Cell Communication and Signaling最新文献

{"title":"Adenosine A_2A receptor-mediated interactions between Th1⁺ T cells and the choroid plexus epithelium via IFN-γ signalling control T-Cell infiltration in experimental autoimmune encephalomyelitis.","authors":"Chenxing Qi, Yuwen Yang, Ping Tang, Cheng Zheng, Xuhang Li, Nan Jiang, Jia Qu, Jiang-Fan Chen, Wu Zheng","doi":"10.1186/s12964-025-02100-7","DOIUrl":"10.1186/s12964-025-02100-7","url":null,"abstract":"<p><strong>Background: </strong>Adenosine A_2A receptor (A_2AR) antagonists have been consistently demonstrated to protect against multiple sclerosis (MS) pathology, but A_2AR knockout (A_2AR^-/-) mice exhibit exacerbated immune injury, raising concerns regarding the use of A_2AR antagonists for MS treatment. Here, we revealed the critical involvement of A_2AR-mediated interactions between Th1⁺ T cells and the choroid plexus (ChP) epithelium in the pathology of experimental autoimmune encephalomyelitis (EAE).</p><p><strong>Methods: </strong>We assessed the effects of A_2AR knockout on ChP gateway activity and the interferon gamma (IFN-γ)-secreting capacity of Th1⁺ T cells in an EAE model by immunofluorescence, qPCR and flow cytometry (FCM). We also investigated the effects of A_2AR-mediated interactions between Th1⁺ T cells and the ChP epithelium on ChP gateway activity in vivo via intracerebroventricular (ICV) injection of Th1⁺ T cells and in vitro via coculture of ChP epithelial cells and splenic Th1⁺ T cells. We further knocked down IFN-γ receptor 1 (IFNGR1) specifically in the ChP of A_2AR^-/- mice via ICV injection of AAV2/5-shRNA (IFNGR1) to disrupt the interactions between Th1⁺ T cells and the ChP epithelium and thus assess the roles of these interactions in the development of EAE pathology.</p><p><strong>Results: </strong>A_2AR knockout disrupted the ChP barrier and increased T-cell infiltration across the ChP in EAE model mice. Coculture of splenic Th1⁺ T cells and ChP epithelial cells revealed that A_2AR knockout in ChP epithelial cells strengthened the ChP barrier and attenuated T-cell migration, whereas A_2AR knockout in Th1⁺ T cells increased the accumulation of Th1⁺ T cells in the ChP via the secretion of IFN-γ. Consistent with the coculture results, ICV injection of activated splenic Th1⁺ T cells from A_2AR^-/- mice increased the accumulation of T cells in the ChP to a greater extent than did injection of Th1⁺ T cells from A_2AR^+/+ mice. This effect was due to the increased secretion of IFN-γ in A_2AR^-/- mice compared with A_2AR^+/+ mice. Finally, ChP-specific knockdown of IFNGR1 attenuated A_2AR knockout-induced T-cell infiltration, brain inflammation and EAE pathology.</p><p><strong>Conclusion: </strong>A_2AR-mediated interactions between Th1⁺ T cells and the ChP epithelium via the secretion of IFN-γ from CD4⁺ T cells and the binding IFN-γ to IFNGR1 in the ChP epithelium control immune cell invasion and the development of EAE pathology in A_2AR^-/- mice.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"94"},"PeriodicalIF":8.2,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IgA displays site- and subclass-specific glycoform differences despite equal glycoenzyme expression.","authors":"David Falck, Maria V Sokolova, Carolien A M Koeleman, Vanessa Irumva, Philipp Kirchner, Sebastian R Schulz, Katja G Schmidt, Thomas Harrer, Arif B Ekici, Bernd Spriewald, Georg Schett, Manfred Wuhrer, Martin Herrmann, Ulrike Steffen","doi":"10.1186/s12964-025-02088-0","DOIUrl":"10.1186/s12964-025-02088-0","url":null,"abstract":"<p><strong>Background: </strong>Glycosylation is an important posttranslational modification of proteins and in most cases indispensable for proper protein function. Like most soluble proteins, IgA, the second most prevalent antibody in human serum, contains several N- and O-glycosylation sites. While for IgG the impact of Fc glycosylation on effector functions and inflammatory potential has been studied intensively, only little is known for IgA. In addition, only glimpses exist regarding the regulation of IgA glycosylation. We have previously shown that IgA1 and IgA2 differ functionally and also show differences in their glycosylation pattern. The more pro-inflammatory IgA2 which is linked to autoimmune diseases displays decreased sialylation, galactosylation, fucosylation and bisection as compared to IgA1. In the present study, we aimed to investigate these differences in glycosylation in detail and to explore the mechanisms underlying them.