Daylan T Pritchard, Caio J Nicholson de Figueiroa, Niels C Bols, Lucy E J Lee
{"title":"Response of epithelial cell lines from the rainbow trout gut and gill to ammonia.","authors":"Daylan T Pritchard, Caio J Nicholson de Figueiroa, Niels C Bols, Lucy E J Lee","doi":"10.1007/s11626-024-01010-1","DOIUrl":"https://doi.org/10.1007/s11626-024-01010-1","url":null,"abstract":"<p><p>Rainbow trout epithelial cell lines from the gill, RTgill-W1, and gut, RTgutGC, were exposed to NH<sub>4</sub>Cl at 18-21 °C in L15 (basal medium) with fetal bovine serum and were found to undergo cytoplasmic vacuolization and cell death, depending on NH<sub>4</sub>Cl concentration and exposure time. Vacuolization arose within 24 h of cultures being exposed to 10-100 mM NH<sub>4</sub>Cl, and vacuoles disappeared over 24 h after NH<sub>4</sub>Cl-exposed cultures were returned to just L15/FBS. RTgill-W1 appeared more sensitive to vacuolization, with one indicator being the maximal proportion of vacuolated cells in a culture, which approached 100% in 50 mM NH<sub>4</sub>Cl for 72 h. RTgill-W1 also were more sensitive to NH<sub>4</sub>Cl-induced cell killing. For 7-d exposures, the inhibitory concentrations (IC50s) for the 50% loss of cell viability as evaluated with Alamar Blue were 30 mM NH<sub>4</sub>Cl for RTgill-W1 and 80 mM for RTgutGC. In a wound-healing assay, RTgutGC cells in 0.1 and 1 mM NH<sub>4</sub>Cl were able to migrate and cover a 500-μm gap in 5 d, like the control, but in 50 mM NH<sub>4</sub>Cl healing was blocked. In 10 mM NH<sub>4</sub>Cl, repair was slowed but by 14 d the gap was covered with cells and many of these were vacuolated. Overall, the results provide a foundation for using these two cell lines to study the physiology and toxicology of ammonia in fish.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188085","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}
Vivian R Dayeh, Anita Solhaug, Mark E Hamilton, Laura E Linton, Lucy E J Lee, Niels C Bols
{"title":"The impact of beauvericin on rainbow trout intestinal epithelial cells at different temperatures and dosing methods.","authors":"Vivian R Dayeh, Anita Solhaug, Mark E Hamilton, Laura E Linton, Lucy E J Lee, Niels C Bols","doi":"10.1007/s11626-025-01014-5","DOIUrl":"https://doi.org/10.1007/s11626-025-01014-5","url":null,"abstract":"<p><p>Mycotoxins in aquatic feeds and their effects on fish are becoming more important in aquaculture, as fishmeal and fish oil in feeds are being replaced with more sustainable plant protein. Here, we investigated the potential of the mycotoxin, beauvericin (BEA), to impact the rainbow trout (RT) intestine by using cultures of the epithelial cell line, RTgutGC. BEA was dosed in different ways and exposed at temperatures ranging from 4 to 26 °C before being evaluated for cell viability by the metabolic reduction of Alamar Blue, by the accumulation of Neutral Red (lysosomal activity), cytotoxicity (CellTox Green), and for wound healing. BEA induces cell death in RTgutGC cells. The lysosomes are the main target (Neutral Red assay is the most sensitive) while cytotoxicity and plasma membrane rupture (CellTox Green) occur at considerably higher concentrations. BEA caused a dose-dependent decline in Neutral Red reading at all tested temperatures but Alamar Blue readings did not decline at 4 °C. Under these conditions, BEA appears to impair only lysosomal activity. Wound healing was reduced at 4, 10, and 26 °C compared to 18 °C. Also BEA treatment, at non-cytotoxic concentrations, reduced wound healing, but the temperature had little influence on this. Different carrier vehicles (methanol, DMSO) and exposure methods (passive or active dispersal) for BEA exposure were also studied. Here, methanol and passive dispersal gave comparable results to exposure with DMSO and active dispersal. In contrast, when DMSO was dosed with passive dispersal, immediate cytotoxicity in combination with BEA was induced.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122812","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}
