Tissue & cell最新文献

{"title":"Corrigendum to \"PDE4B abrogation extenuates angiotensin II-induced endothelial dysfunction related to hypertension through up-regulation of AMPK/Sirt1/Nrf2/ARE signaling\" [Tissue Cell 91 (2024) 102637].","authors":"Yong Chen, Suipeng Li, Xuqing Hou, Yinfeng Jia","doi":"10.1016/j.tice.2025.102738","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102738","url":null,"abstract":"","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":" ","pages":"102738"},"PeriodicalIF":2.7,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PCSK9 exacerbates sevoflurane-induced neuroinflammatory response and apoptosis by up-regulating cGAS-STING signal","authors":"Tao Su,&nbsp;Yuting Si","doi":"10.1016/j.tice.2025.102739","DOIUrl":"10.1016/j.tice.2025.102739","url":null,"abstract":"<div><h3>Background</h3><div>Postoperative cognitive dysfunction (POCD) is a postoperative complication that can be induced by anaesthesia. PCSK9 has been shown to have a role in neuronal development and apoptosis. However, PCSK9 has not been studied in sevoflurane-induced POCD-related disorders.</div></div><div><h3>Objective</h3><div>To explore whether PCSK9 can exacerbate sevoflurane-induced neuroinflammatory response and apoptosis by up-regulating cGAS-STING signalling.</div></div><div><h3>Methods</h3><div>A POCD model was constructed by stimulating BV2 microglia with Sevoflurane. CCK8 was used to detect the cell viability, and immunofluorescence was used to observe the expression of microglial activation markers (Iba-1, CD11b) and BDNF to determine the activation of BV2 microglia. Cell proliferation was measured by EDU staining, and apoptosis was analyzed by flow cytometry and western blot. The levels of inflammatory cytokines, ROS, MDA, SOD and CAT were respectively detected by ELISA, DCFH-DA staining, and kits to determine the neuroinflammation and oxidative stress of cells. Mitochondrial ROS, mitochondrial membrane potential, mtDNA and ATP levels were measured to evaluate cellular mitochondrial function.</div></div><div><h3>Results</h3><div>Transfection of si-PCSK9 inhibited Sevoflurane-induced microglial activation and restored cellular viability, promoted cell proliferation, inhibited apoptosis and neuroinflammation, decreased ROS and MDA levels in the cells while up-regulating the levels of SOD and CAT, thus inhibiting oxidative stress, restored the mitochondrial membrane potential to normal and decreased mitochondrial ROS and mtDNA levels and increased ATP production, thereby alleviating mitochondrial dysfunction. Moreover, PCSK9 depletion also down-regulated the expression of cGAS and STING to inactivate cGAS-STING signaling. However, cGAS overexpression partially reversed the effects of si-PCSK9.</div></div><div><h3>Conclusion</h3><div>PCSK9 exacerbates sevoflurane-induced neuroinflammatory response and apoptosis by upregulating cGAS-STING signaling.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102739"},"PeriodicalIF":2.7,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elderberry diet improves sperm quality and histological parameters of testicular tissue in adult male rats exposed to methamphetamine","authors":"Haleh Hemmatparast ,&nbsp;Zahra Shams Mofarahe ,&nbsp;Mohammad-Amin Abdollahifar ,&nbsp;Samira Ezi ,&nbsp;Ghazal Khanjari ,&nbsp;Nahal Babaeian Amini ,&nbsp;Zahra Niakan ,&nbsp;Pourya Raee ,&nbsp;Meysam Hassani Moghaddam ,&nbsp;Mobina Fathi ,&nbsp;Kimia Vakili ,&nbsp;Amirreza Beirami ,&nbsp;Maral Hasanzadeh ,&nbsp;Ramtin Hajibeygi ,&nbsp;Abbas Aliaghaei ,&nbsp;Mojtaba Sani ,&nbsp;Mohsen Norouzian","doi":"10.1016/j.tice.2025.102732","DOIUrl":"10.1016/j.tice.2025.102732","url":null,"abstract":"<div><div>Psychotropic stimulants like methamphetamine (METH) have an impact on the physiology, behavior, and psychology of human beings and can damage the reproductive and neuroendocrine systems in them. These deleterious impacts include a temporary drop in the relative weight of the testis along with adverse effects on spermatogenesis. Sambucus nigra, also known as elderberry (EB) or sweet elder, is a source of bioactive compounds that has drawn growing attention for its