Cytotechnology最新文献_第9页

Dietary Zinc activates the Nrf2 signaling pathway to inhibit pyroptosis and attenuate the lung inflammatory response in COPD. 膳食锌可激活 Nrf2 信号通路，从而抑制慢性阻塞性肺病患者的脓毒症并减轻肺部炎症反应。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-18 DOI: 10.1007/s10616-025-00725-7

Yanqiu Huang, Tao Liang, Junfei Liu, Hongyan Yu, Jingna Li, Li Han

{"title":"Dietary Zinc activates the Nrf2 signaling pathway to inhibit pyroptosis and attenuate the lung inflammatory response in COPD.","authors":"Yanqiu Huang, Tao Liang, Junfei Liu, Hongyan Yu, Jingna Li, Li Han","doi":"10.1007/s10616-025-00725-7","DOIUrl":"10.1007/s10616-025-00725-7","url":null,"abstract":"Pyroptosis and inflammation play crucial roles in the development of chronic obstructive pulmonary disease (COPD), and Zinc deficiency is commonly observed in COPD patients. In this study, we aimed to explore the impact of Zinc supplementation on pyroptosis and inflammation in a cigarette smoke (CS)-induced COPD mouse model, as well as the underlying mechanisms. The COPD mouse model was established through CS exposure, and mouse pulmonary epithelial cells (MLE-12) were exposed to cigarette smoke extract (CSE) to further validate the effects of Zinc supplementation. CS exposure resulted in significant alveolar wall damage, increased thickening of the alveolar walls, and elevated levels of interleukin-1β (IL-1β), IL-6, IL-18, and tumor necrosis factor-α (TNF-α) in the lung tissues of COPD mice. However, treatment with dexamethasone (a positive control) or Zinc supplementation alleviated these damages. Furthermore, the expressions of pyroptosis markers, including NLRP3, cleaved-Caspase-1, and GSDMD-N proteins, were upregulated in the lung tissues after CS exposure. Zinc supplementation, however, reversed these changes. Additionally, Zinc supplementation upregulated the protein expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and quinone oxidoreductase-1 (NQO-1), and promoted the ubiquitination of Kelch-like ECH-associated protein 1 (Keap1) mediated by tripartite motif 25 (TRIM25) in the lung tissues of CS-induced mice. Importantly, the Nrf2 signaling inhibitor ML385 abolished the beneficial effects of Zinc in CS-exposed mice. Similar results were observed in MLE-12 lung epithelial cells exposed to CSE. In summary, Zinc supplementation inhibits pyroptosis and attenuates inflammation in COPD mice by activating the Nrf2 pathway.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-025-00725-7.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"62"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11836256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467264","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

Fermented plant product (FPP) suppresses immediate hypersensitivity reactions with impaired high-affinity IgE receptor (FcεRI) signaling. 发酵植物产物（FPP）抑制高亲和IgE受体（FcεRI）信号通路受损的即时超敏反应。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-25 DOI: 10.1007/s10616-025-00729-3

Tomoki Kodama, Ayana Yokoyama, Yuki Nishioka, Riku Kawasaki, Aiko Teshima, Akira Maeda, Ayano Hojo, Takumi Suizu, Hideto Torii, Kotaro Fujioka, Shinsuke Kishida, Takashi Fujimura, Kenji Arakawa, Atsushi Ikeda, Seiji Kawamoto

