Archives of biochemistry and biophysics最新文献

{"title":"TNF promotes osteoclastogenesis by secreting miR-31-5p into small extracellular vesicles via the autotaxin–LPA–LPAR1 axis in arthritic fibroblast-like synoviocytes","authors":"Thanh Nam Phan ,&nbsp;Minju Gal ,&nbsp;Okhwa Kim ,&nbsp;Hoang Long Le ,&nbsp;Cheol Hwangbo ,&nbsp;Jeong-Hyung Lee","doi":"10.1016/j.abb.2025.110631","DOIUrl":"10.1016/j.abb.2025.110631","url":null,"abstract":"<div><div>Fibroblast-like synoviocytes (FLSs) play a crucial role in the pathogenesis of arthritis. However, the impact of small extracellular vesicles (sEVs) secreted by FLSs on osteoclastogenesis remains incompletely understood. In this study, we aimed to investigate the role of tumor necrosis factor (TNF)- and lysophosphatidic acid (LPA)-activated FLSs in sEV-mediated release of osteoclastogenic miRNAs and elucidate their functional contribution to osteoclastogenesis. Stimulation of SW982 cells with LPA or TNF significantly increased sEV secretion. TNF upregulated autotaxin expression and promoted sEV release; however, small interfering RNA (siRNA)-mediated knockdown (KD) of <em>LPAR1</em> attenuated the increase in sEV release induced by the TNF–autotaxin–LPA axis. Notably, stimulation with TNF or LPA elevated syntenin-1 expression without altering its mRNA level. Furthermore, KD of the syntenin-1 gene (<em>SDCBP</em>) suppressed the LPA-induced increase in sEV release, indicating that syntenin-1 may mediate sEV secretion induced by the TNF–autotaxin–LPA–LPAR1 axis. sEVs derived from TNF- or LPA-treated SW982 cells stimulated osteoclastogenesis. We identified <em>miR-31-5p</em> as an osteoclastogenic miRNA enriched in sEVs. Expression levels of <em>miR-31-5p</em> in sEVs from TNF- and LPA-stimulated rheumatoid arthritis (RA) FLSs were significantly higher than in those from unstimulated RA FLSs. Treatment with a <em>miR-31-5p</em> mimic enhanced osteoclastogenesis by targeting large tumor suppressor kinase 2 (<em>LATS2</em>), whereas treatment with its inhibitor suppressed the sEV-mediated promotion of osteoclastogenesis. These findings reveal a mechanism by which TNF- and LPA-activated FLSs may facilitate sEV-mediated delivery of osteoclastogenic miRNAs, such as <em>miR-31-5p</em>, to osteoclast precursors, thereby contributing to osteoclast formation and bone destruction.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110631"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145217861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal FGG promotes colorectal cancer liver metastases through inducing angiogenic pre-metastatic niche formation","authors":"Lingling Yang ,&nbsp;Lifang Chen ,&nbsp;Xin Chen ,&nbsp;Haiqiang Huang ,&nbsp;Hui Zhu ,&nbsp;Liangtao Zeng ,&nbsp;Jun Huang ,&nbsp;Hao Ding","doi":"10.1016/j.abb.2025.110625","DOIUrl":"10.1016/j.abb.2025.110625","url":null,"abstract":"<div><div>Angiogenesis is a defining feature of a pre-metastatic niche and is essential for primary colorectal cancer (CRC) tumor metastasis. Epithelial-mesenchymal transition (EMT) also serves as a critical driver of CRC tumor metastatic progression. Here, we hypothesized that exosomes from CRC cells promoted liver metastasis by remodeling tumor microenvironment. To verify this hypothesis, exosomes from CRC cells were isolated and identified, and the effects of these exosomes on human umbilical vein endothelial cells (HUVECs) were investigated. Exosomes from CRC cells promoted vascularization, permeability and migration of HUVECs. Mechanistically, exosomes derived from CRC cells delivered Fibrinogen gamma (FGG) to exert their effects on HUVECs. Furthermore, FGG downregulated the levels of VE-cadherin and E-cadherin in CRC cells, while upregulating N-cadherin and vimentin levels, thereby enhancing endothelial permeability and promoting EMT. <em>In vivo</em> experiments demonstrated that FGG downregulated VE-cadherin in CRC tissues and upregulated CD31 in liver tissues, ultimately leading to an increased number of metastatic liver nodules in a mouse model of CRC liver metastasis. In conclusion, FGG facilitates CRC liver metastasis by regulating key angiogenic, adhesion and mesenchymal markers via exosome-mediated mechanisms, resulting enhanced angiogenesis, vascular permeability, and EMT induction. These findings offer new insights into the mechanisms and treatment strategies of CRC liver metastasis.