potential beneficial impact in preventing and treating several diseases. In this experimental research, 36 adult male rats were classified into three groups: (1) control, (2) METH, and (3) METH receiving the EB diet. The rats were injected with METH at a dose of 20 mg/kg for 28 days during treatment with the EB diet. Then, the rats were euthanized, and their sperm samples were collected for sperm parameters analysis. Afterward, the testis samples were taken for histopathological experimentations, immunohistochemistry against TNF-α and caspase-3, and serum testosterone levels. Our findings indicated largely improved sperm and stereological parameters, like spermatogonia, primary spermatocyte, round spermatid, and Leydig cells, and an increased serum testosterone level in the METH group receiving the EB diet compared to the other METH group. The results also revealed a significantly decreased TNF-α and caspase-3 expression in the METH+EB group compared to the METH group. In conclusion, the EB diet is regarded as an alternative treatment for improving the spermatogenesis process in reproductive toxicity induced by METH exposure.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102732"},"PeriodicalIF":2.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of TGF-β1, PI3K/PIP3/Akt, Nrf-2/Keap-1 and NF-κB signaling pathways to avert bifenthrin induced hepatic injury: A palliative role of daidzein","authors":"Mahmoud El Safadi ,&nbsp;Tawaf Ali Shah ,&nbsp;Syeda Sania Zahara ,&nbsp;Yousef A. Bin Jardan ,&nbsp;Mohammed Bourhia","doi":"10.1016/j.tice.2025.102733","DOIUrl":"10.1016/j.tice.2025.102733","url":null,"abstract":"<div><div>Bifenthrin (BFN) is a noxious insecticide which is reported to damage various body organs. Daidzein (DZN) is a natural flavone with excellent pharmacological properties. This research was conducted to evaluate the alleviative strength of DZN to counteract BFN prompted liver toxicity in male albino rats. Thirty-two rats were divided into 4 groups i.e., the control, BFN (7 mg /kg), BFN (7 mg/kg) + DZN (20 mg/kg) and DZN (20 mg/kg) alone group. The biochemical assessment was performed by using qRT PCR as well as standard ELISA protocols. The findings are validated by applying pharmacodynamic techniques including molecular simulation. It was observed that BFN reduced the gene expressions of phosphoinositide 3-kinase (<em>PI3K), phosphatidylinositol-3, 4, 5-triphosphate (PIP3), Protein kinase B (Akt), nuclear factor erythroid 2–related factor 2 (Nrf-2)</em> while promoting the gene expressions of Kelch-like ECH-associated protein 1 (Keap-1). Moreover, BFN notably reduced the activities of glutathione reductase (GSR), heme-oxygenase-1 (HO-1), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) while elevating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). BFN promoted the levels of matrix metallopeptidase 2 (MMP-2), Procollagen III N-terminal Pro-peptide (PIIINP), alkaline phosphatase (ALP), transforming growth factor-beta-1 (TGF-β1), aspartate aminotransferase (AST), tissue inhibitor of matrix metalloproteinases 1 (TIMP1), and alanine aminotransferase (ALT). The levels of nuclear factor- kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2) were increased following the BFN intoxication. BFN enhanced the expressions of cysteine-aspartic acid protease-3 (Caspase-3) and Bcl-2-associated X protein (Bax) while suppressing the gene expression of B-cell lymphoma-2 (Bcl-2). Moreover, BFN disrupted the normal histology of liver tissues. Nonetheless, DZN treatment remarkably alleviated hepatic damages owing to its antioxidative, anti-apoptotic as well as anti-inflammatory abilities. However, DZN supplementation remarkably safeguarded which is further confirmed by <em>in-silico</em> assessment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102733"},"PeriodicalIF":2.7,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gold nanoparticles “AuNPs” -mediated amelioration of experimentally toxic-induced cerebellar syndrome: Insights into cytomolecular and immuno-histochemical modifications, with a focus on CREB/ Tau modulation","authors":"Mai A. Samak ,&nbsp;Yara M. Elfakharany ,&nbsp;Nancy Huessiny ,&nbsp;Amira Ebrahim Alsemeh","doi":"10.1016/j.tice.2025.102725","DOIUrl":"10.1016/j.tice.2025.102725","url":null,"abstract":"<div><div>Toxic-induced cerebellar syndrome (TOICS) poses substantial neurological challenges, given its diverse causes and complex manifestations. Gold nanoparticles (AuNPs) have gained significant attention owing to enhanced biocompatibility for therapeutic interventions. We aimed to investigate the impacts of AuNPs on cerebellar cytomolecular, immunohistochemical and ultrastructural alterations in the context of phenytoin-experimentally induced TOICS. Thirty male albino rats were assigned randomly to three equal groups; control, phenytoin (PHT) and PHT+ AuNPs groups. Cerebellar sections were examined histopathologically, ultra-structurally and immunohistochemically for GFAP and p-Tau. Cerebellar tissues were evaluated for TNF-α, IL-1β, MDA, CAT, SOD and CREB mRNA. Our data confirmed observable amelioration of histopathological and ultrastructural cerebellar alterations of Purkinje and granule cells after AuNPs cotreatment. Histomorphometric measures revealed AuNPs-induced significant downregulation of p-Tau and GFAP immune-expression. Concurrently, TNF-α, IL-1β, MDA were significantly quenched in cerebellar tissues after AuNPs cotreatment, on contrary to notable restoration of CAT, SOD and CREB mRNA levels. These outcomes confirm that AuNPs hold promise as a therapeutic strategy for TOICS, warranting further exploration of their mechanisms and clinical applications in cerebellar disorders.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102725"},"PeriodicalIF":2.7,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anatomy, histology and ultrastructure of the adult human olfactory peduncle: Blood vessel and corpora amylacea assessment","authors":"J.F. Raspeño-García ,&nbsp;S. González-Granero ,&nbsp;V. Herranz-Pérez ,&nbsp;A. Cózar-Cuesta ,&nbsp;E. Artacho-Pérula ,&nbsp;R. Insausti ,&nbsp;J.M. García-Verdugo ,&nbsp;C. de la Rosa-Prieto","doi":"10.1016/j.tice.2025.102737","DOIUrl":"10.1016/j.tice.2025.102737","url":null,"abstract":"<div><div>The mammalian olfactory system is responsible for processing environmental chemical stimuli and comprises several structures, including the olfactory epithelium, olfactory bulb, olfactory peduncle (OP), and olfactory cortices. Despite the critical role played by the OP in the conduction of olfactory information, it has remained understudied. In this work, optical, confocal, and electron microscopy were employed to examine the anatomy, histology, and ultrastructure of six human OP specimens (ages 37–84 years). Three concentric layers were identified in coronal sections: the external layer (EL), the axonal layer (AL), and the internal layer (IL). Immunohistochemistry revealed the distribution of neurons and glial cells throughout the OP. Two neuronal morphologies were observed: granule cells and larger pyramidal cells, the latter associated with projection neurons of the anterior olfactory nucleus. Astrocytes were uniformly distributed with a more radial morphology in the EL. Oligodendrocytes were mainly located in the AL. Blood vessels (BVs) were evenly distributed along the OP, with a mean luminal area of 82.9 µm² and a density of 1.26 %, with a significant increase in the IL. <em>Corpora amylacea</em> (CA) were abundant, with an average size of 49.3 µm² and a density of 3.23 %. CA clustered near BVs, particularly at tissue edges, with both size and density increasing with age. Notably, CA showed strong associations with astrocytes. This study provides the first detailed qualitative and quantitative data on the internal organization of the human OP, which may contribute to a better understanding of the pathophysiology of some neuropathological disorders.