efavirenz(EFV)could inhibit drug-induced SG to destabilize LINE-1.Our study provides the first evidence of the regulation of LINE-1 by SGs that could be an important survival mechanism for cancer cells exposed to chemotherapy drugs.The findings provide a useful clue for developing new chemotherapeutic strategies against TNBCs.

关键词： LINE-1 stress granules RNA stability neoplasm drug resistance triple negative breast cancer

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Mechanism and effect of stress granule formation in cancer and its potential roles in breast cancer therapy

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Genes & Diseases 2022年第3期9卷 659-667页

作者： Taobo Hu Wei Hou Enhua Xiao Mengping Long Department of Breast Surgery Peking University People’s HospitalBeijing 100044PR China Department of Pathology Peking University Cancer HospitalBeijing 100142PR China Department of Radiology The Second Xiangya HospitalCentral South UniversityChangshaHunan 410011PR China

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.

关键词： Apoptosis Breast cancer Drug resistance stress granules Translation initiation

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A genome-wide RNAi screen identifies genes regulating the formation of P bodies in C. elegans and their functions in NMD and RNAi

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Protein & Cell 2011年第11期2卷 918-939页

作者： Yinyan Sun Peiguo Yang Yuxia Zhang Xin Bao Jun Li Wenru Hou Xiangyu Yao Jinghua Han Hong Zhang National Institute of Biological Sciences Beijing 102206China College of Life Sciences Beijing Normal UniversityBeijing 100875China

Cytoplasmic processing bodies,termed P bodies,are involved in diverse post-transcriptional processes including mRNA decay,nonsense-mediated RNA decay(NMD),RNAi,miRNA-mediated translational repression and storage of translationally silenced mRNAs.Regulation of the formation of P bodies in the context of multicellular organisms is poorly understood.Here we describe a systematic RNAi screen in C.elegans that identified 224 genes with diverse cellular functions whose inactivations result in a dramatic increase in the number of P bodies.83 of these genes form a complex functional interaction network regulating NMD.We demonstrate that NMD interfaces with many cellular processes including translation,ubiquitin-mediated protein degradation,intracellular trafficking and cytoskeleton structure.We also uncover an extensive link between translation and RNAi,with different steps in protein synthesis appearing to have distinct effects on RNAi efficiency.Moreover,the intracellular vesicular trafficking network plays an important role in the regulation of RNAi.A subset of genes enhancing P body formation also regulate the formation of stress granules in C.elegans.Our study offers insights into the cellular mechanisms that regulate the formation of P bodies and also provides a framework for system-level understanding of NMD and RNAi in the context of the development of multicellular organisms.

关键词： P body stress granules nonsensemediated RNA decay(NMD) RNA interference C.elegans

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The protective role of m A during stress-induced granulation

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Journal of Molecular Cell Biology 2020年第11期12卷 870-880页

作者： Marion Alriquet Giulia Calloni Adrian Martinez-Limon Riccardo Delli Ponti Gerd Hanspach Martin Hengesbach Gian G.Tartaglia R.Martin Vabulas Buchmann Institute for Molecular Life Sciences Goethe University Frankfurt60438 Frankfurt am MainGermany Institute of Biophysical Chemistry Goethe University Frankfurt60438 Frankfurt am MainGermany Centre for Genomic Regulation(CRG) The Barcelona Institute for Science and Technology08003 BarcelonaSpain Universitat Pompeu Fabra(UPF) 08003 BarcelonaSpain Institucio Catalana de Recerca i Estudis Avanqats(ICREA) 08010 BarcelonaSpain Institute for Organic Chemistry and Chemical Biology Goethe University Frankfurt60438 Frankfurt am MainGermany Department of Biology'Charles Darwin Sapienza University of Rome00185 RomeItaly Department of Neuroscience and Brain Technologies Istituto Italiano di Tecnologia16163 GenoaItaly Present address:Charite-Universitatsmedizin Berlin Institute of Biochemistry10117 BerlinGermany

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.***.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.

关键词： stress response stress granules N1-methyladenine

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