{"title":"Fermented plant product (FPP) suppresses immediate hypersensitivity reactions with impaired high-affinity IgE receptor (FcεRI) signaling.","authors":"Tomoki Kodama, Ayana Yokoyama, Yuki Nishioka, Riku Kawasaki, Aiko Teshima, Akira Maeda, Ayano Hojo, Takumi Suizu, Hideto Torii, Kotaro Fujioka, Shinsuke Kishida, Takashi Fujimura, Kenji Arakawa, Atsushi Ikeda, Seiji Kawamoto","doi":"10.1007/s10616-025-00729-3","DOIUrl":"10.1007/s10616-025-00729-3","url":null,"abstract":"Fermented plant product (FPP) is a dietary supplement made by fermentation and aging of a variety of plants, including fruits, vegetables, and grains. A previous study has shown that oral FPP supplementation prevents the development of allergic rhinitis-like nasal symptoms in a murine model of Japanese cedar pollinosis without affecting systemic immune response. However,　the mode of action by which FPP exerts an anti-allergic effect remains to be elucidated. Here, we show that FPP acts on mast cells to suppress immediate hypersensitivity reactions in vitro as well as in vivo. We found that stimulation with FPP potently suppressed IgE antibody-mediated degranulation of RBL-2H3 rat basophilic leukemia cells. We also found that oral feeding with FPP significantly suppressed passive cutaneous anaphylaxis (PCA), an in vivo model of IgE- and mast cell-mediated hypersensitivity reactions. Mechanistic analysis revealed that FPP extensively suppressed the high-affinity IgE receptor (FcεRI) signaling pathway, in which FPP not only inhibited intracellular Ca2+ influx upon FcεRI ligation but also negatively regulated another Ca2+-independent FcεRI signaling pathway leading to granule translocation through microtubule formation. These results suggest that FPP fulfills its anti-allergic activity by acting on the IgE-mast cell axis to suppress immediate hypersensitivity reactions.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"69"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11861467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514901","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

Mechanism of microRNA-124-3p targeting calpain-1 to affect the function of intervertebral disc nucleus pulposus cells. microRNA-124-3p靶向calpain-1影响椎间盘髓核细胞功能的机制。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-31 DOI: 10.1007/s10616-024-00693-4

Xunan Xu, Yong Liu, Chun Jiang, Peng Jia, Pengfei Cao, Yi He, Yin Zhang

{"title":"Mechanism of microRNA-124-3p targeting calpain-1 to affect the function of intervertebral disc nucleus pulposus cells.","authors":"Xunan Xu, Yong Liu, Chun Jiang, Peng Jia, Pengfei Cao, Yi He, Yin Zhang","doi":"10.1007/s10616-024-00693-4","DOIUrl":"10.1007/s10616-024-00693-4","url":null,"abstract":"Intervertebral disc degeneration (IVDD) represents a major cause of lower back pain, whose prevalence rises with age. This study probed into the mechanism of microRNA (miR)-124-3p regulating function of nucleus pulposus cells (NPCs) by targeting calpain-1 (CAPN1). Rat IVD NPCs were cultured in vitro and transfected with miR-124-3p mimics, miR-124-3p inhibitor, oe-CAPN1 and their negative controls. The mRNA levels of miR-124-3p and CAPN1 were assessed by RT-qPCR. Cell proliferation, apoptosis and migration were evaluated by CCK-8, flow cytometry and Transwell assays. Levels of CAPN1 protein, apoptosis-related proteins (BAX, Cleaved-Caspase3, BCL-2) and extracellular matrix (ECM) proteins (Collagen II, Aggrecan, Fibronectin, Collagen I, matrix metalloproteinase [MMP]-13) were determined by Western blot. The target binding relationship between miR-124-3p and CAPN1 was verified by dual-luciferase assay. miR-124-3p overexpression facilitated NPC function and the maintenance of ECM homeostasis, as evidenced by increased NPC proliferation and migration, decreased apoptosis, elevated apoptosis-related protein BCL-2 level, diminished BAX and Cleaved-Caspase3 levels, reduced levels of ECM homeostasis-associated factors Collagen I and MMP-13 proteins, as well as raised levels of Collagen II, Aggrecan and Fibronectin proteins. Conversely, miR-124-3p knockdown brought about the opposite results. miR-124-3p targeted CAPN1. Furthermore, overexpression of CAPN1 partially reversed the regulatory effects of miR-124-3p on the ECM homeostasis, proliferation and migration in NPCs, and promoted apoptosis. miR-124-3p contributed to proliferation and migration of IVD NPCs, and reduced their apoptosis by inhibiting CAPN1 expression, thereby modulating ECM homeostasis and maintaining the function of IVD NPCs.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"53"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078820","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

Advancing brain tumor therapy: unveiling the potential of PROTACs for targeted protein degradation. 推进脑肿瘤治疗：揭示PROTACs靶向蛋白降解的潜力。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-31 DOI: 10.1007/s10616-025-00716-8

