In Vitro Cellular & Developmental Biology. Animal最新文献

{"title":"Wogonin improves high glucose-induced ARPE-19 cell damage by inhibiting ferroptosis via suppressing the cGAS-STING pathway.","authors":"Hongjuan Wang, Song Wan, Xueping Zhu","doi":"10.1007/s11626-025-01115-1","DOIUrl":"https://doi.org/10.1007/s11626-025-01115-1","url":null,"abstract":"<p><p>To investigate the protective effect of wogonin against high glucose (HG)-induced ARPE-19 cell injury and to elucidate its mechanism of action. The effects of Wogonin on cell proliferation and apoptosis were systematically evaluated by a high glucose-induced ARPE-19 cell injury model using different doses of Wogonin for intervention. Meanwhile, intracellular reactive oxygen species (ROS) levels, iron ion accumulation and glutathione (GSH) depletion were detected, and the expression changes of apoptosis-related proteins, ferroptosis -related proteins, and cGAS-STING pathway proteins were analyzed. In addition, the cGAS agonist SR-717 was co-administered on the basis of Wogonin intervention to further investigate whether SR-717 could reverse the effects of Wogonin on cells. Wogonin significantly increased cell viability and reduced apoptosis in response to HG. Wogonin also alleviated oxidative stress by decreasing intracellular ROS and iron accumulation while inhibiting glutathione depletion. In addition, wogonin inhibited HG-induced ARPE-19 cell injury by inhibiting the cGAS‒STING signaling pathway and promoting the expression of the cellular GPX4 and SLC7A11 proteins. Wogonin inhibits ferroptosis by suppressing the cGAS-STING signaling pathway and has a protective effect against HG-induced ARPE-19 cell injury, suggesting that it may be used as a therapeutic agent to alleviate DR.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206332","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":"Retraction Note: CD142 promotes trophoblast cell migration by inhibiting BCL2-related autophagic degradation of IL-8.","authors":"Linmei Zheng, Rong Tang, Lei Shi, Zhongyi Zhou, Jie Song, Zhicheng Lu","doi":"10.1007/s11626-025-01125-z","DOIUrl":"https://doi.org/10.1007/s11626-025-01125-z","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206414","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":"A co-culture system to study the effects of Poly I:C-activated microglia on the differentiation of murine primary neural stem cells.","authors":"Marie Pierre Manitz, Karina Violou, Malin Hedstück, Kimberly Bösing, Maria Kottmann, Nadja Freund, Georg Juckel","doi":"10.1007/s11626-025-01091-6","DOIUrl":"https://doi.org/10.1007/s11626-025-01091-6","url":null,"abstract":"<p><p>Studies in rodents have shown that systemic inflammation induced by prenatal exposure to the viral mimetic polyinosinic:polycytidylic acid (Poly I:C) triggers maternal immune activation. Cytokines released by the maternal immune system can cross the placenta and enter fetal circulation. In the fetal brain, embryonic microglia may produce additional cytokines and other inflammatory mediators in response to maternally derived cytokines. This resulting cytokine imbalance is suggested to impair neurogenesis and brain development, potentially contributing to the onset of neuropsychiatric disorders in offspring. To investigate microglial involvement in neurogenesis under pathological conditions, we used the spontaneously immortalized microglial cell line (SIM-A9), and confirmed the expression of Iba1 and CD68 via immunocytochemistry. Additionally, SIM-A9 cells expressed CX3CR1, Ki67, and isolectin. Upon Poly I:C stimulation, SIM-A9 cells released the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), as well as nitric oxide (NO), as determined by ELISA and Griess assay, respectively. After confirming SIM-A9 cell activation by Poly I:C, we co-cultured these cells with neural stem/progenitor cells (NSPCs) from embryonic mouse neocortex using a transwell system. We examined how chronically activated microglia influence NSPC differentiation and characterized the resulting cell phenotypes using immunocytochemistry. Our results demonstrate that SIM-A9 cells support NSPC differentiation into neurons as early as three days in culture. However, the number of neurons decreased with prolonged culture. Furthermore, Poly I:C in the NSPC culture media, as well as cytokines secreted by Poly I:C-activated SIM-A9 cells, showed a supportive effect on astrocyte differentiation.