Cytotechnology最新文献

{"title":"Green synthesis of silver nanoparticles using <i>Amomum nilgiricum</i> leaf extracts: preparation, physicochemical characterization and ameliorative effect against human cancer cell lines.","authors":"Narasimhamurthy Konappa, Rajeshwari H Patil, Anupama S Kariyappa, Soumya Krishnamurthy, Niranjana Siddapura Ramachandrappa, Rahul Krishnappa, Srinivas Chowdappa","doi":"10.1007/s10616-024-00674-7","DOIUrl":"10.1007/s10616-024-00674-7","url":null,"abstract":"<p><p>The present study to production of silver nanoparticles (AgNPs) by leaf extracts of <i>A. nilgiricum</i> and to evaluate the activity of anticancer by using AgNPs against cancer cell lines such as MCF-7, HEPG2, H9C2, HEK293 and H1975. The synthesized AgNPs were characterized by using UV-Vis spectroscopy, EDS, FT-IR, XRD, DLS, SEM and HRTEM with SAED patterns. The surface plasmon resonance (SPR) of AgNPs formed a peak centered at 427 nm by UV-Vis analysis. FTIR analysis reveals that existence of functional groups subjected to silver ions reduction to metallic silver. Crystalline form of the AgNPs was assessed by XRD analysis, four spectral peaks at 111, 200, 220, and 311 were formed and zeta potential peak was found at 28.5 mV indicating the higher stability. The size average diameter of the AgNPs was between 27 and 30 nm by TEM and SEM analysis was reveals the morphology of AgNPs as elongated, irregular and aggregated and some particles are spherical. EDX analysis confirmed the elemental composition of AgNPs with 81.43% Ag. The average diameter of AgNPs was found 21.49 nm in diameter and width was about 12.01 nm by DLS analysis. Cytotoxicity of AgNPs was investigated by using MTT, SRB assay and comet assay was performed as a genotoxicity. The results revealed that AgNPs decreased the viability of cancer cells in a concentration dependent pattern (50 to 350 µg/ml). The influence of AgNPs on cell cycle stop was studied on H1975, HEP-G2 and MCF-7 cells and found that AgNPs could induce sub G0 cell cycle arrest. The AgNPs was also induced DNA fragmentation confirms the DNA damage in nanoparticles treated cell lines. The anticancer action of nanoparticles was analyzed using proapoptotic and antiapoptotic caspase 8 and caspase 3 mRNA expression levels. Finally the results suggested that AgNPs is an effective anticancer agent which induces apoptosis in H1975, HEP-G2 and MCF-7 cells. Based on our studies, further identification of the major compounds of leaf extracts is acceptable.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00674-7.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"16"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817502","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":"Current opinion on pluripotent stem cell technology in Gaucher's disease: challenges and future prospects.","authors":"Pankaj Gurra, Raja Babu, Bhaskaranand Pancholi, Bibhash Chandra Mohanta, Debapriya Garabadu","doi":"10.1007/s10616-024-00687-2","DOIUrl":"10.1007/s10616-024-00687-2","url":null,"abstract":"<p><p>Gaucher's disease (GD) is a rare autosomal recessive genetic disorder caused by mutations in the <i>GBA1</i> gene. Mutations in the gene lead to the deficiency of glucocerebrosidase, an enzyme that helps in the breakdown of glucosylceramide (GlcCer) into ceramide and glucose. The lack of the enzyme causes GlcCer accumulation in macrophages, resulting in various phenotypic characteristics of GD. The currently available therapies, including enzyme replacement therapy and substrate reduction therapy, only provide symptomatic relief. However, they grapple with limitations in efficacy, accessibility, and potential side effects. These observations laid the foundation to search for new approaches in the management of GD. Induced pluripotent stem cells (iPSCs) technology emerges as a beacon of hope, offering novel avenues for future GD therapies. The true magic of iPSCs lies in their ability to differentiate into various cell types. By reprogramming patient-derived cells into iPSCs, researchers can generate personalized models that recapitulate the genetic and phenotypic characteristics of the GD. These models are valuable tools for dissecting intricate disease pathways, developing novel therapeutic targets, and enhancing the drug development process for GD. This review emphasizes the significance of iPSCs technology in GD management. Further, it addresses several challenges that are being encountered in the application of iPSC technology in the management of GD. In addition, it provides several insights into the future aspects of iPSC technology in the management of GD.