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102737"},"PeriodicalIF":2.7,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leveraging the nanotopography of filamentous fungal chitin-glucan nano/microfibrous spheres (FNS) coated with collagen (type I) for scaffolded fibroblast spheroids in regenerative medicine","authors":"Kannan Badri Narayanan ,&nbsp;Rakesh Bhaskar ,&nbsp;Sung Soo Han","doi":"10.1016/j.tice.2025.102734","DOIUrl":"10.1016/j.tice.2025.102734","url":null,"abstract":"<div><div>Numerous naturally occurring biological structures have inspired the development of innovative biomaterials for a wide range of applications. Notably, the nanotopographical architectures found in natural materials have been leveraged in biomaterial design to enhance cell adhesion and proliferation and improve tissue regeneration for biomedical applications. In this study, we fabricated three-dimensional (3D) chitin-glucan micro/nanofibrous fungal-based spheres coated with collagen (type I) to mimic the native extracellular matrix (ECM) microenvironment. These collagen-coated fungal nano/microfibrous spheres (C-FNS) were utilized to construct 3D scaffolded spheroids of human fibroblasts through suspension culture for tissue engineering and regenerative medicine. The particle sizes of C-FNS ranged from 1.4 to 3.25 µm (average: 2.27 ± 0.38 µm), with a porosity of 81.17 %. Field emission-scanning electron microscopy (FE-SEM) revealed that C-FNS comprised continuous chitin-glucan fibers with an average diameter of 363 ± 61 nm (range: 203–512 nm), exhibiting a highly interconnected structure. The reduced arithmetic average roughness (Ra) and root mean square roughness (Rq) values of C-FNS compared to uncoated FNS suggested that collagen coating reduced surface roughness, resulting in a smoother surface that enhanced hydrophilicity, crucial for mammalian cell adhesion and spheroid formation. Moreover, the <em>in vitro</em> cytocompatibility of C-FNS with fibroblasts was evaluated using a resazurin-based PrestoBlue assay, which demonstrated a time-dependent increase in the metabolic activity of C-FNS/fibroblast spheroids during suspension culture for up to 14 days. FE-SEM images of C-FNS/fibroblast spheroids further revealed enhanced adhesion and proliferation of fibroblasts on the nano/microfibrous mycelial architecture, accompanied by the secretion of ECM components and formation of multilayered cell sheets over the 14-day culture period. Similarly, an assessment of the hemocompatibility of C-FNS with erythrocytes revealed the non-hemolytic properties of the biomaterial. Overall, the interaction between collagen-coated fungal chitin-glucan nano/microfibrous structures and mammalian cells holds significant potential for the development of novel, sustainable biomaterials with tailored properties for a myriad of biomedical applications, including tissue engineering, regenerative medicine, drug screening, and wound healing.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102734"},"PeriodicalIF":2.7,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights into reductive stress responses and its clinical relation in cancer","authors":"Suman Kumar Ray ,&nbsp;Sukhes Mukherjee","doi":"10.1016/j.tice.2025.102736","DOIUrl":"10.1016/j.tice.2025.102736","url":null,"abstract":"<div><div>Cells are susceptible to both oxidative and reductive stresses, with reductive stress being less studied and potentially therapeutic in cancer. Reductive stress, characterized by an excess of reducing equivalents exceeding the activity of endogenous oxidoreductases, can lead to an imbalance in homeostasis, causing an increase in reactive oxygen species induction, affecting cellular antioxidant load and flux. Unlike oxidative stress, reductive stress has been understudied and poorly understood, and there is still much to learn about its mechanisms in cancer, its therapeutic potential, and how cancer cells react to it. Changes in redox balance and interference with redox signaling are linked to cancer cell growth, metastasis, and resistance to chemotherapy and radiation. Overconsumption of reducing equivalents can reduce metabolism, alter protein disulfide bond formation, disrupt mitochondrial homeostasis, and disrupt cancer cell signaling pathways. Novel approaches to delivering or using cancer medicines and techniques to influence redox biology have been discovered. Under reductive stress, cancer cells may coordinate separate pools of redox pairs, potentially impacting biology.