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199254","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":"lncRNA PVT1 regulates chondrocyte proliferation and apoptosis through the glycolysis process mediated by miR-552-3p/PKM2 to promote osteoarthritis.","authors":"Demiao Zeng, Bin Li, Longhua Zhang, Guodong Zhang, Xiangjia Yan, Mengshi Huang, Jun Jiang, Zenggao Han","doi":"10.1007/s11626-025-01090-7","DOIUrl":"https://doi.org/10.1007/s11626-025-01090-7","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a common degenerative joint disease, and cartilage dysfunction is the main cause of OA. Long non-coding RNAs (lncRNAs) have been reported to be involved in the development of OA, but the mechanism of action of lncRNA PVT1 (PVT1) in the progression of OA is still poorly understood. The purpose of this study was to explore the effect of lncRNA PVT1 on the progression of OA and the specific molecular mechanism. A rat OA model was constructed by surgery for medial meniscus instability of the right knee joint, and HC-a cells were treated with 10 μg/mL lipopolysaccharide (LPS) for 24 h to establish the OA cell model. The expression of related genes and proteins was detected by RT-qPCR and Western blot, and the damage of HC-a cells and articular cartilage tissue was evaluated by CCK-8, ELISA, flow cytometry, and HE staining. In this study, PVT1 was found to be upregulated in human or rat OA cartilage tissue, as well as in LPS-induced HC-a cells. Knockdown of PVT1 can alleviate the effect of LPS; promote the proliferation of HC-a cells; inhibit glycolysis, apoptosis, and the secretion of inflammatory cytokines TNF-α, IL-1β, and IL-6; alleviate HC-a cell damage; and alleviate the development process of OA in vivo. Mechanistically, PVT1 upregulates the expression of PKM2 by inhibiting the expression of miR-552-3p, thereby promoting the glycolysis process and cell damage, and ultimately accelerating the occurrence and development of OA. Our study suggests that inhibition of PVT1 expression may be a new target for the treatment of OA.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191715","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":"Overexpression of long non‑coding RNA H19 enhances cell viability and inhibits apoptosis in recurrent spontaneous abortion by targeting the miR-29a-3p/SOCS3 axis.","authors":"Zhengli Qian, Keyan Luo, Mingzhe Zhang, Dejing Wang, Yu Hu, Qinghan Li","doi":"10.1007/s11626-024-00922-2","DOIUrl":"https://doi.org/10.1007/s11626-024-00922-2","url":null,"abstract":"<p><p>Recurrent spontaneous abortion (RSA) represents a substantial challenge in reproductive medicine, attributed to a variety of complex factors, among which aberrations in long non-coding RNAs (lncRNAs) play a crucial role. The present study delves into the functional dynamics of the lncRNA H19 in the context of RSA, particularly focusing on its regulatory interplay with miR-29a-3p and the Suppressor of Cytokine Signaling 3 (SOCS3). A notable downregulation of H19 in villous tissues from RSA patients was observed, highlighting its potential involvement in RSA pathophysiology. Functional assays demonstrated that overexpression of H19 in HTR-8/SVneo cells enhances cellular viability while concurrently attenuating apoptotic processes, thereby indicating a pivotal role of H19 in cellular survival pathways. This study identifies miR-29a-3p as a direct regulatory target of H19, exerting significant influence on cellular viability and apoptosis. The inhibition of miR-29a-3p was observed to mitigate its pro-apoptotic effects, thereby reinforcing its critical regulatory capacity in cellular homeostasis. Moreover, SOCS3 was delineated as a downstream effector of miR-29a-3p, with its expression being inversely modulated by miR-29a-3p. Co-transfection experiments involving H19, miR-29a-3p, and SOCS3 unraveled their intricate regulatory nexus in modulating cellular survival mechanisms. Collectively, these findings elucidate that H19 orchestrates the regulation of cell viability and apoptosis in RSA through the miR-29a-3p/SOCS3 signaling axis, thereby providing valuable insights into the molecular underpinnings of RSA and unveiling novel avenues for therapeutic intervention.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191698","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":"The active ingredient of Ginkgo biloba extract (quercetin) improved H₂O₂-induced microglia injury by activating NQO1-PI3K/Akt/mTOR signaling.","authors":"Jingchi Sun, Zhousong Zheng","doi":"10.1007/s11626-025-01106-2","DOIUrl":"https://doi.org/10.1007/s11626-025-01106-2","url":null,"abstract":"<p><p>Activated microglia are considered to be closely related to brain senescence and the pathogenesis of neurodegenerative diseases. Ginkgo biloba extract (GBE) is widely used to treat cognitive impairment and Alzheimer's disease (AD). This study aims to investigate the active ingredients of GBE and the underlying molecular mechanisms. The active ingredients of GBE in AD treatment were first analyzed by network pharmacology, culminating in the identification of the key ingredient, quercetin, and its targeted protein, NQO1. GO function enriched the oxidative stress pathway, while KEGG enriched the PI3K/Akt/mTOR pathway. Quercetin