Haicheng Yang, Zhuo Han, Ying Yang, Shuai Zhou, Bo Zhang, Jiaxing He, Xianli He, Nan Wang
{"title":"Expression, prognosis, immunological infiltration, and DNA methylation of members of the SFRP gene family in colorectal cancer: a comparative bioinformatic and experimental analysis.","authors":"Haicheng Yang, Zhuo Han, Ying Yang, Shuai Zhou, Bo Zhang, Jiaxing He, Xianli He, Nan Wang","doi":"10.1007/s11626-024-00998-w","DOIUrl":"10.1007/s11626-024-00998-w","url":null,"abstract":"<p><p>This study aimed to investigate the expression, prognostic significance, methylation, and immune invasion levels of secreted frizzled-related proteins (SFRP1-5) in colorectal cancer (CRC). Additionally, the relationship between SFRP1/2 methylation and immune infiltration in CRC was explored. The expression of SFRP1-5 was analyzed using several databases, including GEO, TCGA, TIMER, STRING, and GEPIA. Molecular interactions with SFRPs were examined via Cytoscape software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes, and Genomes (KEGG) pathway analyses were conducted using the DAVID database. Methylation levels of SFRP1/2 in CRC were assessed through methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) experiments. Apoptosis and proliferation in CRC cells following the knockdown of SFRP1/2 expression were evaluated using flow cytometry and CCK-8 assays. The TISIDB database was used to analyze the relationship between SFRP1/2 methylation levels and immune infiltration. The expression of SFRP1, SFRP2, and SFRP5 was significantly lower in CRC patients, while SFRP4 expression was higher compared to that in healthy individuals. Elevated mRNA expression of SFRP2 was significantly associated with improved overall survival (OS), disease-specific survival, and progression-free intervals. SFRP1/2 expression was also linked to immune invasion, with higher levels correlating with increased immune infiltration. Both SFRP1 and SFRP2 showed hypermethylation in CRC. Knockdown of SFRP1/2 expression resulted in increased proliferation of CRC cells, and their methylation levels were inversely correlated with immune cell presence. The expression, methylation, and immune cell infiltration patterns of the SFRP family in CRC differed markedly from those in healthy individuals. These findings suggest that SFRPs may serve as potential therapeutic targets and key genes associated with immune cell infiltration in CRC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"149-164"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11865182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894245","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":"Chlorogenic acid suppresses the expression of matrix metalloproteinase-7 and cell invasiveness to almost the same extent as isofraxidin in human colorectal cancer cells.","authors":"Takayoshi Tokiwa, Taisuke Yamazaki, Takashi Yokoyama","doi":"10.1007/s11626-024-00993-1","DOIUrl":"10.1007/s11626-024-00993-1","url":null,"abstract":"<p><p>The expression of matrix metalloproteinase (MMP)-7 is reported to be correlated with invasion and metastasis of colorectal cancer (CRC). Therefore, the inhibition of MMP-7 would be beneficial for the suppression or prevention of CRC cell invasion and metastasis. The stem bark of Acanthopanax senticosus, a widely used medicinal herb, contains isofraxidin (IF) and chlorogenic acid (CGA) as major components. Previously we reported that IF suppressed the expression of MMP-7 and cell invasion in human hepatoma cells. In this study, we investigated the effects of CGA on cell invasion, MMP-7 mRNA expression and the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and compared it with those of IF in human CRC cells (HT-29). We found that CGA significantly suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell invasion, MMP-7 expression and the expression of activated form of MMP-7 to almost the same extent as IF. Meanwhile, we also found that TPA-induced expression of MMP-7 