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110625"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPP1-mediated crosstalk between macrophage and fibroblasts promotes benign airway stenosis","authors":"Fu Niu ,&nbsp;Bo Sun ,&nbsp;Ying Yu ,&nbsp;Xiaolan Xu ,&nbsp;Haitao Li ,&nbsp;Lining Huang ,&nbsp;Yan Wang ,&nbsp;Zhigang Cai","doi":"10.1016/j.abb.2025.110627","DOIUrl":"10.1016/j.abb.2025.110627","url":null,"abstract":"<div><h3>Objective</h3><div>The aim of this study is to elucidate the role of M2 macrophages in the pathogenesis of benign airway stenosis using a Sprague Dawley (SD) rat model and in vitro macrophage–fibroblast co-culture systems.</div></div><div><h3>Methods</h3><div>Ligand–receptor interactions mediating cellular crosstalk between macrophages and fibroblasts were identified through single-cell RNA sequencing-based bioinformatics analysis. An airway stenosis model was established in SD rats, which were assigned to five experimental groups: normal control and post-modeling days 1 (D1), 4 (D4), 7 (D7), and 14 (D14). Temporal changes in M2 macrophage infiltration and their involvement in airway remodeling were assessed. Fibroblasts isolated from human granulation tissue and normal airway tissue were evaluated for differential activation of intracellular signaling pathways. In vitro macrophage–fibroblast co-culture systems involving M2 macrophages and fibroblasts were conducted to assess molecular signaling interactions.</div></div><div><h3>Results</h3><div>A progressive increase in M2 macrophage infiltration was observed during the development of airway stenosis, accompanied by upregulation of secreted phosphoprotein-1 (SPP1) and activation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway. Fibroblasts derived from granulation tissue exhibited higher levels of pathway activation compared to normal fibroblasts.In co-culture, M2 macrophages induced fibroblast activation and fibrogenesis via SPP1-mediated signaling. Administration of rapamycin, an mTOR pathway inhibitor, significantly reduced granulation tissue formation and improved airway patency in the rat model.</div></div><div><h3>Conclusion</h3><div>M2 macrophages contribute to fibrotic airway remodeling in benign airway stenosis through SPP1-mediated activation of the PI3K/AKT/mTOR signaling pathway in fibroblasts. Pharmacological targeting of this axis with rapamycin may represent a potential therapeutic strategy for mitigating fibrosis in benign airway stenosis.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110627"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen sulfide (H2S) alleviates diabetic myocardial fibrosis by suppressing pyroptosis via inhibiting DNMT3a-mediated Sestrin2 CpG promoter hypermethylation","authors":"Yi Liu ,&nbsp;Ting Yang ,&nbsp;Hongming Hu ,&nbsp;Qi Yang ,&nbsp;Jun Yang ,&nbsp;Chun Chu","doi":"10.1016/j.abb.2025.110605","DOIUrl":"10.1016/j.abb.2025.110605","url":null,"abstract":"<div><h3>Background</h3><div>Diabetic cardiomyopathy (DCM) represents an important concern associated with diabetes, inhibiting pyroptosis has shown promising results in alleviating DCM symptoms. The objective of this work is to investigate the role and underlying mechanism of hydrogen sulfide (H₂S) in the suppression of pyroptosis in the context of diabetic myocardial fibrosis (MF).