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Corrigendum to "Sample size estimation for AQP4-IgG seropositive optic neuritis: retinal damage detection by optical coherence tomography". “AQP4-IgG血清阳性视神经炎的样本量估计:光学相干断层扫描检测视网膜损伤”的勘误。
IF 1.7 4区 生物学
Open Life Sciences Pub Date : 2026-05-18 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1335
Shuwen Lu, Chao Ma, Yi Du
{"title":"Corrigendum to \"Sample size estimation for AQP4-IgG seropositive optic neuritis: retinal damage detection by optical coherence tomography\".","authors":"Shuwen Lu, Chao Ma, Yi Du","doi":"10.1515/biol-2025-1335","DOIUrl":"https://doi.org/10.1515/biol-2025-1335","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1515/biol-2022-0866.].</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251335"},"PeriodicalIF":1.7,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148138634","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}
引用次数: 0
Effects of luteolin on proliferation and apoptosis of breast cancer cells by regulating EGFR/STAT3/AKt pathway. 木犀草素通过调控EGFR/STAT3/AKt通路对乳腺癌细胞增殖和凋亡的影响
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-18 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1270
Xueyu Zheng, Pinting Fu, Zhihua Xia, Wen Feng, Bingbao Song
{"title":"Effects of luteolin on proliferation and apoptosis of breast cancer cells by regulating EGFR/STAT3/AKt pathway.","authors":"Xueyu Zheng, Pinting Fu, Zhihua Xia, Wen Feng, Bingbao Song","doi":"10.1515/biol-2025-1270","DOIUrl":"10.1515/biol-2025-1270","url":null,"abstract":"<p><p>Breast cancer (BC) is a common malignant tumor in women, characterized by high recurrence rates, a significant risk of metastasis, and limitations of existing treatments. The anticancer activity of the natural compound luteolin (LU) has been confirmed, but its specific mechanism of action in breast cancer cells (BCCs) has not been fully elucidated. This study aimed to investigate the effects of LU on the proliferation and apoptosis of BCCs and to clarify its association with the epidermal growth factor receptor (EGFR)/signal transducer and activator of transcription 3 (STAT3)/protein kinase B (Akt) pathway. Using MCF-7 breast cancer cells as the research subject, experimental groups were set up with 5, 15, 25, 35, and 45 μmol/L LU treatment and a dimethyl sulfoxide (DMSO) solvent control group. Cell proliferation activity, reactive oxygen species (ROS) levels, apoptosis rate (AR), and the expression of phosphorylated Akt (p-Akt), phosphorylated EGFR (p-EGFR), and phosphorylated STAT3 (p-STAT3) were detected. LU at concentrations of 25, 35, and 45 μmol/L significantly inhibited the proliferation of MCF-7 cells (<i>P</i> < 0.05), while increasing the cell apoptosis rate and ROS levels (<i>P </i><<i> </i>0.05). Within this concentration range, the expression of p-EGFR, p-STAT3, and p-Akt was significantly downregulated (<i>P </i><<i> </i>0.05), whereas the total protein expression levels of EGFR, Akt, and STAT3 showed no significant change (<i>P </i>><i> </i>0.05). The inhibitory effect of LU on MCF-7 cell proliferation and its pro-apoptotic effect were dose-dependent, with half-maximal inhibitory concentrations (IC<sub>50</sub>) of 28.7 ± 1.5 μmol/L and 29.4 ± 1.8 μmol/L, respectively. LU dose-dependently inhibits the proliferation and promotes the apoptosis of MCF-7 cells by specifically inhibiting the phosphorylation activation of the EGFR/STAT3/Akt pathway and inducing ROS accumulation. This provides experimental evidence for LU as a potential therapeutic agent for breast cancer.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251270"},"PeriodicalIF":2.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13178185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974411","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}
引用次数: 0
Norepinephrine promotes lung cancer cell progression via PFKFB3-promoted histone lactylation-mediated activation of the NF-κB signaling pathway. 去甲肾上腺素通过pfkfb3促进组蛋白乳酸化介导的NF-κB信号通路激活促进肺癌细胞进展。
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-18 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1321
Han Ma, Wenlong Yang, Yiwei Fan, Hui Zou, Xiaoxia Lv