mRNA and ERK1/2 phosphorylation were significantly suppressed when cells were exposed to the ERK1/2 inhibitor U0126 and that CGA was a little more potent than IF at inhibiting TPA-induced ERK1/2 phosphorylation. Taken together, the present results indicate that CGA suppresses cell invasion, MMP-7 expression and ERK1/2 phosphorylation to almost the same extent as IF and suggest that not only IF but also CGA suppresses cell invasion by inhibiting MMP-7 expression via the inhibition of at least ERK1/2 phosphorylation and Acanthopanax senticosus, which contains two components with anti-MMP-7 activity, may be a beneficial herb with anti-invasive effects against human CRC cells.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"205-213"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853967","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}
Minjie He, Yongheng Yang, Xing He, Rong Lei, Hong Liu, Mei Yang
{"title":"Melatonin inhibits ferroptosis through the ATF3/GPX4 signaling pathway to relieve myocardial ischemia-reperfusion injury in rats.","authors":"Minjie He, Yongheng Yang, Xing He, Rong Lei, Hong Liu, Mei Yang","doi":"10.1007/s11626-024-00995-z","DOIUrl":"10.1007/s11626-024-00995-z","url":null,"abstract":"<p><p>Melatonin (MEL), functioning as a circulating hormone, is important for the regulation of ferroptosis in different health scenarios and acts as a crucial antioxidant in cardiovascular diseases. However, its specific function in ferroptosis related to myocardial ischemia-reperfusion injury (MIRI) remains to be fully elucidated. In our research, we utilized a rat model of MIRI induced by coronary artery ligation, along with a cell model subjected to hypoxia/reoxygenation (H/R). We evaluated relevant genes and proteins by real-time fluorescent quantitative PCR and Western blot analysis. To evaluate myocardial tissue damage and cell injury, we employed cell counting kit-8 assays, flow cytometry, hematoxylin-eosin staining, and 2,3,5-triphenyltetrazolium chloride staining techniques. Our results show that administering MEL notably reduces the concentrations of cTnT, CK-MB, and lactate dehydrogenase in the serum of MIRI rats, mitigates the extent of myocardial infarction, improves the recovery of pathological conditions in myocardial tissues, and reduces the concentrations of Fe<sup>2+</sup>, malondialdehyde (MDA), and reactive oxygen species (ROS) in the myocardial tissue, while also promoting increased glutathione levels. Moreover, MEL can also restore the reduced viability of H9C2 cells caused by H/R or ferroptosis inducers (RSL3), reduce the cellular content of Fe<sup>2+</sup>, MDA, and ROS, and inhibit ferroptosis. Mechanistically, MEL promotes the expression of GPX4 by downregulating the expression of ATF3, thereby inhibiting ferroptosis in cardiomyocytes and ultimately alleviating the process of MIRI. Our study demonstrates that MEL ameliorates MIRI by inhibiting ferroptosis.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"135-148"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004831","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}
Yuling Bin, Minji Liu, Rong He, Pingfei Tang, Weiming Qu, Dajun Wu, Lin Tan, Qian Wang, Peng Jiang, Hongsai Hu
{"title":"LINC01224 promotes the Warburg effect in gastric cancer by activating the miR-486-5p/PI3K axis.","authors":"Yuling Bin, Minji Liu, Rong He, Pingfei Tang, Weiming Qu, Dajun Wu, Lin Tan, Qian Wang, Peng Jiang, Hongsai Hu","doi":"10.1007/s11626-024-01001-2","DOIUrl":"10.1007/s11626-024-01001-2","url":null,"abstract":"<p><p>The Warburg effect, a common feature of solid tumors, rewires the metabolism and promotes growth, survival, proliferation, and long-term maintenance in gastric cancer (GC). We performed in vitro and in vivo studies of the pathogenesis of GC to investigate the effects and mechanism of LINC01224 in this cancer. qRT-PCR was used to measure the expression of LINC01224 or miR-486-5p in GC cells, and the expression of LINC01224 in GC tissues by FISH (Fluorescence