</p><p><strong>Methods: </strong>IgA1 and IgA2 was isolated from serum of 12 healthy donors. Site specific glycosylation was analyzed by mass spectrometry. In addition, human bone marrow plasma cells were investigated using single cell mRNA sequencing, flow cytometry and ELISpot.</p><p><strong>Results: </strong>We found that certain glycoforms greatly differ in their abundance between IgA1 and IgA2 while others are equally abundant. Overall, the IgA2 glycans displayed a more immature phenotype with a higher prevalence of oligomannose and fewer fully processed glycans. Of note, these differences can't be explained by differences in the glycosylation enzyme machinery as mRNA sequencing and flow cytometry analysis showed equal enzyme expression in IgA1 and IgA2 producing plasma cells. ELISpot analysis suggested a slightly increased antibody production rate in IgA2 producing plasma cells which might contribute to its lower glycan processing rates. But this difference was only minor, suggesting that further factors such as steric accessibility determine glycan processing. This is supported by the fact that glycans at different positions on the same IgA chain differ dramatically in fucosylation, sialylation and bisection.</p><p><strong>Conclusion: </strong>In summary, our detailed overview of IgA1 and IgA2 glycosylation shows a class, subclass, and site-specific glycosylation fingerprint, most likely due to structural differences of the protein backbones.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"92"},"PeriodicalIF":8.2,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglial depletion decreases Müller cell maturation and inner retinal vascular density.","authors":"Nathaniel Rowthorn-Apel, Naveen Vridhachalam, Kip M Connor, Gracia M Bonilla, Ruslan Sadreyev, Charandeep Singh, Gopalan Gnanaguru","doi":"10.1186/s12964-025-02083-5","DOIUrl":"10.1186/s12964-025-02083-5","url":null,"abstract":"<p><strong>Background: </strong>The neuroretinal vascular system is comprised of three interconnected layers. The initial superficial vascular plexus formation is guided by astrocytes around birth in mice. The formation of the deep and intermediate vascular plexuses occurs in the second postnatal week and is driven by Müller-cell-derived angiogenic signaling. Previously, we reported that microglia play an important role in regulating astrocyte density during superficial vascular plexus formation. Here, we investigated the role of microglia in regulating Müller-cell-dependent inner retinal vascular development.</p><p><strong>Methodology: </strong>In this study, we depleted microglia during retinal development using Csf1R antagonist (PLX5622). We characterized the developmental progression of inner retinal vascular growth, effect of microglial depletion on inner retinal vascular growth and Müller cell marker expressions by immunostaining. Differential expressions of genes in the control and microglia depleted groups were analyzed by mRNA-seq and qPCR. Unpaired t-test was performed to determine the statistical differences between groups.</p><p><strong>Results: </strong>This study show that microglia interact with Müller cells and the growing inner retinal vasculature. Depletion of microglia resulted in reduced inner retinal vascular layers densities and decreased Vegfa isoforms transcript levels. RNA-seq analysis further revealed that microglial depletion significantly reduced specific Müller cell maturation markers including glutamine synthetase, responsible for glutamine biosynthesis, necessary for angiogenesis.</p><p><strong>Conclusions: </strong>Our study reveals an important role for microglia in facilitating inner retinal angiogenesis and Müller cell maturation.