Saooda Ibrahim, Muhammad Umer Khan, Saadia Noreen, Safia Firdous, Iqra Khurram, Raima Rehman, Muhammad Arshad Javed, Qurban Ali

{"title":"Advancing brain tumor therapy: unveiling the potential of PROTACs for targeted protein degradation.","authors":"Saooda Ibrahim, Muhammad Umer Khan, Saadia Noreen, Safia Firdous, Iqra Khurram, Raima Rehman, Muhammad Arshad Javed, Qurban Ali","doi":"10.1007/s10616-025-00716-8","DOIUrl":"10.1007/s10616-025-00716-8","url":null,"abstract":"The long-term treatment of malignancies, particularly brain tumors, is challenged by abnormal protein expression and drug resistance. In terms of potency, selectivity, and overcoming drug resistance, Proteolysis Targeting Chimeras (PROTACs), a cutting-edge method used to selectively degrade target proteins, beats traditional inhibitors. This review summarizes recent research on using PROTACs as a therapeutic strategy for brain tumors, focusing on their mechanism, benefits, limitations, and the need for optimization. The review draws from a comprehensive search of peer-reviewed literature, scientific databases, and clinical trial databases. Articles published up to the knowledge cutoff date up to 14 April 2023 were included. Inclusion criteria covered PROTAC-based brain tumor therapies, including preclinical and early clinical studies, with no restrictions on design or publication type. We included studies using in vitro, in vivo brain tumor models, and human subjects. Eligible treatments involved PROTACs targeting proteins linked to brain tumor progression. We evaluated the selected studies for methodology, including design, sample size, and data analysis techniques. A narrative synthesis summarized key outcomes and trends in PROTAC-based brain tumor therapy. Recent research shows PROTACs selectively degrade brain tumor-related proteins with minimal off-target effects. They offer enhanced potency, selectivity, and the ability to combat resistance compared to traditional inhibitors. PROTACs hold promise for brain tumor treatment offering advantages over traditional inhibitors, but more research is needed to refine their mechanisms, efficacy, and safety. Larger-scale trials and translational studies are essential for assessing their clinical utility.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"54"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078814","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

miR-372-3p represses hepatic stellate cell activation via the RhoC/ROCK pathway. miR-372-3p通过RhoC/ROCK途径抑制肝星状细胞活化。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-14 DOI: 10.1007/s10616-025-00715-9

Shiyu Ou, Xiaoling Tang, Zhongzhuan Li, Rong Ouyang, Yuan Lei, Gang Chen, Ling Du

{"title":"miR-372-3p represses hepatic stellate cell activation via the RhoC/ROCK pathway.","authors":"Shiyu Ou, Xiaoling Tang, Zhongzhuan Li, Rong Ouyang, Yuan Lei, Gang Chen, Ling Du","doi":"10.1007/s10616-025-00715-9","DOIUrl":"10.1007/s10616-025-00715-9","url":null,"abstract":"The study was undertaken to determine the mechanism of miR-372-3p activating hepatic stellate cell (HSC). Transforming growth factor-β1 (TGF-β1) induced LX-2 cells were transfected with miR-372-3p mimics and/or RhoC overexpression vector (oe-RhoC), after which the miR-372-3 and RhoC expressions were detected and the biological functions of transfected cells were assessed. The relation between miR-372-3p and RhoC predicted online was validated using the dual-luciferase assay. Protein level of Collagen I (COL I), α-smooth muscle actin (α-SMA), and key proteins in the RhoC/ROCK pathway were determined using western blot. Activated LX-2 cells had decreased miR-372-3p and increased RhoC expression. Overexpression of miR-372-3p led to inhibited LX-2 cell proliferation, accelerated apoptosis, and decreased protein level of COL I and α-SMA, while such an expression pattern can be partially reversed by RhoC overexpression. miR-372-3p can bind and target RhoC expression. miR-372-3p inhibited RhoC expression to block the activation of the Rho/ROCK pathway and thus mediate LX-2 cell proliferation and apoptosis. miR-372-3p mediated RhoC/ROCK pathway to inhibit HSC activation.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"60"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11828770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432684","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