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"26"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11680541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902674","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":"Evaluation of the Ki-67 labeling index on immediate pre-ablation biopsies as a predictive biomarker of local recurrence of colorectal cancer liver metastases.","authors":"Vlasios S Sotirchos, Efsevia Vakiani, Carlie Sigel, Rami Imam, Henry S Kunin, Timothy M Cooke, Mithat Gönen, Stephen B Solomon, Joseph P Erinjeri, Constantinos T Sofocleous","doi":"10.1007/s10616-024-00700-8","DOIUrl":"10.1007/s10616-024-00700-8","url":null,"abstract":"<p><p>The aim of this study was to evaluate if the Ki-67 labeling index (LI) on immediate pre-ablation biopsies of colorectal liver metastases (CLM) is associated with the presence of viable tumor cells in subsequent ablation zone biopsies and/or local tumor progression-free survival (LTPFS). Biopsies of CLM were performed before and after microwave ablation (MWA), as part of a prospective clinical trial between October 2013 and May 2019. Pre-ablation biopsy slides were examined for the Ki-67 LI using light microscopy. Ablation zone biopsy specimens were evaluated for the presence of viable tumor using hematoxylin-eosin and immunohistochemistry. Differences in CLM Ki-67 LI between positive and negative for viable tumor ablation zone biopsies were assessed using the Mann-Whitney U test. Biopsy, tumor and margin data were evaluated as predictors of LTPFS using Kaplan-Meier/Cox methods. Thirty-four patients with 48 CLM underwent biopsy before and after MWA. Sufficient tissue for Ki-67 labeling was obtained in 43/48 (89.6%) CLM. Viable tumor cells were detected in 11 ablation zones (22.9%). There was no significant difference in the CLM Ki-67 LI between the positive and negative for viable tumor ablation zones (mean: 69.2% vs. 64.3% respectively, p = 0.4). Adequate ablation zone margins (> 5 mm; p = 0.029) and negative ablation zone biopsies (p = 0.009) were significant predictors of longer LTPFS. <i>KRAS</i> status, tumor size and Ki-67 LI were not significant predictors of LTPFS. Complete tumor ablation (with adequate margins and negative ablation zone biopsies) is the most important factor in achieving local control of CLM, even for tumors exhibiting aggressive tumor biology.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"31"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11685365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913883","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":"E2F8-TPX2 axis regulates glycolysis and angiogenesis to promote progression and reduce chemosensitivity of liver cancer.","authors":"Xiao-Qing Li, Zhen-Rui Cao, Min Deng, Yun Qing, Lan Sun, Zhong-Jun Wu","doi":"10.1007/s10616-024-00655-w","DOIUrl":"10.1007/s10616-024-00655-w","url":null,"abstract":"<p><p>Liver cancer (LC) is a global health concern, marked by its high prevalence and mortality rates and known for its resistance to chemotherapy. The treatment of LC patients is facing great challenges. Targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a LC marker that has been discovered in recent years, and there are sporadic data suggesting that it has an impact on the level of chemoresistance, but the exact mechanism remains to be deciphered. Our investigation, grounded in bioinformatics strategies including the TCGA database, GEO database, K-M plot database, GSEA, Pearson correlation analysis, and detection of clinical samples, led to the identification of TPX2 and its upstream transcription factor E2F8 as differentially expressed elements in LC tissues. We also probed the role of the axis in glycolysis, angiogenesis, tumor progression, and chemoresistance in LC cells. This was achieved by a battery of molecular and cellular experiments, such as qRT-PCR, CCK-8, Transwell, flow cytometry, and angiogenesis assays. Both TPX2 and E2F8 were upregulated in LC tissues and cells with E2F8 being responsible for the upregulation of TPX2. Through bioinformatics analysis, we observed a significant enrichment of TPX2 in the glycolysis and angiogenesis pathways. Cell-based experiments corroborated these findings, demonstrating that TPX2 knockdown led to significant inhibition of glycolysis and angiogenesis, along with a suppression of the malignant progression of LC cells. This was mirrored by a reduction in the IC₅₀ values for cisplatin and apatinib to 0.8257 µM and 10.79 µM, respectively. In contrast, E2F8 overexpression reversed these effects in LC cells, increasing the IC₅₀ values to 3.375 and 16.06 µM, respectively. The E2F8-TPX2 axis promotes glycolysis and angiogenesis in LC cells, which in turn accelerates cancer progression and reduces chemosensitivity.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00655-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"76 6","pages":"817-832"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460027","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":"Retraction Note: MiR-522-3p inhibits proliferation and activation by regulating the expression of SLC31A1 in T cells.","authors":"Hengxiao Lu, Hao Wang, Peidao Sun, Jiang Wang, Shuhai Li, Tongzhen Xu","doi":"10.1007/s10616-024-00658-7","DOIUrl":"https://doi.org/10.1007/s10616-024-00658-7","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1007/s10616-021-00472-5.