in situ hybridization) analysis was evaluated. Bioinformatics predicted the target gene of LINC01224, Western blotting was used to measure the protein expression of genes in the PI3K/AKT/mTOR/HIF-1α axis and Warburg effect in GC cells. The function of LINC01224 in GC cells was determined using measurements of EDU assay, colony formation, apoptosis, cell migration, and cell invasion. Glucose metabolism was evaluated using a glucose uptake assay and measurements of lactate. A tumor xenograft model was used to examine the effect of LINC01224 on GC growth in vivo. We found that upregulation of LINC01224 in GC cells activated the miR-486-5p/PI3K axis and promoted aerobic glycolysis, thereby increasing cell viability, proliferation, migration, invasion and anti-apoptosis. LINC01224 downregulation had the opposite effect. LINC01224 expression promoted the in vitro and in vivo pathogenesis of GC by promoting aerobic glycolysis. LINC01224 is a promising target in the treatment of GC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"228-244"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052377","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}
Yessica Zamudio-Cuevas, Javier Fernández-Torres, Octavio Gamaliel Aztatzi-Aguilar, Pedro Raymundo Martínez-Cabello, Ambar López-Macay, Victor Ilizaliturri-Sánchez, Bertha Vargas-Sandoval, Roberto Sánchez-Sánchez, Karina Martínez-Flores
{"title":"Preliminary study on the potential damage of cigarette smoke extract in 3D human chondrocyte culture.","authors":"Yessica Zamudio-Cuevas, Javier Fernández-Torres, Octavio Gamaliel Aztatzi-Aguilar, Pedro Raymundo Martínez-Cabello, Ambar López-Macay, Victor Ilizaliturri-Sánchez, Bertha Vargas-Sandoval, Roberto Sánchez-Sánchez, Karina Martínez-Flores","doi":"10.1007/s11626-024-00999-9","DOIUrl":"10.1007/s11626-024-00999-9","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a chronic degenerative disease characterized by the progressive loss of articular cartilage. The role of cigarette smoke (CS) in OA is debated, with some studies suggesting a protective effect while others indicate it may pose a risk. Our preliminary findings suggest a link between smoking in young adults and severe knee OA, though the extent of this contribution is unclear. This study investigates the impact of cigarette smoke extract (CSE) on human chondrocytes. Human chondrocyte cultures were exposed to varying concentrations (0-10%) of CSE for 7 d. We evaluated cell viability, extracellular matrix (ECM) components, metalloproteinase expression and cytokines levels, and antioxidant enzymes (SOD1 and CAT) using calcein staining, immunohistochemistry and ELISA. Oxidative stress (OS) was assessed by measuring hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and nitric oxide (NO) levels. Results were analyzed using ANOVA with Tukey post hoc tests, and Pearson correlation coefficients were calculated. Cell viability decreased at 10% CSE, and ECM components were diminished. MMP9 and MMP13 expression significantly increased at 5% and 10% CSE. H<sub>2</sub>O<sub>2</sub> levels peaked at 1%, while IL-1β peaked at 2.5%. Antioxidant expression (SOD1 and CAT) decreased at higher concentrations, and heat shock protein 70 (HSP70) was notably expressed. MMPs expression was negatively correlated with both viability and ECM components. CSE induces cellular damage, alters ECM composition, and upregulates MMP expression via OS and IL-1β, while diminishing antioxidant defenses. These findings suggest that smoking may disrupt articular cartilage homeostasis, highlighting the need for further investigation into oxidative stress and inflammatory mediators.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"214-227"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893513","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}
YanYun Jiang, Cong Han, WanLi Xu, YuQiu Li, Yao Liu
