Cytotechnology最新文献_第2页

Identification of plasma exosomal microRNAs and bioinformatics analysis of the microRNA-messenger RNA regulatory pathways in mice with status epilepticus.

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-20 DOI: 10.1007/s10616-025-00708-8

Wei Wang, Jian Yin

{"title":"Identification of plasma exosomal microRNAs and bioinformatics analysis of the microRNA-messenger RNA regulatory pathways in mice with status epilepticus.","authors":"Wei Wang, Jian Yin","doi":"10.1007/s10616-025-00708-8","DOIUrl":"10.1007/s10616-025-00708-8","url":null,"abstract":"Status epilepticus (SE) is a serious neurological emergency that brings significant risks to health and life. microRNAs (miRNAs) and their targets show involvement in the pathophysiology of SE. We identified plasma exosomal miRNAs and analyzed the miRNA-messenger RNA (mRNA) regulatory pathways in SE mice. Mice were subjected to SE induction by kainic acid injection, and plasma exosome (Exo) extraction. Exo morphology, particle size distribution, and Exo-positive marker proteins were evaluated. Differentially-expressed miRNAs in Exos of SE mice were analyzed and verified by sequencing and RT-qPCR. Functional enrichment analysis on target genes and protein-protein interaction (PPI) network were performed. Hippocampal neuron cells HT-22 were cultured in vitro, and the targeted binding association between Exos-derived miR-205-5p and target genes was invalidated. There were 64 differentially-expressed miRNAs in plasma Exos of SE mice from healthy mice (32 up-regulated, 32 down-regulated). Among the top 10 differentially-expressed miRNAs, 5 were up-regulated, and 5 were down-regulated. The PPI network of collective target genes was developed, including 11 edges and 9 nodes. The genes related to nerve injury were phosphatase and tensin homolog (Pten), glycogen synthase kinase 3 beta (Gsk3b), and leucine-rich repeat kinase 2 (Lrrk2). SE mouse plasma Exos targeted Gsk3b, Lrrk2 and Pten in neuronal cells and reduced cell viability. Plasma exosomal miRNAs of SE mice were differentially expressed, and their target genes participated in the regulation of multiple pathways, mainly related to nervous system development. miR-205-5p could target Gsk3b, Lrrk2 and Pten, and suppress neuronal viability.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-025-00708-8.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"65"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482473","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.

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

Proanthocyanidin B2 alleviates Pg.LPS-induced RAW264.7 cellular inflammation and oxidative stress via PI3K/Akt/NFkB pathway.

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

miR-372-3p represses hepatic stellate cell activation via the RhoC/ROCK pathway.

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

Advancing brain tumor therapy: unveiling the potential of PROTACs for targeted protein degradation.

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

Mechanism of microRNA-124-3p targeting calpain-1 to affect the function of intervertebral disc nucleus pulposus cells.

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

Cancer-associated fibroblast-derived exosomal FAM83F regulates KIF23 expression to promote the malignant progression and reduce radiosensitivity in non-small cell lung cancer.

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

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.

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

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

Yunnan medicine Jiangzhi ointment alleviates hyperlipid-induced hepatocyte ferroptosis by activating AMPK and promoting autophagy.

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-03-05 DOI: 10.1007/s10616-025-00737-3

Xin Hong, Haijing Liu, Hongli Sun, Yan Zhuang, Meizhen Xiao, Shaoping Li, Yandong Li, Ming Jing

{"title":"Yunnan medicine Jiangzhi ointment alleviates hyperlipid-induced hepatocyte ferroptosis by activating AMPK and promoting autophagy.","authors":"Xin Hong, Haijing Liu, Hongli Sun, Yan Zhuang, Meizhen Xiao, Shaoping Li, Yandong Li, Ming Jing","doi":"10.1007/s10616-025-00737-3","DOIUrl":"10.1007/s10616-025-00737-3","url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is a serious public health problem worldwide. The purpose of this study was to investigate whether Yunnan medicine Jiangzhi ointment (YMJO) can relieve the progression of NAFLD and to elucidate the specific mechanism involved. A NAFLD model was established in high-fat diet (HFD)-induced SD rats and free fatty acid (FFA)-induced BRL 3A cells. The expression of autophagy-related proteins and ferroptosis-related proteins was detected using Western blotting. The histopathological features of the livers of NAFLD rats were evaluated using hematoxylin and eosin (HE) and Oil Red O staining. The results revealed that in a successfully established HFD-induced NAFLD rat model, YMJO alleviated the progression of NAFLD, promoted autophagy, and inhibited ferroptosis. This regulatory mechanism is related to the activation of the AMPK pathway. Further study of the molecular mechanism via cell experiments revealed that YMJO activated FFA-induced liver cell autophagy through the AMPK signaling pathway and inhibited ferroptosis, thus alleviating the development of NAFLD. This study revealed that YMJO promotes phosphorylation by activating the AMPK pathway, enhances autophagy, ameliorates ferroptosis induced by high fat, and alleviates the occurrence and development of NAFLD.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"73"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585008","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