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"76 6","pages":"859"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460028","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":"MiR-133 promotes the multidrug resistance of acute myeloid leukemia cells (HL-60/ADR) to daunorubicin","authors":"Lin Liu, Kun Yu, Jingxing Yu, Wei Tao, Yueping Wei","doi":"10.1007/s10616-024-00656-9","DOIUrl":"https://doi.org/10.1007/s10616-024-00656-9","url":null,"abstract":"<p>This study aimed to explore the role and molecular mechanism of miR-133 in multidrug resistance in acute myeloid leukemia (AML) and provide a new theoretical basis for the treatment and prognosis of AML patients. We performed experiments at the cellular level. RT‒qPCR and Western blotting were used to detect gene and protein expression; cell viability was measured with CCK-8 assays; apoptosis was detected via flow cytometry; and a dual-luciferase reporter gene assay was used to verify the binding between miR-133 and CXCL12. In this study, we found that miR-133 was upregulated in HL-60/ADR multidrug-resistant cells. Functionally, the inhibition of miR-133 alleviated the resistance of HL-60/ADR cells to daunorubicin (DNR). After inhibiting miR-133 in HL-60/ADR cells treated with DNR, the expression of the intracellular drug resistance-related proteins MRP562 and P-gp was inhibited, cell proliferation decreased, and apoptosis increased. Mechanistically, the NF-κB signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-κB signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"31 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142258711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrolyzed cow colostrum extract (BCFM) inhibits alpha-MSH-induced melanogenesis in B16F1 cells via regulation of the MC1R-cAMP signaling pathway","authors":"Jae Hyeok Choi, Taeil Kwak, Heejung Shin, Yang Hee Jo, Junil Kim, Younghwa Kim, Junoh Kim, Woo-Ram Lee","doi":"10.1007/s10616-024-00657-8","DOIUrl":"https://doi.org/10.1007/s10616-024-00657-8","url":null,"abstract":"<p>Cow colostrum is the first milk produced after birth and is a rich natural source of nutrients, immunoglobulins, peptides, and growth factors. The bioconversion of milk and whey changes the immobilization and biochemical characterization. However, the cellular mechanism and the anti-melanin synthesis effects of hydrolyzed cow colostrum extract (BCFM) in alpha-MSH-induced B16F1 cells have not been examined. In this study, we investigated the anti-melanogenesis mechanism by examining the effects of BCFM in alpha-MSH-induced B16F1 cells. Cells were treated with BCFM in the presence or absence of alpha-MSH and co-cultured for 24, 48, and 72 h. The treatment of B16F1 cells with alpha-MSH resulted in the darkening of the color of the cells and induction of melanin synthesis. In addition, the expression levels of MC1R and cAMP, as well as phosphorylation levels of CREB and PKA, were increased by alpha-MSH treatment. However, concomitant treatment with BCFM resulted in a significant decrease in these factors and phosphorylated MITF. At the same time, the expressive amount of TRP-1 and tyrosinase was also decreased in B16F1 cells. These results demonstrate the potential of BCFM for the prevention of melanogenesis progression via the regulation of the MC1R-cAMP signaling pathway in alpha-MSH-induced B16F1 cells. The administration of BCFM suppressed the expression of TRP-1 and/or tyrosinase by regulating the CREB/MITF signaling pathways in the B16F1 cells. We propose that hydrolyzed cow colostrum extract (BCFM) is suitable for use as a novel active agent for skin whitening or pharmaceutical applications.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"65 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142258708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of combined blue light and 5-ALA on mitochondrial functions and cellular responses in B16F1 melanoma and HaCaT cells","authors":"Kazuomi Sato, Taiki Sato, Riku Hirotani, Munetsugu Bam","doi":"10.1007/s10616-024-00654-x","DOIUrl":"https://doi.org/10.1007/s10616-024-00654-x","url":null,"abstract":"<p>In this study, we investigated the effects of blue light and 5-aminolevulinic acid (5-ALA) co-treatment on B16F1 melanoma cells and HaCaT keratinocytes. We focused on cellular responses, including mitochondrial function, DNA integrity, and gene expression. Co-treatment significantly damaged the mitochondria, altered their morphology, induced mitochondrial membrane depolarization, increased intracellular reactive oxygen species, and led to cardiolipin peroxidation in both cell types. This approach promoted DNA fragmentation and apoptosis. However, blue light and co-treatment with 5-ALA did not enhance the formation of cyclobutane pyrimidine dimers, 6–4 photoproducts, or Dewar photoproducts. Moreover, it triggered complex, time-dependent changes in gene expression, particularly the upregulation of MMP-1 and p21 in HaCaT cells. Our findings revealed that blue light and 5-ALA co-treatment caused substantial cellular stress and damage, suggesting their therapeutic potential against melanoma and highlighting the need for caution and precision in their application to avoid harming normal cells. This underscores the necessity for further research to refine therapeutic approaches.