binding to NQO1 was verified by molecular docking and DARTS analysis. Cytotoxicity assay revealed no significant toxicity of GBE (0-1 mg/mL) and quercetin (0-0.4 μM) over 48 h. Subsequently, we constructed the microglial injury model by H₂O₂-induced HMC3 and BV2 cell lines. GBE and quercetin suppressed the senescence characteristics in H₂O₂-induced microglia. Further investigation revealed that the expression of NQO1 was downregulated in the injury model, and treatment with GBE and quercetin facilitated the protein expression of NQO1. In addition, silencing NQO1 reduced the promoting effect of quercetin on microglia viability and phosphorylation levels of PI3K, Akt, and mTOR. At the same time, it significantly increased the levels of p53, p21, p16 and β-galactosidase (SA-β-gal). Collectively, GBE mitigated H₂O₂-induced microglial injury, which activated the PI3K/Akt/mTOR pathway through the quercetin/NQO1 axis. These findings highlight quercetin/NQO1 signaling as a possible therapeutic target for senescence-related neurodegeneration.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124652","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":"Immunomodulatory properties of mesenchymal stem cells within three-dimensional collagen matrices.","authors":"Yenny Yustisia, Koichi Kato","doi":"10.1007/s11626-025-01109-z","DOIUrl":"https://doi.org/10.1007/s11626-025-01109-z","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) hold promise for treating inflammatory and immune-related diseases; however, their clinical application is limited by poor survival and function post-transplantation. Collagen hydrogels may support MSC viability and function by mimicking the extracellular matrix. This study aimed to evaluate how cell density and collagen concentration within three-dimensional (3D) collagen matrices affect the immunomodulatory behavior of MSCs under inflammatory conditions. MSCs were embedded in collagen hydrogels of varying stiffness and seeded at different densities. Constructs were stimulated with proinflammatory cytokines (tumor necrosis factor-α and interferon-γ), and changes in Gene expression, hydrogel contraction, and cell viability were analyzed. Lower collagen concentrations and higher seeding densities enhanced MSC immunomodulatory Gene expression and matrix contraction. High cell density increased contraction but reduced cell viability in softer gels. Mechanical properties of the matrix, such as stiffness and viscoelasticity, influenced cell behavior via mechanotransduction pathways. Both physical and biological cues within 3D collagen hydrogels significantly regulated MSC immunomodulatory responses. Optimizing collagen concentration and seeding density may improve the therapeutic potential of MSC-based treatments.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145064375","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 LCN-2/PI3K/Akt on TNF-α induced inflammatory response of porcine intramuscular adipocytes.","authors":"Xiaoying Dong, Xiaona Zeng, Yongjian Li, Yiming Yan, Shuang Gao, Yanfei Chen, Shengqiu Tang, Meiqi Liang, Yiyi Pan, Xiaonan Zhou, Wei Luo, Yuchen Tang","doi":"10.1007/s11626-025-01087-2","DOIUrl":"https://doi.org/10.1007/s11626-025-01087-2","url":null,"abstract":"<p><p>Lipocalin-2 (LCN-2) has a variety of biological functions and produces various effects on adipocytes, such as promoting cell apoptosis, inhibiting preadipocyte differentiation, and weakening insulin signaling. Tumor necrosis factor-α (TNF-α) is one of the first secreted products discovered in adipocytes, which plays an important role in the regulation of adipose metabolism. This experiment was conducted to investigate the regulatory effect of LCN-2 on TNF-α induced inflammatory response in porcine intramuscular adipocytes. Porcine intramuscular adipocytes were cultured in vitro and treated with LCN-2 overexpression or silencing plasmids. After TNF-α treatment, the expressions of LCN-2, interleukin 6 (IL-6), IL-8, and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Western blot analysis was used to detect the expression of phosphatidylinositol 3-kinase (PI3K), total protein kinase B (Akt), and phosphorylated Akt (pAkt) proteins. After the action of the PI3K/Akt pathway inhibitor LY294002, the effects of LCN-2 overexpression on IL-6, IL-8, and IL-1β were evaluated. The results showed that TNF-α induced LCN-2 expression in a dose-/time-dependent manner. Overexpression or silencing of LCN-2 had an impact on TNF-α induced IL-6, IL-8, and IL-1β in porcine intramuscular adipocytes. Overexpression of LCN-2 significantly promoted inflammatory factors IL-6, IL-8, and IL-1β secretion while silencing of LCN-2 inhibited the secretion of these inflammatory factors (P < 0.01). Overexpression of LCN-2 significantly increased the expression of pAkt protein in cells, while silencing of LCN-2 decreased pAkt protein expression (P < 0.01). After blocking the PI3K/Akt signaling pathway, compared with the control group, overexpression of LCN-2 affected IL-6, IL-8, and IL-1β secretion, but the impact was not significant (P > 0.05). This study suggests that LCN-2 regulates TNF-ɑ induced IL-6, IL-8, and IL-1β secretion in porcine intramuscular adipocytes by targeting the PI3K/Akt pathway, which provides a theoretical basis for LCN-2 regulating the inflammatory response of porcine intramuscular adipocytes.