Proanthocyanidin B2 alleviates Pg.LPS-induced RAW264.7 cellular inflammation and oxidative stress via PI3K/Akt/NFkB pathway. 原花青素B2通过PI3K/Akt/NFkB通路缓解pg . lps诱导的RAW264.7细胞炎症和氧化应激。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-03-10 DOI: 10.1007/s10616-025-00734-6

Xiaoyan Ou, Xin Chen, Zhichun Fang, Junwei Zhao

{"title":"Proanthocyanidin B2 alleviates Pg.LPS-induced RAW264.7 cellular inflammation and oxidative stress via PI3K/Akt/NFkB pathway.","authors":"Xiaoyan Ou, Xin Chen, Zhichun Fang, Junwei Zhao","doi":"10.1007/s10616-025-00734-6","DOIUrl":"10.1007/s10616-025-00734-6","url":null,"abstract":"Periodontitis is a multifactorial chronic inflammatory infectious disease associated with systemic diseases. Proanthocyanidin B2 (PB2), a polyphenol, has been investigated to exhibit antioxidant, anti-inflammatory and anti-cancer pharmacological properties. PB2 has shown good efficacy in treating hepatocellular carcinoma, type 2 diabetes mellitus, and ulcerative colitis. There are few studies on PB2 in treating periodontitis, and the molecular mechanism is unknown. This research focused on the effects of PB2 in Porphyromonas gingivalis-derived lipopolysaccharide (Pg. LPS)-stimulated RAW264.7 cells, as well as the potential mechanisms. CCK-8 assay was used to assess the cytotoxic effects of PB2. qRT-PCR assay and ELISA assay were used to evaluate the expression of inflammatory cytokines. DCFH-DA probe and other assay kits were employed to detect oxidative stress indicators. Western blot was conducted to assess important proteins of the PI3K/Akt/NFκB pathway. The results showed that PB2 downregulated the overproduction of pro-inflammatory mediators IL-1β, IL-6, and TNF-α; reduced the generation of ROS, MDA, and NO; Enhanced the activities of anti-inflammatory factor IL-10 and the total antioxidant capacity; and inhibited the activation of PI3K/Akt/NFκB pathway. In addition, the PI3K agonist 740Y-P was able to partially reverse the effects of PB2. This study indicates that PB2 exhibits significant anti-inflammatory and antioxidant effects in P. gingivalis LPS-stimulated RAW264.7 cells, primarily through the inhibition of the PI3K/Akt/NFκB signaling pathway.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"77"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613874","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

Type IV collagen derived non-collagenous domain α6 (IV) NC1 and its derivative fragments inhibit endothelial cell proliferation and attenuates in-vivo chorioallantoic membrane angiogenesis. IV型胶原来源的非胶原结构域α6 (IV) NC1及其衍生物片段抑制内皮细胞增殖，减弱体内绒毛膜尿囊膜血管生成。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-25 DOI: 10.1007/s10616-025-00709-7

Aravind Setti, Akbar Pasha, Venkata Krishna Kanth Makani, Manika Pal Bhadra, Smita C Pawar

{"title":"Type IV collagen derived non-collagenous domain α6 (IV) NC1 and its derivative fragments inhibit endothelial cell proliferation and attenuates in-vivo chorioallantoic membrane angiogenesis.","authors":"Aravind Setti, Akbar Pasha, Venkata Krishna Kanth Makani, Manika Pal Bhadra, Smita C Pawar","doi":"10.1007/s10616-025-00709-7","DOIUrl":"10.1007/s10616-025-00709-7","url":null,"abstract":"Targeting tumor angiogenesis with safe endogenous protein inhibitors is a promising therapeutic approach despite the plethora of the first line of emerging chemotherapeutic drugs. The extracellular matrix network in the blood vessel basement membrane and growth factors released from endothelial and tumor cells promote the neovascularization which supports the tumor growth. Contrastingly, small cleaved cryptic fragments of the C-terminal non collagenous domains of the same basement membrane display antiangiogenic effect. In the present study, full length α6(IV)NC1(Hexastatin) and its three subfragments α6S1(IV)NC1, α6S2(IV)NC1, and α6S3(IV)NC1 were validated for their pro-apoptotic and angio-inhibitory property. In order to construct the coding sequence of hexastatin and its three derivative partial peptide fragments were constructed with our proposed method, where the corresponding exons were amplified from the genomic DNA and then assembled together. Coding sequences were cloned and expressed using pLATE31 vector and recombinant proteins were purified with C-terminal His tag. The endogenous NC protein fragments of collagen IV were evaluated in vitro for their role in cytotoxicity on human umbilical vein endothelial cells (HUVECs). The results showed that the NC1 domain and its fragments inhibited the HUVECs cell proliferation, migration, invasion and induced apoptosis. The neovascularization inhibition was studied in in-vitro, via tube formation assay and in-vivo via the CAM Assay. The results showed that blood vessels and inter capillary network were inhibited in endothelial cells and also, in chick embryo treated with recombinant α6(IV)NC1 and its derivatives, except for α6S1(IV)NC1 and these endogenous protein inhibitors act as bio-therapeutics in inhibition of angiogenesis.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"47"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045806","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

