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Article ; Online: Selective autophagy of the immunoproteasomes suppresses innate inflammation.

Zhou, Jiao / Li, Huihui / Lu, Kefeng

2024 , Page(s) 1–2

Abstract: Immunoproteasomes are involved in various inflammatory diseases. Upon stimulation, standard constitutive proteasomes are partially replaced by newly formed immunoproteasomes that promote inflammatory responses. How the upregulated immunoproteasomes are ... ...

Abstract	Immunoproteasomes are involved in various inflammatory diseases. Upon stimulation, standard constitutive proteasomes are partially replaced by newly formed immunoproteasomes that promote inflammatory responses. How the upregulated immunoproteasomes are cleared to constrain hyper-inflammation is unknown. Recently, our studies showed that the pan-FGFR inhibitor LY2874455 efficiently activates macroautophagy/autophagy in macrophages, leading to the degradation of the immunoproteasomes. Immunoproteasome subunits are ubiquitinated and recognized by the selective autophagy receptor SQSTM1/p62. LY2874455 suppresses inflammation induced by lipopolysaccharide both
Language	English
Publishing date	2024-05-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2024.2353437
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Article: Proteomics and Autophagy Research.

Lu, Kefeng / Li, Huihui

Advances in experimental medicine and biology

2021 Volume 1208, Page(s) 373–386

Abstract: Autophagy is an evolutionarily conserved intracellular degradation process. Autophagy is closely involved in human health and diseases. In recent years, mass spectrometry-based proteomic methods have become important and powerful tools for autophagy ... ...

Abstract	Autophagy is an evolutionarily conserved intracellular degradation process. Autophagy is closely involved in human health and diseases. In recent years, mass spectrometry-based proteomic methods have become important and powerful tools for autophagy studies. These types of techniques have been especially helpful to reveal the range of degradation substrates of autophagy through large-scale, unbiased analysis of cellular proteomes. At present, a variety of mass spectrometry-based proteomics methods have been successfully applied to autophagy research.
MeSH term(s)	Autophagy ; Humans ; Mass Spectrometry ; Proteome/genetics ; Proteomics
Chemical Substances	Proteome
Language	English
Publishing date	2021-07-14
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-981-16-2830-6_17
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Article: Screening for Genes Involved in Autophagy.

Lu, Kefeng / Li, Huihui

Advances in experimental medicine and biology

2021 Volume 1208, Page(s) 357–371

Abstract: Autophagy is an important intracellular lysosomal degradation process in cells, which is highly conserved from yeast to mammals. The process of autophagy is roughly divided into the following key steps: the formation of a membrane structure called ISM ( ... ...

Abstract	Autophagy is an important intracellular lysosomal degradation process in cells, which is highly conserved from yeast to mammals. The process of autophagy is roughly divided into the following key steps: the formation of a membrane structure called ISM (isolated membrane) after stimulation, the biogenesis and maturation of autophagosomes, and finally the degradation of autophagosomes. A number of proteins are required to function in the whole process of autophagy. Since the initial genetic screening in yeast cells, multiple genes that play pivotal roles in autophagy have been discovered. These molecules have been named ATG genes (AuTophaGy related genes). The screening for new key molecules involved in autophagy has greatly promoted the characterization of the mechanism of the autophagy machinery and provides multiple targets for the development of autophagy-based regulatory drugs.
MeSH term(s)	Animals ; Autophagosomes ; Autophagy/genetics ; Autophagy-Related Proteins/genetics ; Lysosomes ; Saccharomyces cerevisiae
Chemical Substances	Autophagy-Related Proteins
Language	English
Publishing date	2021-07-14
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-981-16-2830-6_16
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Article ; Online: Pharmacological induction of autophagy reduces inflammation in macrophages by degrading immunoproteasome subunits.

Zhou, Jiao / Li, Chunxia / Lu, Meng / Jiang, Gaoyue / Chen, Shanze / Li, Huihui / Lu, Kefeng

PLoS biology

2024 Volume 22, Issue 3, Page(s) e3002537

Abstract: Defective autophagy is linked to proinflammatory diseases. However, the mechanisms by which autophagy limits inflammation remain elusive. Here, we found that the pan-FGFR inhibitor LY2874455 efficiently activated autophagy and suppressed expression of ... ...