{"title":"Compatibility of Calycosin-Tanshinone IIA improves Ang II-induced renal artery endothelial cell dysfunction through lncRNA-mRNA co-expression network.","authors":"YanYun Jiang, Cong Han, WanLi Xu, YuQiu Li, Yao Liu","doi":"10.1007/s11626-024-00990-4","DOIUrl":"10.1007/s11626-024-00990-4","url":null,"abstract":"<p><p>This study aimed to investigate the effect of the compatibility of Calycosin and Tanshinone IIA on dysfunction of rat renal artery endothelial cells (RRAECs) induced by angiotensin II (Ang II) and to elucidate the underlying molecular mechanisms. We utilized cell culture to optimize Calycosin and Tanshinone IIA concentrations and assessed autophagy, apoptosis, ATP levels, and cell migration using MDC staining, Annexin V-FITC/PI staining, ATP assay, and Transwell assays, respectively. RNA-seq identified differentially expressed lncRNAs and mRNAs, which were validated by qRT-PCR. The compatibility of Calycosin and Tanshinone IIA significantly enhanced the proliferative capacity of Ang II-induced RRAECs, increased autophagosome formation, reduced cell apoptosis, elevated ATP production, and enhanced cell migration ability. RNA sequencing analysis revealed 146 differentially expressed lncRNAs and 43 differentially expressed mRNAs, and co-expression network analysis identified interactions between 28 lncRNAs and 7 mRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these differentially expressed mRNAs were primarily involved in the regulation of ATPase activity and metabolic processes related to serine family amino acids, triglycerides, arachidonic acid, etc., as well as the MAPK signaling pathway. The compatibility of Calycosin and Tanshinone IIA improved Ang II-induced dysfunction in RRAECs by modulating the lncRNA-mRNA co-expression network, providing new molecular targets and therapeutic strategies for the prevention and treatment of hypertensive renal damage.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"189-204"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143407411","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}
Yuqiang Yin, Zhenxin Ma, Siwen Yuan, Kangfeng Xu, Xiaofeng Wang
{"title":"OPA3 inhibits the cGAS-STING pathway mediated by mtDNA stress to promote colorectal cancer progression.","authors":"Yuqiang Yin, Zhenxin Ma, Siwen Yuan, Kangfeng Xu, Xiaofeng Wang","doi":"10.1007/s11626-024-01000-3","DOIUrl":"10.1007/s11626-024-01000-3","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is an extremely harmful malignant tumor. Optic atrophy 3 (OPA3) is highly expressed in multiple tumors, but its action in CRC is still unknown. This research aims to explore the role of OPA3 and its related molecular mechanisms for CRC. Firstly, we overexpressed and knocked down OPA3 to examine its effect on CRC cell (HT29 cell) growth. CRC cell viability, migration, invasion, and levels of proliferation markers and cell cycle-associated proteins were measured. Then, we treated cells with carbonyl cyanide m-chlorophenyl hydrazone (CCCP) to explore mitochondrial dysfunction and mtDNA stress in HT29 cells. Next, we overexpressed cGAS and STING to examine their correlation with OPA3. The results showed that OPA3 overexpression enhanced CRC cell viability, migration, invasion, and the levels of PCNA, Cyclin A2, and Cyclin B1. Knockdown of OPA3 had the opposite effects. Moreover, OPA3 knockdown facilitated mitochondrial dysfunction and mtDNA stress in CRC cells. OPA3 overexpression also inhibited CCCP-induced mitochondrial stress disorder. Additionally, OPA3 knockdown elevated the protein levels of p-STING and cGAS and the mRNA level of STING target genes. Furthermore, overexpression of either cGAS or STING partially alleviated the enhancement of HT29 cell proliferation, migration, and invasion mediated by OPA3 overexpression. In conclusion, OPA3 promotes CRC progression via inhibiting the cGAS-STING pathway, which is mediated by mtDNA stress. OPA3 may be a new potential target for CRC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"165-177"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894246","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}