Cancer-associated fibroblast-derived exosomal FAM83F regulates KIF23 expression to promote the malignant progression and reduce radiosensitivity in non-small cell lung cancer. 癌症相关成纤维细胞来源的外泌体FAM83F调节KIF23的表达，促进非小细胞肺癌的恶性进展并降低放射敏感性。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-25 DOI: 10.1007/s10616-025-00713-x

Yi Li, Mingming Zhou, Xiaogang Hu, Tingting Xie, Wenli Peng, Lina Zhang, Minxin Tang, Rui Hu, Yongpeng He

{"title":"Cancer-associated fibroblast-derived exosomal FAM83F regulates KIF23 expression to promote the malignant progression and reduce radiosensitivity in non-small cell lung cancer.","authors":"Yi Li, Mingming Zhou, Xiaogang Hu, Tingting Xie, Wenli Peng, Lina Zhang, Minxin Tang, Rui Hu, Yongpeng He","doi":"10.1007/s10616-025-00713-x","DOIUrl":"10.1007/s10616-025-00713-x","url":null,"abstract":"Cancer-associated fibroblasts (CAFs) have been shown to play a crucial role in the progression of non-small cell lung cancer (NSCLC). Exosomes derived from CAFs have emerged as important mediators of intercellular communication in the tumor microenvironment, contributing to cancer progression. Therefore, it is essential to further investigate the mechanisms by which CAF-derived exosomes regulate NSCLC. CAFs promoted NSCLC cell proliferation, invasion, and migration, while also suppressing radiosensitivity. We observed an upregulation of FAM83F expression in both NSCLC cells and NSCLC cells treated with conditioned medium from CAFs. Notably, CAF-derived exosomes were found to transfer FAM83F to NSCLC cells, thereby enhancing the malignant properties of the cancer cells. In contrast, FAM83F-deficient CAF-derived exosomes exerted inhibitory effects on NSCLC cell proliferation, invasion, and migration, while also sensitizing the cells to radiotherapy. FAM83F was found to interact with KIF23 in NSCLC cells, and the overexpression of KIF23 attenuated the effects induced by FAM83F-deficient exosomes in NSCLC cells. Moreover, FAM83F-deficient CAF-derived exosomes were effective in inhibiting tumor formation in vivo. Our findings highlight the crucial role of CAF-derived exosomal FAM83F in promoting NSCLC progression and conferring resistance to radiotherapy. Targeting this signaling pathway may offer promising therapeutic strategies for combating NSCLC progression and improving patient outcomes.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-025-00713-x.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"50"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045438","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

In vitro and in vivo evidence of the effectiveness of gallic acid on glycerol-induced acute kidney injuries. 没食子酸对甘油诱导的急性肾损伤的体内和体外实验证据。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-25 DOI: 10.1007/s10616-025-00706-w

Khojasteh Hoseinynejad, Zahra Tafazzoli, Fereshteh Nejaddehbashi, Mehrnoosh Moosavi, Zahra Mansouri