Abstract	Defective autophagy is linked to proinflammatory diseases. However, the mechanisms by which autophagy limits inflammation remain elusive. Here, we found that the pan-FGFR inhibitor LY2874455 efficiently activated autophagy and suppressed expression of proinflammatory factors in macrophages stimulated by lipopolysaccharide (LPS). Multiplex proteomic profiling identified the immunoproteasome, which is a specific isoform of the 20s constitutive proteasome, as a substrate that is degraded by selective autophagy. SQSTM1/p62 was found to be a selective autophagy-related receptor that mediated this degradation. Autophagy deficiency or p62 knockdown blocked the effects of LY2874455, leading to the accumulation of immunoproteasomes and increases in inflammatory reactions. Expression of proinflammatory factors in autophagy-deficient macrophages could be reversed by immunoproteasome inhibitors, confirming the pivotal role of immunoproteasome turnover in the autophagy-mediated suppression on the expression of proinflammatory factors. In mice, LY2874455 protected against LPS-induced acute lung injury and dextran sulfate sodium (DSS)-induced colitis and caused low levels of proinflammatory cytokines and immunoproteasomes. These findings suggested that selective autophagy of the immunoproteasome was a key regulator of signaling via the innate immune system.
MeSH term(s)	Animals ; Mice ; Lipopolysaccharides/pharmacology ; Proteomics ; Autophagy ; Inflammation ; Macrophages ; Proteasome Endopeptidase Complex
Chemical Substances	Lipopolysaccharides ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002537
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Article ; Online: PAK inhibitor FRAX486 decreases the metastatic potential of triple-negative breast cancer cells by blocking autophagy.

Lyu, Liang / Li, Haiyan / Lu, Kefeng / Jiang, Shu / Li, Huihui

British journal of cancer

2023 Volume 130, Issue 3, Page(s) 394–405

Abstract: Background: Triple-negative breast cancer (TNBC) is a unique breast cancer subtype with a high risk of metastasis and recurrence and a poor prognosis. Epithelial-mesenchymal transition (EMT) endows epithelial cells with the ability to move to distant ... ...

Abstract	Background: Triple-negative breast cancer (TNBC) is a unique breast cancer subtype with a high risk of metastasis and recurrence and a poor prognosis. Epithelial-mesenchymal transition (EMT) endows epithelial cells with the ability to move to distant sites, which is essential for the metastasis of TNBC to organs, including the lung. Autophagy, an intracellular degradation process that involves formation of double-layered lipid autophagosomes that transport cytosolic cargoes into lysosomes via autophagosome-lysosome fusion, is involved in various diseases, including cancer and neurodegenerative, metabolic, cardiovascular, and infectious diseases. The relationship between autophagy and cancer has become relatively clear. However, research on pharmacological drugs that block cancer EMT by targeting autophagy is still in the initial stages. Therefore, the re-evaluation of old drugs for their potential in blocking both autophagy and EMT was conducted. Methods: More than 2000 small molecule chemicals were screened for dual autophagy/EMT inhibitors, and FRAX486 was identified as the best candidate inhibitor of autophagy/EMT. The functions of FRAX486 in TNBC metastasis were detected by CCK-8, migration and wound healing assays. The effects of FRAX486 on autophagy and its target PAK2 were determined by immunoblotting, immunofluorescence, immunoprecipitation analysis and transmission electron microscopy. The findings were validated in mouse models. Results: Here, we report that FRAX486, a potent P21-activated kinase 2 (PAK2) inhibitor, facilitates TNBC suppression both in vitro and in vivo by blocking autophagy. Mechanistically, FRAX486 inhibits autophagy in TNBC cells by targeting PAK2, leading to the ubiquitination and proteasomal degradation of STX17, which mediates autophagosome-lysosome fusion. The inhibition of autophagy by FRAX486 causes upregulation of the epithelial marker protein E-cadherin and thus suppresses the migration and metastasis of TNBC cells. Conclusions: The effects of FRAX486 on TNBC metastasis suppression were verified to be dependent on PAK2 and autophagy inhibition. Together, our results provide a molecular basis for the application of FRAX486 as a potential treatment for inhibiting the metastasis of TNBC.
MeSH term(s)	Mice ; Humans ; Animals ; Triple Negative Breast Neoplasms/pathology ; Cell Line, Tumor ; Pyrimidines/pharmacology ; Cell Movement ; Autophagy ; Epithelial-Mesenchymal Transition ; Cell Proliferation ; Pyridones
Chemical Substances	6-(2,4-dichlorophenyl)-8-ethyl-2-(3-fluoro-4-(piperazin-1-yl)phenylamino)pyrido(2,3-d)pyrimidin-7(8H)-one ; Pyrimidines ; Pyridones
Language	English
Publishing date	2023-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-023-02523-4
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Article ; Online: Oligomerization of Selective Autophagy Receptors for the Targeting and Degradation of Protein Aggregates.