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032985","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":"The ability of the polysaccharide extract Cissus sicyoides L. leaves to maintain normal follicle structure in ovarian tissue culture.","authors":"Camila Maria Araújo de Aguiar, Solano Dantas Martins, Alesandro Silva Ferreira, Hyandra Emilly Oliveira Santos-Saboia, João Eudes Farias Cavalcante-Filho, Maria Alice Felipe Oliveira, Maria Joana Nogueira de Moura, Rafael Aires Lessa, Maria Gonçalves Pereira, Cibele Dos Santos Borges, Vânia Marilande Ceccatto, Sônia Nair Báo, Valdevane Rocha Araújo","doi":"10.1007/s11626-025-01110-6","DOIUrl":"https://doi.org/10.1007/s11626-025-01110-6","url":null,"abstract":"<p><p>The present study aimed to (1) evaluate the effects of different concentrations of the polysaccharide extract of Cissus sicyoides (PE-Cs) during in vitro culture of preantral follicles included in goat ovarian tissue on (i) follicular morphology and activation, (ii) ovarian stromal density, (iii) follicular and oocyte diameters, (iv) antioxidant enzymes activity (SOD, CAT, and GPx), (v) quantification of MDA, thiol, and nitrite levels; as well as to (2) measure the total antioxidant capacity of the extract. The ovarian cortex fragments were cultured at 39 °C in a humidified atmosphere with 5% CO₂ for 6 d in alpha-modified minimum essential medium (αMEM) supplemented with insulin, transferrin, and selenium; hypoxanthine; glutamine; and bovine serum albumin, which was called αMEM⁺ alone or added of PE-Cs at 20, 40, or 80 µg/mL. At the end of the culture period, a reduction in the percentage of normal follicles in all treatments using PE-Cs compared to fresh control and αMEM⁺. Moreover, 80 µg/mL of PE-Cs reduced stromal density and follicular diameter, as well as ultrastructural changes were observed in ovarian tissue. On the other hand, a decrease in MDA levels was observed in all treatments cultured with PE-Cs, although its antioxidant capacity was proven. In summary, supplementation of the culture medium with PE-Cs induced in vitro follicular degeneration. Thus, more studies are needed to evaluate the effect of Cissus sicyoides in reproductive cells and culture systems.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023119","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":"S100A8/A9-MCAM signaling promotes gastric cancer cell progression via ERK-c-Jun activation.","authors":"Youyi Chen, Xu Yang, Rie Kinoshita, Nahoko Tomonobu, Bo Pan, Fangping Wu, Xu Zhang, Kazumi Sagayama, Bei Sun, Masakiyo Sakaguchi","doi":"10.1007/s11626-025-01105-3","DOIUrl":"https://doi.org/10.1007/s11626-025-01105-3","url":null,"abstract":"<p><p>S100 protein family members S100A8 and S100A9 function primarily as a heterodimer complex (S100A8/A9) in vivo. This complex has been implicated in various cancers, including gastric cancer (GC). Recent studies suggest that these proteins play significant roles in tumor progression, inflammation, and metastasis. However, the exact mechanisms by which S100A8/A9 contributes to GC pathogenesis remain unclear. This study investigates the role of S100A8/A9 and its receptor in GC. Immunohistochemical analysis was performed on GC tissue samples to assess the expression of the S100A8/A9 receptor melanoma cell adhesion molecule (MCAM). In vitro transwell migration and invasion assays were used to evaluate the motility and invasiveness of GC cells. Cell proliferation was assessed using a growth assay, and Western blotting (WB) was employed to examine downstream signaling pathways, including ERK and the transcription factor c-Jun, in response to S100A8/A9-MCAM interaction. S100A8/A9 stimulation enhanced both proliferation and migration through MCAM binding in GC cell lines. These cellular events were accompanied by ERK activation and c-Jun induction. Downregulation of MCAM suppressed both ERK phosphorylation and c-Jun expression, highlighting the importance of the S100A8/A9‒MCAM‒ERK‒c-Jun axis in promoting GC progression. These findings indicate that S100A8/A9 contributes to GC progression via MCAM, which activates the ERK‒c-Jun pathway. The S100A8/A9‒signaling axis may represent a novel therapeutic target in GC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023191","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}