{"title":"Norepinephrine promotes lung cancer cell progression via PFKFB3-promoted histone lactylation-mediated activation of the NF-κB signaling pathway.","authors":"Han Ma, Wenlong Yang, Yiwei Fan, Hui Zou, Xiaoxia Lv","doi":"10.1515/biol-2025-1321","DOIUrl":"10.1515/biol-2025-1321","url":null,"abstract":"<p><p>This study aims to investigate molecular mechanisms by which norepinephrine (NE) exposure influences lung cancer cell behavior, identify key factors and pathways involved in stress-related signaling in lung cancer cells. NE was used to treat lung cancer cells (H1975) to simulate a stress-related signaling environment. PFKFB3 mRNA expression and phosphorylation levels of epithelial-mesenchymal transition (EMT) markers and key proteins in NF-κB signaling pathway were evaluated. NE significantly enhanced lung cancer cell proliferation, specifically upregulated PFKFB3 mRNA expression, promoted EMT marker (N-cadherin and Vimentin) expression, and increased cell migration capacity. Knockdown of PFKFB3 or inhibition of glycolysis reduced cell viability, lactate production, ATP levels, and expression of glycolysis-related enzymes (LDHA and GLUT1) and EMT markers, while suppressing cell migration. Combined interventions exhibited synergistic inhibitory effects. Mechanistic studies revealed that PFKFB3 knockdown inhibited phosphorylation of NF-κB pathway proteins (IKKβ, IκBα, and p65), blocked pathway activation, and reduced histone lactylation levels, particularly at the H4K12la modification site. These effects were reversed by NE intervention. This study suggests a mechanism whereby NE upregulates PFKFB3, activates glycolysis, promotes lactate production to drive histone lactylation, and activates the NF-κB signaling pathway, which is associated with EMT and cell migration.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251321"},"PeriodicalIF":2.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13182856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974488","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}
引用次数: 0
Characterization of nitroreductase gene A of Enterococcus faecalis isolates from fecal samples of patients with colorectal cancer and healthy people. 结直肠癌患者和健康人粪便中分离的粪肠球菌硝基还原酶基因A的鉴定
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-18 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1276
Ping Li, Xiang Li, Jianing Li, Yuqi Tan, Mingcheng Li
{"title":"Characterization of nitroreductase gene A of <i>Enterococcus faecalis</i> isolates from fecal samples of patients with colorectal cancer and healthy people.","authors":"Ping Li, Xiang Li, Jianing Li, Yuqi Tan, Mingcheng Li","doi":"10.1515/biol-2025-1276","DOIUrl":"10.1515/biol-2025-1276","url":null,"abstract":"<p><p>The mechanisms of <i>Enterococcus faecalis</i> (<i>E. faecalis</i>) in the oncogenesis of colorectal cancer (CRC) remain to be revealed. The study aims to identify oxygen-insensitive nitroreductase gene A (NfsA) in <i>E. faecalis</i> between patients with CRC and healthy subjects. A total of 51 patients with CRC were enrolled as an observational group and 30 healthy controls were included in this study during July 2022 to July 2024. <i>E. faecalis</i> isolates were selectively identified from stool samples from two groups. The NfsA genes were analyzed using cloning and sequencing techniques. The fluorescence quantitative PCR targeting the NfsA gene was employed to explore difference of gene expression levels. The differences of the enzymatic activity were also evaluated. A total of 81 isolates were selectively isolated and identified as <i>E. faecalis</i> from stool samples. The exact point mutation exhibited that the base mutated from GA to AC at 52 and 53rd, G to A at 67th, G to A at 105th, C to T at 506th, A to C at 509th in addition to a base deletation at 408, 409th. The mutations frequencies showed statistically significant (<i>P</i> < 0.05). The mRNA expression of the NfsA and the enzymatic activity in fecal samples of patients with CRC was significantly higher than that in healthy controls (<i>P</i> < 0 05). The mutation, expression, and activity of NfsA in <i>E. faecalis</i> from feces of patients with CRC are closely related to the occurrence and development of CRC. Our findings showed that <i>E. faecalis</i> colonizing within intestine may play a role in the tumorigenesis.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251276"},"PeriodicalIF":2.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13183265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974439","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}