Chen, Wenjun / Shen, Tianyun / Wang, Lijun / Lu, Kefeng

Cells

2021 Volume 10, Issue 8

Abstract: The selective targeting and disposal of solid protein aggregates are essential for cells to maintain protein homoeostasis. Autophagy receptors including p62, NBR1, Cue5/TOLLIP (CUET), and Tax1-binding protein 1 (TAX1BP1) proteins function in selective ... ...

Abstract	The selective targeting and disposal of solid protein aggregates are essential for cells to maintain protein homoeostasis. Autophagy receptors including p62, NBR1, Cue5/TOLLIP (CUET), and Tax1-binding protein 1 (TAX1BP1) proteins function in selective autophagy by targeting ubiquitinated aggregates through ubiquitin-binding domains. Here, we summarize previous beliefs and recent findings on selective receptors in aggregate autophagy. Since there are many reviews on selective autophagy receptors, we focus on their oligomerization, which enables receptors to function as pathway determinants and promotes phase separation.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy ; Autophagy-Related Proteins/metabolism ; Humans ; Proteasome Endopeptidase Complex/metabolism ; Protein Aggregates ; Protein Multimerization ; Proteolysis ; Proteostasis ; Signal Transduction ; Structure-Activity Relationship ; Ubiquitination
Chemical Substances	Autophagy-Related Proteins ; Protein Aggregates ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2021-08-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10081989
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Article ; Online: Cleavage of the selective autophagy receptor SQSTM1/p62 by the SARS-CoV-2 main protease NSP5 prevents the autophagic degradation of viral membrane proteins.

Zhang, Yabin / Liu, Shiyan / Xu, Qingjia / Li, Huihui / Lu, Kefeng

Molecular biomedicine

2022 Volume 3, Issue 1, Page(s) 17

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the coronavirus disease 2019 (COVID-19) global pandemic. Omicron, a new variant of SARS-CoV-2, has the characteristics of strong transmission and pathogenicity, short incubation ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the coronavirus disease 2019 (COVID-19) global pandemic. Omicron, a new variant of SARS-CoV-2, has the characteristics of strong transmission and pathogenicity, short incubation period, and rapid onset progression, and has spread rapidly around the world. The high replication rate and intracellular accumulation of SARS-CoV-2 are remarkable, but the underlying molecular mechanisms remain unclear. Autophagy acts as a conservative cellular defence mechanism against invading pathogens. Here, we provide evidence that the main protease of SARS-CoV-2, NSP5, effectively cleaves the selective autophagy receptor p62. NSP5 targets p62 for cleavage at glutamic acid 354 and thus abolishes the capacity of p62 to mediate selective autophagy. It was further shown that p62 specifically interacted with ubiquitinated SARS-CoV-2 M, the viral membrane protein, to promote its autophagic degradation. In the presence of NSP5, p62-mediated autophagic degradation of the M protein was inhibited. The cleaved products of p62 also cannot facilitate the degradation of the M protein. Collectively, our findings reveal that p62 is a novel host target of SARS-CoV-2 NSP5 and suggest that selective autophagy targets viruses and potential strategies by which the virus evades autophagic clearance. Our results may provide new ideas for the development of anti-COVID-19 drugs based on autophagy and NSP5.
Language	English
Publishing date	2022-06-03
Publishing country	Singapore
Document type	Journal Article
ISSN	2662-8651
ISSN (online)	2662-8651
DOI	10.1186/s43556-022-00083-2
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Article ; Online: Risk factors for the development of severe breast cancer-related lymphedema: a retrospective cohort study.

Liu, Xiaozhen / Sun, Kewang / Yang, Hongjian / Xia, Lingli / Lu, Kefeng / Meng, Xuli / Li, Yongfeng

BMC cancer

2023 Volume 23, Issue 1, Page(s) 361

Abstract: Background: Severe lymphedema presents a challenge in terms of treatment due to the significant formation of scar tissue that accompanies it. The aim of this study was to identify intraoperative and preoperative risk factors of severe lymphedema and to ... ...