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102736"},"PeriodicalIF":2.7,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragalus polysaccharide mediates lnc-GD2H to regulate proliferation and differentiation of C2C12 muscle cells under hypoxic condition","authors":"Wannian Liang ,&nbsp;Yang Li ,&nbsp;Si Lei ,&nbsp;Rui Chen ,&nbsp;Huacai Shi ,&nbsp;Feimeng Li ,&nbsp;Zhiyuan Liao ,&nbsp;Chao Zhong ,&nbsp;Yanling She","doi":"10.1016/j.tice.2025.102731","DOIUrl":"10.1016/j.tice.2025.102731","url":null,"abstract":"<div><div><em>Astragalus</em> polysaccharide (APS) is a bioactive component of <em>Astragalus</em> species that shows protective effects on C2C12 muscle cell proliferation and differentiation under hypoxic conditions. In this study, EdU staining, cell scratch testing, quantitative reverse-transcription polymerase chain reaction, Western blotting, immunofluorescence analysis, and lnc-GD2H silencing were used to investigated the protective effects and mechanisms of action of APS against CoCl₂-induced hypoxic injury of muscle cells. Our results showed that APS promoted cell proliferation and increased the expression of lnc-GD2H, c-Myc, and Ki-67. In addition, APS protected against the effect of CoCl₂ on differentiation and increased the levels of Myog and MyHC expression. Silencing lnc-GD2H attenuated the protective effects of APS outlined above. Considering that APS may mediate the regulation of proliferation and differentiation by lnc-GD2H in C2C12 cells, and alleviates hypoxic injury induced by CoCl₂.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102731"},"PeriodicalIF":2.7,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of mTOR/HK2 signaling mitigates effects of PYCR2 depletion in colorectal cells","authors":"Li Chen ,&nbsp;Yuan Yuan ,&nbsp;Nian Zhang,&nbsp;Qianqian Huang,&nbsp;Yu Zhou","doi":"10.1016/j.tice.2025.102729","DOIUrl":"10.1016/j.tice.2025.102729","url":null,"abstract":"<div><h3>Background</h3><div>Colorectal cancer (CRC) is one of the aggressive malignant tumors. Studies have shown that glycolysis promotes the proliferation of colorectal cancer cells and that PYCR2 is involved in cancer progression by affecting cellular glycolysis. In addition, PYCR2 is upregulated in colorectal cancer cell lines and can affect cellular autophagy.</div></div><div><h3>Methods</h3><div>Si-PYCR2 was used to interfere with PYCR2 in colorectal cancer cells, and the cells were treated with the addition of autophagy inhibitor 3-MA or mTOR agonist MHY1485. The expression of LC3B was detected by immunofluorescence, and the expression of autophagy and glycolytic proteins was detected by Western blot. XF96 extracellular flux analyzer was used to detect the ECAR and OCR of the cells, and biochemical kits were used to detect the levels of glucose consumption, lactate secretion, and ATP production in the cells.</div></div><div><h3>Results</h3><div>PYCR2 expression was up-regulated in colorectal cancer cell lines. si-PYCR2 interference enhanced the fluorescence intensity of LC3B in the cells, inhibited the expression of p62 proteins but enhanced the expression of ATG5, ATG7, and LC3-II/I proteins, which indicated an enhanced level of autophagy in colorectal cancer cells. In addition, PYCR2 depletion also inhibited cellular glycolysis as well as mTOR/HK2 signaling. However, the addition of 3-MA resulted in an increase in cellular ECAR while a decrease in OCR, and an increase in the levels of glucose consumption, lactate and ATP production, as well as the expressions of glycolytic proteins (GLUT1, PGK1, ENO1, PKM2), which suggested the glycolysis of cells was enhanced. In addition, MHY1485 treatment not only inhibited autophagy but also enhanced glycolysis in colorectal cancer cells.</div></div><div><h3>Conclusion</h3><div>Interference with PYCR2 corrected autophagy-dependent glycolysis levels in colorectal cancer cells via mTOR/HK2 signaling. Activation of mTOR/HK2 signaling mitigated the effects of PYCR2 depletion in colorectal cells.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102729"},"PeriodicalIF":2.7,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}