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"90"},"PeriodicalIF":8.2,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11831819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting membrane contact sites to mediate lipid dynamics: innovative cancer therapies.","authors":"Jie Wang, Meifeng Wang, Xueni Zeng, Yanhan Li, Lingzhi Lei, Changan Chen, Xi Lin, Peiyuan Fang, Yuxuan Guo, Xianjie Jiang, Yian Wang, Lihong Chen, Jun Long","doi":"10.1186/s12964-025-02089-z","DOIUrl":"10.1186/s12964-025-02089-z","url":null,"abstract":"<p><p>Membrane contact sites (MCS) are specialized regions where organelles are closely interconnected through membrane structures, facilitating the transfer and exchange of ions, lipids, and other molecules. This proximity enables a synergistic regulation of cellular homeostasis and functions. The formation and maintenance of these contact sites are governed by specific proteins that bring organelle membranes into close apposition, thereby enabling functional crosstalk between cellular compartments. In eukaryotic cells, lipids are primarily synthesized and metabolized within distinct organelles and must be transported through MCS to ensure proper cellular function. Consequently, MCS act as pivotal platforms for lipid synthesis and trafficking, particularly in cancer cells and immune cells within the tumor microenvironment, where dynamic alterations are critical for maintaining lipid homeostasis. This article provides a comprehensive analysis of how these cells exploit membrane contact sites to modulate lipid synthesis, metabolism, and transport, with a specific focus on how MCS-mediated lipid dynamics influence tumor progression. We also examine the differences in MCS and associated molecules across various cancer types, exploring novel therapeutic strategies targeting MCS-related lipid metabolism for the development of anticancer drugs, while also addressing the challenges involved.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"89"},"PeriodicalIF":8.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11830217/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel 5'tRNA-derived fragment tRF-Tyr inhibits tumor progression by targeting hnRNPD in gastric cancer.","authors":"Huaiping Cui, Zhaodong Liu, Lipan Peng, Lijun Liu, Xiaozhou Xie, Yudi Zhang, Zi Gao, Chi Zhang, Xinshuai Yu, Yonghao Hu, Jin Liu, Liang Shang, Leping Li","doi":"10.1186/s12964-025-02086-2","DOIUrl":"10.1186/s12964-025-02086-2","url":null,"abstract":"<p><strong>Background: </strong>Transfer RNA-derived small RNAs (tsRNAs), including tRNA-derived fragments (tRFs) and tRNA halves (tiRNAs), constitute a novel class of small noncoding RNAs (sncRNAs). tsRNAs have been linked to tumorigenesis and the progression of carcinogenesis; however, the precise molecular mechanism through which tRFs act in gastric cancer (GC) remains unknown.</p><p><strong>Methods: </strong>tRF-Tyr is a potential GC tumor suppressor that was identified through high-throughput sequencing technology. The expression and subcellular localization of tRF-Tyr in GC were detected by via qRT‒PCR and FISH. RNA pull-down, mass spectrometry, RNA immunoprecipitation (RIP), dual-luciferase reporter and rescue assays were performed to explore the regulatory mechanisms through which tRF-Tyr acts in GC.</p><p><strong>Results: </strong>tRF-Tyr was significantly downregulated and the downregulation of its mainly concentrated in the nuclei of GC cells. Functionally, tRF-Tyr inhibited the proliferation, invasiveness and migration of GC cells and promoted GC cells apoptosis in vitro; meanwhile, tRF-Tyr inhibited tumor growth in vivo. Mechanistically, tRF-Tyr bound directly to the hnRNPD protein and competitively inhibited the binding of hnRNPD to the c-Myc 3'UTR, thereby, regulating the c-Myc/Bcl2/Bax pathway and ultimately inhibiting the progression of GC.</p><p><strong>Conclusions: </strong>This study focused on a novel GC suppressor, tRF-Tyr, and revealed a previously undiscovered mechanism that tRF-Tyr inhibits tumor progression by targeting hnRNPD. These findings provide new insight into the involvement of tRFs in GC and suggest a novel target for GC treatment.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"88"},"PeriodicalIF":8.2,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of neutrophil in sepsis: recent insights and advances.","authors":"Ji Zhang, Yuwen Shao, Jingyi Wu, Jing Zhang, Xiangsheng Xiong, Jingjing Mao, Yunwei Wei, Changhong Miao, Hao Zhang","doi":"10.1186/s12964-025-02098-y","DOIUrl":"10.1186/s12964-025-02098-y","url":null,"abstract":"<p><p>Sepsis remains the leading cause of death in intensive care units. Despite newer antimicrobial and supportive therapies, specific treatments are still lacking. Neutrophils are pivotal components of the effector phase of the host immune defense against pathogens and play a crucial role in the control of infections under normal circumstances. In addition to its anti-infective effects, the dysregulation and overactivation of neutrophils may lead to severe inflammation or tissue damage and are potential mechanisms for poor prognosis in sepsis. This review focuses on recent advancements in the understanding of the functional status of neutrophils across various pathological stages of sepsis to explore the mechanisms by which neutrophils participate in sepsis progression and provide insights for the treatment of sepsis by targeting neutrophils.