</div></div><div><h3>Methods</h3><div>The effect of H₂S on pyroptosis was detected using CCK-8, ELISA, and flow cytometry. The expression of Sestrin2 and its DNA methylation modification, as well as the quantification of pyroptosis-related proteins and the activation of the TLR4/MyD88/NF-κB signaling pathway, were measured using Western blot, ChIP, Immunofluorescence, and methylation-specific quantitative PCR. To establish a type 2 diabetes rat model, a high-fat diet was administered, followed by injection of streptozotocin (HFD/STZ). After five weeks, the rats received H₂S treatment for four weeks, either with or without sh-Sestrin2. The effects of H₂S treatment on myocardial function, tissue structure, and myocardial cell apoptosis were assessed. Furthermore, the CCK-8 assay was used to detect the cell viability induced by TGF-β. Cellular oxidative stress levels were measured by the ELISA method. Western blotting was applied to determine the protein expression levels of Collagen I, Fibronectin, α-SMA, NLRP3, caspase-1, GSDMD-N, and Sestrin2.</div></div><div><h3>Results</h3><div>H₂S ameliorates HG-induced fibrosis, injury, pyroptosis, and inflammatory response of cardiac fibroblasts (CFs). H₂S inhibits Sestrin2 methylation and up-regulates its expression through DNMT3a. H₂S ameliorates HG-induced CFs pyroptosis and fibrosis through Sestrin2. Sestrin2 regulates HG-induced CFs pyroptosis and fibrosis through the TLR4/MyD88/NF-κB pathway. The myocardial tissue injury was improved after H₂S treatment, and the results of the H₂S treatment were reversed after knockdown of Sestrin2. In addition, TGF-β1 can induce an increase in the activity of cardiac fibroblasts and enhance cellular oxidative stress. Meanwhile, it significantly upregulates the expression of Collagen I, Fibronectin, α-SMA, as well as NLRP3, caspase-1, and GSDMD-N, and remarkably downregulates the expression of Sestrin2. However, H₂S intervention can reverse the aforementioned phenomena.</div></div><div><h3>Conclusion</h3><div>H₂S can suppress pyroptosis and ameliorate diabetic MF by inhibiting DNMT3a-mediated DNA methylation of Sestrin2 promoter through the TLR4/MyD88/NF-κB pathway.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110605"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA CTB-31O20.2 promotes the progression of hepatocellular carcinoma by targeting the miR-139-5p/ROCK1 axis","authors":"Dizhong Ye ,&nbsp;Biyan Chen ,&nbsp;Xiangfa Wang,&nbsp;Weiwei Chen,&nbsp;Feng Ye,&nbsp;Guangqian Quan","doi":"10.1016/j.abb.2025.110619","DOIUrl":"10.1016/j.abb.2025.110619","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a primary cause of mortality from cancer, necessitating novel insights into its molecular underpinnings. Recent evidence points to the significant roles of lncRNAs in HCC progression, among which CTB-31O20.2 has emerged as a potentially crucial player. This study utilized RNA sequencing to identify differentially expressed lncRNAs in HCC tissues, focusing on CTB-31O20.2. We employed RT-qPCR, Western blotting, and dual-luciferase reporter assays to evaluate the expression patterns of CTB-31O20.2 in HCC cells and its interactions with miR-139-5p and Rho-associated coiled-coil containing protein kinase1 (ROCK1). In vivo effects were analyzed using a xenograft mouse model. CTB-31O20.2 was significantly upregulated in HCC tissues and cell lines. Silencing CTB-31O20.2 in Hep3B and HepG2 cells reduced malignancy, evidenced by decreased viability, colony formation, and invasion, and increased apoptosis. These cellular behaviors were associated with alterations in apoptosis-related proteins and epithelial-mesenchymal transition (EMT) markers. CTB-31O20.2 was shown to interact with miR-139-5p, and its silencing upregulated miR-139-5p, leading to reduced ROCK1 expression. Conversely, miR-139-5p inhibition reversed the anti-tumor effects of CTB-31O20.2 silencing. Overexpression of ROCK1 negated the inhibitory effects on HCC cell malignancy induced by CTB-31O20.2 depletion. In vivo, CTB-31O20.2 silencing significantly reduced tumor growth in a xenograft model. Our findings reveal that CTB-31O20.2 contributes to HCC progression by modulating miR-139-5p and ROCK1 expression. These results highlight CTB-31O20.2 as a potential therapeutic target in HCC, providing a new perspective on the mechanisms driving HCC pathogenesis and progression.