Abstract	Background: Severe lymphedema presents a challenge in terms of treatment due to the significant formation of scar tissue that accompanies it. The aim of this study was to identify intraoperative and preoperative risk factors of severe lymphedema and to develop a nomogram for estimating the risk of severe lymphedema within 3 years of surgery. Method: Data was collected from a retrospective cohort of 326 patients with BCRL at the Zhejiang Cancer Hospital from November 2015 to November 2018. Univariate and multivariate logistic regression analysis was conducted to identify predictive indicators of severe lymphedema. A nomogram was developed to further improve the clinical applicability. Results: In the retrospective cohort, the ratio of severe/non-severe lymphedema within 3 years of surgery was 1:3. Independent risk factors for severe lymphedema were determined to be age, positive lymph nodes, interpectoral (Rotter's) lymph nodes (IPNs) dissection, and educational level. IPNs dissection was found to contribute greatly to the development of severe lymphedema with a higher odds ratio (7.76; 95% CI: 3.87-15.54) than other risk factors. A nomogram was developed by integrating age, positive lymph nodes, IPNs dissection, and educational level, which yielded a C-index of 0.810 and 0.681 in the training and validation cohort, respectively. This suggested a moderate performance of the nomogram in predicting the risk of severe lymphedema within 3 years of surgery. The cut-off values of the low-, medium- and high-risk probabilities were 0.0876 and 0.3498, and the severe lymphedema exhibited a significantly higher risk probability as compared with the non-severe lymphedema. Conclusion: This study identified the risk factors of severe lymphedema and highlighted the substantial contribution of IPNs dissection to the severity of lymphedema.
MeSH term(s)	Humans ; Female ; Retrospective Studies ; Lymph Node Excision/adverse effects ; Breast Neoplasms/complications ; Breast Neoplasms/surgery ; Risk Factors ; Breast Cancer Lymphedema/epidemiology ; Breast Cancer Lymphedema/etiology ; Lymphedema/epidemiology ; Lymphedema/etiology ; Lymph Nodes ; Axilla
Language	English
Publishing date	2023-04-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-023-10814-5
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Article: Molecular subtype identification and prognosis stratification based on lysosome-related genes in breast cancer.

Liu, Xiaozhen / Sun, Kewang / Yang, Hongjian / Zou, Dehomg / Xia, Lingli / Lu, Kefeng / Meng, Xuli / Li, Yongfeng

Heliyon

2024 Volume 10, Issue 4, Page(s) e25643

Abstract: Background: Lysosomes are known to have a significant impact on the development and recurrence of breast cancer. However, the association between lysosome-related genes (LRGs) and breast cancer remains unclear. This study aims to explore the potential ... ...

Abstract	Background: Lysosomes are known to have a significant impact on the development and recurrence of breast cancer. However, the association between lysosome-related genes (LRGs) and breast cancer remains unclear. This study aims to explore the potential role of LRGs in predicting the prognosis and treatment response of breast cancer. Methods: Breast cancer gene expression profile data and clinical information were downloaded from TCGA and GEO databases, and prognosis-related LRGs were screened for consensus clustering analysis. Lasso Cox regression analysis was used to construct risk features derived from LRGs, and immune cell infiltration, immune therapy response, drug sensitivity, and clinical pathological feature differences were evaluated for different molecular subtypes and risk groups. A nomogram based on risk features derived from LRGs was constructed and evaluated. Results: Our study identified 176 differentially expressed LRGs that are associated with breast cancer prognosis. Based on these genes, we divided breast cancer into two molecular subtypes with significant prognostic differences. We also found significant differences in immune cell infiltration between these subtypes. Furthermore, we constructed a prognostic risk model consisting of 7 LRGs, which effectively divides breast cancer patients into high-risk and low-risk groups. Patients in the low-risk group have better prognostic characteristics, respond better to immunotherapy, and have lower sensitivity to chemotherapy drugs, indicating that the low-risk group is more likely to benefit from immunotherapy and chemotherapy. Additionally, the risk score based on LRGs is significantly correlated with immune cell infiltration, including CD8 T cells and macrophages. This risk score model, along with age, chemotherapy, clinical stage, and N stage, is an independent prognostic factor for breast cancer. Finally, the nomogram composed of these factors has excellent performance in predicting overall survival of breast cancer. Conclusions: In conclusion, this study has constructed a novel LRG-derived breast cancer risk feature, which performs well in prognostic prediction when combined with clinical pathological features.
Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2024.e25643
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Article ; Online: The progress in

Jiang, Lan / Zhang, Tizhong / Lu, Kefeng / Qi, Shiqian

Small GTPases

2021 Volume 13, Issue 1, Page(s) 56–76

Abstract: The hexanucleotide repeat (GGGGCC) expansion ... ...

Abstract	The hexanucleotide repeat (GGGGCC) expansion in
MeSH term(s)	Humans ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Frontotemporal Dementia/pathology ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; C9orf72 Protein/genetics ; C9orf72 Protein/metabolism ; Autophagy/genetics ; GTPase-Activating Proteins
Chemical Substances	C9orf72 Protein ; GTPase-Activating Proteins ; C9orf72 protein, human
Language	English
Publishing date	2021-03-05
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2682247-7
ISSN	2154-1256 ; 2154-1248
ISSN (online)	2154-1256
ISSN	2154-1248
DOI	10.1080/21541248.2021.1892443
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