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"68 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142184596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishing an evaluation system for T cell activation and anergy based on CD25 expression levels as an indicator","authors":"Sangwon Seo, Makoto Hattori, Tadashi Yoshida","doi":"10.1007/s10616-024-00651-0","DOIUrl":"https://doi.org/10.1007/s10616-024-00651-0","url":null,"abstract":"<p>T cell anergy refers to a state where T cells become unresponsive, playing an important role in several types of immune tolerance, such as oral tolerance. This tolerance is vital for preventing some diseases, including food allergies. Understanding the mechanism underlying T cell anergy is essential to addressing food allergies. Previous studies often identified anergic T cells by their decreased ability to produce cytokine compared to the control cells. In the studies, unstimulated or naïve T cells were commonly used as the control cells. These systems could evaluate the hyporesponsiveness of anergic T cells; however, it was challenging to distinguish whether the decrease in cytokine production by anergic T cells was owing to anergy induction or merely a temporarily response to a certain stimulation. This complexity arises because some T cell responses are temporarily suppressed, even by activating stimuli. Therefore, this study aims to explore a new evaluation index that can differentiate the responsiveness of activated T cells from that of anergic T cells compared to the control cells. It was demonstrated that CD25 expression levels serve as an appropriate indicator for distinguishing between T-cell activation and anergy. Conversely, cytokine-producing ability proved inadequate for this purpose. It was found that CD25 expression increased in activated T cells than in naïve T cells, whereas it decreased in anergic T cells after restimulation. This occurred despite decreased cytokine production in the activated and anergic T cells than in the naïve T cells. This new evaluation system, centered on CD25 expression, may help in identifying the mechanism for determining T cell activation and anergy.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"24 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142184597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00161 upregulated by M2-like tumor-associated macrophages promotes hepatocellular carcinoma progression by methylating HACE1 promoters","authors":"Yujunya Zhang, Shuying Chen, Lina You, Zhanao He, Peidong Xu, Wukui Huang","doi":"10.1007/s10616-024-00653-y","DOIUrl":"https://doi.org/10.1007/s10616-024-00653-y","url":null,"abstract":"<p>M2-like tumor-associated macrophages (M2-TAM) played an essential part in hepatocellular carcinoma (HCC) progression. Long intergenic noncoding RNA 00161 (LINC00161), is a long non-coding RNA, that was related to HCC development. However, the relationship between LINC00161 and TAM remains indistinct. HCC cells were cocultured with an M2-like conditioned medium (M2-CM). cell counting kit-8 (CCK-8), plate cloning, cell scratch, and transwell assay evaluated cell biological activities of HCC cells. The interactions among molecules were analyzed by chromatin immunoprecipitation (CHIP), dual-luciferase reporter, and RNA immunoprecipitation (RIP). The methylation status of HECT domain and ankyrin repeat-containing, E3 ubiquitin protein ligase 1 (HACE1) was evaluated using methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP). The xenograft model was established in vivo using subcutaneous nude mice. Histological analyses were performed using hematoxylin–eosin (HE) staining. The expression of molecules was determined using immunohistochemistry (IHC), western blot and quantitative real-time PCR (qPCR). LINC00161 expression was promoted in HCC. LINC00161 knockdown significantly reduced HCC cell proliferation, migration, and invasion. Additionally, M2-TAM stimulated LINC00161 transcription and expression in HCC cells by secreting hepatocyte growth factor (HGF) to activate the Met/NFκB pathway. LINC00161 suppressed HACE1 expression, and knockdown of LINC00161 decreased the methylation on the HACE1 promoter. Meanwhile, a binding relationship between the enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and HACE1 was observed. LINC00161 overexpression increased the binding of EZH2 on the HACE1 promoter region. Furthermore, LINC00161 knockdown suppressed tumor growth in vivo and induced HACE1 expression by inhibiting its methylation. LINC00161, induced by M2-TAM, played a pivotal role in contributing to HCC development by recruiting EZH2 to promote the methylation of HACE1. This underscores the significant involvement of LINC00161 in mediating the progression of HCC.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"41 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142184619","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}