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"87"},"PeriodicalIF":8.2,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNFAIP2 promotes NF-κB signaling mediate lymph node metastasis of oral squamous cell carcinoma by protecting IKKβ from ubiquitin proteasome degradation.","authors":"Teng Xu, Yaning Wang, Zechen Zhao, Jinsong Wang, Zhenyuan Zhao, Yuemei Yang, Xiaomeng Song, Qingguo Lai","doi":"10.1186/s12964-025-02077-3","DOIUrl":"10.1186/s12964-025-02077-3","url":null,"abstract":"<p><strong>Background: </strong>Tumor dissemination is a life-threatening event which confers to most cancer-related deaths with limited effective therapeutic option. TNFα-induced protein 2 (TNFAIP2) reveals pro-metastasis potential in several cancers. However, its definite role and underlying mechanism in oral squamous cell carcinoma (OSCC) is largely unknown.</p><p><strong>Methods: </strong>The impact of TNFAIP2 on tumor metastasis was assessed based on the conditional knockout mouse with 4-nitroquinoline-1-oxide (4NQO) induced OSCC model through feature and immunohistochemistry analysis. To explore the specific mechanism, enrichment analysis and co-immunoprecipitation were applied. Meanwhile, the nano-hydroxyapatite (nHAp) and poly-L-lysine (PLL) based RNA interference delivery system was designed to restrict tumor dissemination.</p><p><strong>Results: </strong>The conditional knockout Tnfaip2 in epithelium reduced tumor initiation rate, differentiation degree and cervical lymph node metastasis (LNM) in mouse exposed to 4NQO. Enrichment analysis suggested nuclear factor-kappa B (NF-κB) signaling was associated with these effects. Western blot proved that TNFAIP2 prevented the ubiquitin proteasome degradation of inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta (IKKβ), a classical transcriptional activator protein in NF-κB signaling. Mechanistically, TNFAIP2 was demonstrated to competitively interact with kelch-like ECH-associated protein 1 (KEAP1) to avoid IKKβ from ubiquitination at K63 and proteasomal degradation subsequently, which finally sustained NF-κB signaling and facilitated tumor metastasis by enhancing epithelial-mesenchymal transition (EMT) and lymphangiogenesis. Notably, the synthetic small interfering RNA delivery systems nHAp@PLL-siTnfaip2 showed significant effect in attenuating tumor progression of OSCC mouse.</p><p><strong>Conclusion: </strong>Above results showed TNFAIP2 promoted EMT and lymphangiogenesis of OSCC by regulating NF-κB signaling, a mechanism that was dependent on the interaction with KEAP1 competitively. The nHAp based TNFAIP2 interference might serve as a novel therapeutic in limiting OSCC metastasis.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"83"},"PeriodicalIF":8.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biogenesis of stress granules and their role in the regulation of stress-induced male reproduction disorders.","authors":"Jiaxin Li, Linyuan Shen, Kai Wang, Shuang Wu, Yan Wang, Yuheng Pan, Siyu Chen, Ting Zhao, Ye Zhao, Lili Niu, Lei Chen, Shunhua Zhang, Li Zhu, Mailin Gan","doi":"10.1186/s12964-025-02054-w","DOIUrl":"10.1186/s12964-025-02054-w","url":null,"abstract":"<p><p>Stress granules (SGs) are conserved messenger ribonucleoprotein (mRNP) granules that form through rapid coalescence in the cytoplasm of eukaryotic cells under stressful environments. These dynamic membrane-free organelles can respond to a variety of both intracellular and extracellular stressors. Studies have shown that stress conditions such as heat stress, arsenite exposure, and hypoxic stress can induce SGs formation. The formation of SGs helps mitigates the effects of environmental stimuli on cells, protects them from damage, and promotes cell survival. This paper focuses on the biogenesis of SGs and summarizes the role in regulating environmental stress-induced male reproductive disorders, with the aim of exploring SGs as a potential means of mitigating male reproduction disorders. Numerous studies have demonstrated that the detrimental effects of environmental stress on germ cells can be effectively suppressed by regulating the formation and timely disassembly of SGs. Therefore, regulating the phosphorylation of eIF2α and the assembly and disassembly of SGs could offer a promising therapeutic strategy to alleviate the impacts of environmental stress on male reproduction health.