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110619"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Benzene induces myelodysplasia and hematotoxicity via ferroptosis induction and downregulation of GPX4” [Arch. Biochem. Biophys. 773 (2025) 110606]","authors":"Renjun Bao ,&nbsp;Ti Zhang ,&nbsp;Yuhua Fu ,&nbsp;Hongyun Song ,&nbsp;Mian Wang ,&nbsp;Huijing Hu ,&nbsp;Yonghua Yao","doi":"10.1016/j.abb.2025.110621","DOIUrl":"10.1016/j.abb.2025.110621","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110621"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel tRNA-Derived Fragment, tRF-23-Z87HFK8SDZ inhibits malignant progression of pancreatic cancer through mediating IRS1","authors":"Liping Zheng ,&nbsp;Jing Wang ,&nbsp;Yiyu Shen ,&nbsp;Chundong Hu ,&nbsp;Bin Wu ,&nbsp;Zhongcheng Zhou ,&nbsp;Wei Wang","doi":"10.1016/j.abb.2025.110624","DOIUrl":"10.1016/j.abb.2025.110624","url":null,"abstract":"<div><h3>Background</h3><div>Transfer RNA-derived fragments (tRFs) have emerged as significant actors in cancer progression. Nevertheless, their functions in pancreatic cancer stay poorly understood. This work focuses on the role of tRF-23-Z87HFK8SDZ (tRF-23), a downregulated fragment in pancreatic cancer, and its potential tumor-suppressive functions through the regulation of IRS1.</div></div><div><h3>Methods</h3><div>RNA sequencing was performed on cancerous and adjacent non-cancerous tissues from pancreatic cancer patients to identify differentially expressed tRFs. RT-qPCR, Kaplan-Meier survival analysis, and various <em>in vivo</em> and <em>in vitro</em> functional assays were performed to assess tRF-23 expression, its effects on cellular processes, and its regulation of IRS1. Dual-luciferase and RNA immunoprecipitation assays proved the interaction between tRF-23 and IRS1.</div></div><div><h3>Results</h3><div>tRF-23 was considerably downregulated in pancreatic cancer tissues and cells. Lower tRF-23 expression was correlated with poor patient survival. Overexpression of tRF-23 inhibited cell viability, proliferation, and migration, while advancing cell cycle arrest and apoptosis in pancreatic cancer cells. <em>In vivo,</em> tRF-23 reduced tumor growth in a subcutaneous mouse model. tRF-23 directly targeted IRS1, downregulating its protein and mRNA levels, and IRS1 overexpression partially rescued these effects.</div></div><div><h3>Conclusion</h3><div>tRF-23 suppresses the malignant progression of pancreatic cancer by downregulating IRS1. These findings suggest that the tRF-23/IRS1 axis could act as a prospective therapeutic target in pancreatic cancer.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110624"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial redox imbalance and CoQ10 deficiency in Rett syndrome: Insights from patient-derived fibroblasts","authors":"Francesco Mengarelli ,&nbsp;Valeria Cordone ,&nbsp;Alessandra Pecorelli ,&nbsp;Mascia Benedusi ,&nbsp;Giuseppe Valacchi ,&nbsp;Camilla Morresi ,&nbsp;Tiziana Bacchetti ,&nbsp;Patrick Orlando ,&nbsp;Luca Tiano ,&nbsp;Sonia Silvestri","doi":"10.1016/j.abb.2025.110636","DOIUrl":"10.1016/j.abb.2025.110636","url":null,"abstract":"<div><div>Rett syndrome (RTT), a neurodevelopmental disorder primarily affecting females, is characterized by mutations in the <em>MECP2</em> gene, leading to systemic oxidative stress and mitochondrial dysfunction. This study investigates the role of Coenzyme Q₁₀ (CoQ₁₀), particularly its reduced form ubiquinol, in modulating oxidative stress and mitochondrial function in primary dermal fibroblasts derived from RTT patients with distinct MeCP2 mutations.