引用次数: 0
Neurocritical progression in amyotrophic lateral sclerosis: pathological relevance and validation. 肌萎缩侧索硬化症的神经临界进展:病理相关性和验证。
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-14 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1323
Jiayue Pan, Chengyi Zhang, Jingyao Li, Li Ma
{"title":"Neurocritical progression in amyotrophic lateral sclerosis: pathological relevance and validation.","authors":"Jiayue Pan, Chengyi Zhang, Jingyao Li, Li Ma","doi":"10.1515/biol-2025-1323","DOIUrl":"10.1515/biol-2025-1323","url":null,"abstract":"<p><p>Evidence from multiple clinical studies indicates that amyotrophic lateral sclerosis (ALS) frequently evolves into a condition requiring neurocritical care. In advanced stages or during acute complications, ALS can rapidly transition into a neurocritical state characterized by respiratory insufficiency, systemic dysfunction, and accelerated neurological decline. Although current management strategies for advanced-stage ALS are relatively well established, there remains a significant lack of targeted interventions aimed at preventing or attenuating neurocritical deterioration. This review systematically examines the pathophysiological mechanisms underlying neurocritical progression in ALS, including respiratory failure, metabolic imbalance, autonomic dysfunction, and multisystem involvement. We further evaluate emerging and potential therapeutic strategies designed to mitigate disease severity and stabilize critical neurological function. In addition, we analyze clinical and biological factors that increase susceptibility to neurocritical states and discuss evidence-based approaches to delay disease progression. By integrating clinical observations with mechanistic insights, this review aims to improve early recognition, optimize neurocritical management, and ultimately enhance outcomes for patients with ALS.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251323"},"PeriodicalIF":2.3,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13170975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942260","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}
引用次数: 0
Corrigendum to "Knockdown of Stanniocalcin-1 inhibits growth and glycolysis in oral squamous cell carcinoma cells". “敲低史坦钙素-1抑制口腔鳞状细胞癌细胞的生长和糖酵解”的勘误表。
IF 1.7 4区 生物学
Open Life Sciences Pub Date : 2026-05-14 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1334
Chanyuan Wang, Jianpei Hu, Lijian Wang
{"title":"Corrigendum to \"Knockdown of Stanniocalcin-1 inhibits growth and glycolysis in oral squamous cell carcinoma cells\".","authors":"Chanyuan Wang, Jianpei Hu, Lijian Wang","doi":"10.1515/biol-2025-1334","DOIUrl":"https://doi.org/10.1515/biol-2025-1334","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1515/biol-2022-0907.].</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251334"},"PeriodicalIF":1.7,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13170974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942239","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}
引用次数: 0
Bone marrow stromal cells enhance multiple myeloma cells proliferation through regulating LncRNA OVAAL/ENPP1 axis. 骨髓基质细胞通过调控LncRNA OVAAL/ENPP1轴促进多发性骨髓瘤细胞增殖。
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-14 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1322
Zhenjie Cai, Xiuli Chen, Heyong Zheng, Rongrong Zheng, Rong Zheng, Wuqiang Lin
{"title":"Bone marrow stromal cells enhance multiple myeloma cells proliferation through regulating LncRNA OVAAL/ENPP1 axis.","authors":"Zhenjie Cai, Xiuli Chen, Heyong Zheng, Rongrong Zheng, Rong Zheng, Wuqiang Lin","doi":"10.1515/biol-2025-1322","DOIUrl":"10.1515/biol-2025-1322","url":null,"abstract":"<p><p>Previous research has established the pivotal role of bone marrow stromal cells (BMSCs) in supporting multiple myeloma (MM) pathogenesis. However, the precise molecular mechanisms underlying this role remain elusive. To investigate this, we established a co-culture system of MM cells (U266) with BMSCs (HS-5), demonstrating that HS-5 significantly promoted U266 proliferation. Subsequent RNA sequencing identified HS-5-induced differentially expressed long non-coding RNAs (lncRNAs) and mRNAs. Pathway enrichment analysis, clinical sample validation, and <i>in vitro</i> functional assays were then employed to elucidate the mechanistic basis of HS-5-mediated MM cell proliferation. A