{"title":"In vitro and in vivo evidence of the effectiveness of gallic acid on glycerol-induced acute kidney injuries.","authors":"Khojasteh Hoseinynejad, Zahra Tafazzoli, Fereshteh Nejaddehbashi, Mehrnoosh Moosavi, Zahra Mansouri","doi":"10.1007/s10616-025-00706-w","DOIUrl":"10.1007/s10616-025-00706-w","url":null,"abstract":"Because acute kidney injuries (AKI) are one of the critical health problems worldwide, studies on the risk factors, mechanisms, and treatment strategies seem necessary. Glycerol (GLY), known to induce cell necrosis via myoglobin accumulation in renal tubules, is widely used as an AKI model. This study aimed to evaluate the protective effects of gallic acid (GA) against GLY-induced AKI. The study utilized both in vivo and in vitro models. In vivo, healthy rats were divided into six groups: control (normal saline), GLY (10 mg/kg, intramuscularly), GLY + GA10 (10 mg/kg), GLY + GA50 (50 mg/kg), GLY + GA100 (100 mg/kg), and GA (100 mg/kg). GA was administered by gavage for seven consecutive days, followed by a single intramuscular injection of GLY. Kidney biomarkers, lactate dehydrogenase (LDH), oxidative stress markers, inflammatory indices, and histological parameters were assessed 72 h post-injection. In vitro, human embryonic kidney 2 (HK-2) cells were incubated with GLY and GA at different concentrations (30, 60, and 125 μg/ml) to evaluate cell viability, reactive oxygen species (ROS) production, oxidative stress, and inflammatory cytokines. GLY administration significantly elevated renal dysfunction markers, including blood urea nitrogen and creatinine, alongside oxidative stress and reduced cell viability. GA treatment improved kidney biomarkers, enhanced antioxidant enzyme activity, and reduced inflammatory cytokines. Histological analyses also showed improved kidney structural integrity in GA-treated rats compared to the GLY group. This study confirmed that GLY induces AKI through oxidative stress, inflammation, and structural damage. GA exhibited significant renal protective effects by enhancing antioxidant defenses and reducing inflammation. These findings support GA as a potential natural supplement for preventing or treating renal diseases.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"45"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045782","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

Long non-coding RNA HOXC-AS1 promotes the malignancy by sponging miR-195-5p with ANLN in esophageal cancer. 长非编码 RNA HOXC-AS1 在食管癌中通过与 ANLN 共同作用促进 miR-195-5p 的恶性发展。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-24 DOI: 10.1007/s10616-025-00711-z

Yongchao Su, Feng Kuang, Hongwei Guo, Qu Chen, Yiquan Lai, Ran Jing, Lei Huang

{"title":"Long non-coding RNA HOXC-AS1 promotes the malignancy by sponging miR-195-5p with ANLN in esophageal cancer.","authors":"Yongchao Su, Feng Kuang, Hongwei Guo, Qu Chen, Yiquan Lai, Ran Jing, Lei Huang","doi":"10.1007/s10616-025-00711-z","DOIUrl":"10.1007/s10616-025-00711-z","url":null,"abstract":"Long non-coding RNA HOXC cluster antisense RNA 1 (HOXC-AS1) exhibits elevated expression in gastric and prostate cancers, yet its involvement in esophageal cancer (EC) remains unexplored. This investigation assessed the expression patterns and functional implications of HOXC-AS1 in EC. Quantitative real-time PCR was employed to evaluate HOXC-AS1 expression in EC cell lines, while its impact on cell proliferation, migration, invasion, tumor growth, and metastasis was examined through MTT, EdU, transwell, wound healing assays, and animal models. Mechanistic insights into HOXC-AS1 were pursued using dual-luciferase reporter assays and RNA immunoprecipitation. Analysis of TCGA data demonstrated significant upregulation of HOXC-AS1 in EC tissues, consistent with its enriched expression in EC cell lines. Knockdown experiments revealed that suppressing HOXC-AS1 reduced proliferation, migration, and invasion of EC cells in vitro and inhibited tumor growth and metastasis in vivo. Mechanistically, HOXC-AS1 acted as a molecular sponge for miR-195-5p, with anillin actin-binding protein (ANLN) identified as a direct downstream target of miR-195-5p. Functional rescue experiments showed that inhibiting miR-195-5p or overexpressing ANLN counteracted the suppressive effects induced by HOXC-AS1 silencing on the aggressive phenotypes of EC cells. These findings establish HOXC-AS1 as a promoter of EC progression via regulation of the miR-195-5p/ANLN axis, suggesting its utility as a prospective therapeutic target for EC management.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"68"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515000","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