</div><div>Baseline assessments revealed significant CoQ₁₀ deficiencies and elevated reactive oxygen species (ROS) levels, notably in fibroblasts with the T158M mutation. Ubiquinol supplementation effectively restored CoQ₁₀ levels and improved redox balance in these cells. Additionally, treatment influenced mitochondrial dynamics, as evidenced by alterations in the expression of fission and fusion proteins and modulated the activity of paraoxonase 2 (PON2), an enzyme involved in cellular antioxidant defense.</div><div>In conclusion, our data suggest that CoQ₁₀ supplementation could mitigate oxidative damage and preserve mitochondrial integrity, but we are far from being able to claim that it can represents an effective therapeutic strategy to complement current pharmacological treatments in RTT patients. Further research is warranted to explore the potential of CoQ₁₀ as an adjunctive treatment, particularly during the early stages of RTT.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110636"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lauryl gallate induces apoptosis via p38-MAPK phosphorylation and autophagy in chemoresistant human lung cancer cells","authors":"Yen-Hsiang Huang ,&nbsp;Shur-Hueih Cherng ,&nbsp;Ling-Yen Chiu ,&nbsp;Kuo-Hsuan Hsu ,&nbsp;Jeng-Sen Tseng ,&nbsp;Po-Hsin Lee ,&nbsp;Gwo-Tarng Sheu ,&nbsp;Tsung-Ying Yang","doi":"10.1016/j.abb.2025.110633","DOIUrl":"10.1016/j.abb.2025.110633","url":null,"abstract":"<div><div>Human lung cancer has taken many lives and chemoresistance generally occurs in patients and reduces patients’ survival. Docetaxel (DOC) and vincristine (VCR) have been widely used in cancer chemotherapy but their efficacy is restricted by <em>P</em>-glycoprotein (<em>P</em>-gp) overexpression. Lauryl gallate (LG) is a plant-derived small molecule which acts as antioxidant in normal cells. Surprisingly, LG also has been shown to control several types of cancer cells and induce apoptosis by way of induction of reactive oxygen species (ROS). To further clarify the anti-lung cancer activity of LG, we evaluated the cytotoxicity of LG using a previously established human A549/DOC resistant subline that has high <em>P</em>-gp expression and a A549/VCR resistant subline to determine their LG sensitivity by MTT assay. The apoptosis and autophagy levels were examined by protein analysis and flow cytometry. Interference of p38-MAPK and ATG5 expression by siRNAs was performed to measure the involvement of these two proteins in apoptosis and autophagy. We found that LG exerts higher cytotoxicity to the target cells when compared with tannic acid (TA) and octyl gallate (OG). Furthermore, LG not only induces apoptosis, it also enhances autophagy in both chemoresistant A549 sublines. When p38-MAPK was knocked down, the apoptosis level was reduced but autophagy was not. Knockdown of ATG5 resulted in significant apoptosis reduction in VCR-resistant A549 cells but less effect was found in DOC-resistant A549 cells. In sum, our data suggested that LG promotes p38-MAPK phosphorylation and induces apoptosis in chemoresistant A549 cells independently with <em>P</em>-gp expression. LG also enhances autophagy-regulated cell death in chemoresistant lung cancer cells.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110633"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “WNK1 phosphorylation sites in TBC1D1 and TBC1D4 modulate cell surface expression of GLUT1” [Arch. Biochem. Biophys. 679 (2020) 108223]","authors":"Andreia F.A. Henriques ,&nbsp;Paulo Matos ,&nbsp;Ana Sofia Carvalho ,&nbsp;Mikel Azkargorta ,&nbsp;Felix Elortza ,&nbsp;Rune Matthiesen ,&nbsp;Peter Jordan","doi":"10.1016/j.abb.2025.110614","DOIUrl":"10.1016/j.abb.2025.110614","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110614"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}