total of 79 downregulated RNAs and 619 upregulated RNAs induced by HS-5 were identified. Pathway enrichment analysis of these mRNAs indicated that the pantothenate and coenzyme A biosynthesis pathway functions as a convergence hub enriched by both up-regulated and down-regulated mRNAs, with ENPP1 being enriched in this pathway. Further lncRNA data analysis and validation experiments established lncRNAs OVAAL's targeting of ENPP1 and HS-5-mediated regulation of OVAAL. Additional <i>in vitro</i> experiments showed that OVAAL knockdown reduce the levels of LDH, GLU, and ATP and increase the levels of ROS in MM cells, which were reversed by co-culture with HS-5 cells. Knockdown of ENPP1 significantly suppresseed MM cell proliferation. This suppression could be rescued by co-culture with HS-5 stromal cells. This work indicates that BMSCs drive MM progression via OVAAL upregulation, which activates the ENPP1-mediated cells proliferation and metabolic reprogramming.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251322"},"PeriodicalIF":2.3,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13170762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942302","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}
引用次数: 0
Detection of Deltamethrin resistance level and association between sodium channel domain III gene mutation sites and drug resistance of Rhipicephalus microplus. 微头象对溴氰菊酯抗性水平的检测及钠通道结构域III基因突变位点与耐药性的关系。
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-13 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1287
Zhong-Bo Li, Liangxin Duan, Xin Liu, Tian Yang, Hui Hu, Min Xiang, Cui-Qin Huang
{"title":"Detection of Deltamethrin resistance level and association between sodium channel domain III gene mutation sites and drug resistance of <i>Rhipicephalus microplus</i>.","authors":"Zhong-Bo Li, Liangxin Duan, Xin Liu, Tian Yang, Hui Hu, Min Xiang, Cui-Qin Huang","doi":"10.1515/biol-2025-1287","DOIUrl":"10.1515/biol-2025-1287","url":null,"abstract":"<p><p>To investigate the level of Deltamethrin resistance and mutation sites in the sodium iron channel gene in <i>Rhipicephalus microplus</i> (<i>R. microplus</i>) in Huaihua City, Hunan Province, and to examine the correlation between Deltamethrin resistance and mutation sites in the sodium iron channel gene of <i>R. microplus</i>. A total of 600 <i>R. microplus</i> were sampled from multiple yellow cattle farms in Huaihua City, Hunan Province from June to September 2022, and the level of resistance to Deltamethrin was determined in ticks using the adult immersion test. The sodium iron channel domain III gene was amplified in Deltamethrin-resistant and wild-type <i>R. microplus</i> using PCR assay. Following sequencing and sequence alignment, mutation sites were detected in bases. The sodium iron channel domain III gene in <i>R. microplus</i> was translated, and the signal peptide, transmembrane domain, and phosphorylation and glycosylation sites were detected in amino acid sequences. The tertiary structures of the sodium iron channel domain III protein of Deltamethrin-resistant and wild-type <i>R. microplus</i> were deduced and compared, and the association between mutation sites in bases and resistance to Deltamethrin was examined in <i>R. microplus</i> according the level of Deltamethrin resistance, sequence alignment and protein tertiary structure. The median (LC50) and 95 % lethal concentrations (LC95) of Deltamethrin were 121.39 mg/L and 952.61 mg/L against <i>R. microplus</i>, with a resistance factor of 9.24 and level II resistance. The sequence of the sodium ion channel domain III gene was 1,010 bp in size, and mutation sites were detected in two neighboring bases in the sequence of the sodium ion channel domain III gene in Deltamethrin-resistant <i>R. microplus</i>. Although no signal peptides were found in the sodium iron channel domain III protein of Deltamethrin-resistant or wild-type <i>R. microplus</i>, 6 trans-membrane domains, 42 phosphorylation sites and 8 glycosylation sites were identified, with a significant difference in the tertiary structure of the sodium iron.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251287"},"PeriodicalIF":2.3,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942275","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}
引用次数: 0
A bibliometric analysis of Moringa oleifera during 2000-2024. 2000-2024年辣木文献计量学分析。