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"84"},"PeriodicalIF":8.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF1α controls steroidogenesis under acute hypoxic stress.","authors":"Stephen Ariyeloye, Deepika Watts, Mangesh T Jaykar, Cagdas Ermis, Anja Krüger, Denise Kaden, Barbara K Stepien, Vasileia Ismini Alexaki, Mirko Peitzsch, Nicole Bechmann, Peter Mirtschink, Ali El-Armouche, Ben Wielockx","doi":"10.1186/s12964-025-02080-8","DOIUrl":"10.1186/s12964-025-02080-8","url":null,"abstract":"<p><strong>Background: </strong>Hypoxia is a critical physiological and pathological condition known to influence various cellular processes, including steroidogenesis. While previous studies, including our own, have highlighted the regulatory effects of Hypoxia-Inducible Factor 1α (HIF1α) on steroid production, the specific molecular mechanisms remain poorly understood. This study investigates the role of hypoxia and HIF1α in steroid biosynthesis across multiple experimental models during acute exposure to low oxygen levels.</p><p><strong>Methods: </strong>To assess the extent to which acute hypoxia modulates steroidogenesis, we employed several approaches, including the Y1 adrenocortical cell line, and a conditional HIF1α-deficient mouse line in the adrenal cortex. We focused on various regulatory patterns that may critically suppress steroidogenesis.</p><p><strong>Results: </strong>In Y1 cells, hypoxia upregulated specific microRNAs in a HIF1α-dependent manner, resulting in the suppression of mRNA levels of critical steroidogenic enzymes and a subsequent reduction in steroid hormone production. The hypoxia/HIF1α-dependent induction of these microRNAs and the consequent modulation of steroid production were confirmed in vivo. Notably, using our adrenocortical-specific HIF1α-deficient mouse line, we demonstrated that the increase in miRNA expression in vivo is also directly HIF1α-dependent, while the regulation of steroidogenic enzymes (e.g., StAR and Cyp11a1) and steroid production occurs at the level of protein translation, revealing an unexpected layer of control under hypoxic/HIF1 α conditions in vivo.</p><p><strong>Conclusions: </strong>These findings elucidate the molecular mechanisms underlying acute hypoxia/HIF1α-induced changes in steroid biosynthesis and may also be useful in developing new strategies for various steroid hormone pathologies.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"86"},"PeriodicalIF":8.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes play a crucial role in remodeling the tumor microenvironment and in the treatment of gastric cancer.","authors":"Lingyun Tang, Wenjie Zhang, Teng Qi, Zhengting Jiang, Dong Tang","doi":"10.1186/s12964-024-02009-7","DOIUrl":"10.1186/s12964-024-02009-7","url":null,"abstract":"<p><p>Gastric cancer (GC) is a common and frequent malignant cancer of the digestive system with a poor prognosis. In addition to common therapies such as surgical resection and chemotherapy, novel biological interventions are quite valuable for research. Exosomes are extracellular vesicles (EVs) that originate from various cell types and contain proteins, RNA, DNA, and other components that transmit biological signals and mediate intercellular communication. Numerous studies have shown that exosomes shape the tumor microenvironment (TME) by affecting hypoxia, inflammation, immunity, metabolism, and interstitial changes in the tumor, playing a crucial role in the development and metastasis of GC. This article reviews the important role of exosomes in the TME of GC and explores their potential clinical applications in GC treatment.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"82"},"PeriodicalIF":8.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}