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-13 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1314
Sini Wu, Xiaoyin Li, Guo Zhou, Lijin Pan, Yan Su, Quan Qiu, Junjie Zhang, Qian He
{"title":"A bibliometric analysis of <i>Moringa oleifera</i> during 2000-2024.","authors":"Sini Wu, Xiaoyin Li, Guo Zhou, Lijin Pan, Yan Su, Quan Qiu, Junjie Zhang, Qian He","doi":"10.1515/biol-2025-1314","DOIUrl":"10.1515/biol-2025-1314","url":null,"abstract":"<p><p><i>Moringa oleifera</i> is a fast-growing, high-yielding tree species rich in bioactive compounds, holding significant potential for production and application across various fields. This review provides a comprehensive overview of the development, hotspots, and future trends in its study over the past 25 years, aiming to provide strategic insights for future research and applications. Using bibliometric tools including VOS-viewer, Cite-Space, and Biblio-Metrix R-package, we analyzed publications from the Web of Science Core Collection (2000-2024). The analysis of the 2,704 publications ultimately collected, with 426 from India and 292 from China, indicates that the research has experienced rapid development over the past five years. The extensive participation of various actors has fostered a complex global collaboration network, where countries/regions leverage their unique resources and expertise to create a complementary research landscape. Research on <i>M. oleifera</i> is interdisciplinary. Burst detection, clustering analysis, and thematic evolution analysis revealed that \"leaves\" and \"extraction\" will continue to be keywords. Nutritional components, medicinal uses, and water purification have become mature and stable areas. Growth promotion and quality improvement are gradually emerging as core themes. Biofuels and emissions may become new fields of interest. Overall, <i>M. oleifera</i> holds great promise for sustainable agriculture, health food, and environmental remediation.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251314"},"PeriodicalIF":2.3,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942326","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}
引用次数: 0
The EGR1/caspase-14/HIF-1α axis mediates tamoxifen resistance in MCF-7 breast cancer cells. EGR1/caspase-14/HIF-1α轴介导MCF-7乳腺癌细胞的他莫昔芬耐药。
IF 2.3 4区 生物学
Open Life Sciences Pub Date : 2026-05-11 eCollection Date: 2026-01-01 DOI: 10.1515/biol-2025-1311
Feihu Ji, Anping Zhao, Qiuxu Chen, Chenwei Li, Liyuan Huang
{"title":"The EGR1/caspase-14/HIF-1α axis mediates tamoxifen resistance in MCF-7 breast cancer cells.","authors":"Feihu Ji, Anping Zhao, Qiuxu Chen, Chenwei Li, Liyuan Huang","doi":"10.1515/biol-2025-1311","DOIUrl":"10.1515/biol-2025-1311","url":null,"abstract":"<p><p>Breast cancer therapy is compromised by widespread tamoxifen resistance. The modulatory role of Caspase14 in the early growth response protein 1 (EGR1)/hypoxia-inducible factor 1-alpha (HIF-1α) axis in this context is unclear. We investigated how Caspase14 regulates EGR1/HIF-1α to promote 4-hydroxytamoxifen (4-OHT) resistance in MCF7 cells using cell-based genetic and biochemical assays (small-interference RNA knockdown, plasmid overexpression, Western blotting, qPCR, IC50 assays, and Chromatin immunoprecipitation experiments) across multiple independent experiments. Caspase14 expression correlated with resistance, with IC<sub>50</sub> rising from 0.178 µM to 1.575 µM in resistant variants. EGR1 knockdown reduced Caspase14 and downstream targets GLUT3 and BCRP, implicating EGR1 as a key mediator. Resistant cells displayed elevated HIF-1α that enhanced metabolism and migration, further supporting a role in drug resistance. These data indicate that Caspase14 promotes survival, proliferation, and metabolic reprogramming in resistant MCF7 cells via the EGR1/HIF-1α pathway. Our findings reveal a mechanistic link between Caspase14 and endocrine therapy resistance and nominate Caspase14 as a therapeutic target to overcome tamoxifen resistance, with potential translational relevance.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"21 1","pages":"20251311"},"PeriodicalIF":2.3,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13157251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147875149","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}
引用次数: 0
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