Human Cell最新文献_第2页

Potential reverse functions of GOLPH3 and GOLPH3L in pyroptotic cell death, with implications in resistance to radiotherapy and chemotherapy. GOLPH3和GOLPH3L在热腐细胞死亡中的潜在逆转功能，与放疗和化疗耐药性有关。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-22 DOI: 10.1007/s13577-025-01236-5

Caglar Berkel

引用次数: 0

Establishment and characterization of patient-derived tongue squamous cell carcinoma cell lines. 患者源性舌鳞状细胞癌细胞系的建立与鉴定。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-20 DOI: 10.1007/s13577-025-01231-w

Priyanka Joshi, Sanjay Bane, Pankaj Chaturvedi, Poonam Gera, Sanjeev K Waghmare

{"title":"Establishment and characterization of patient-derived tongue squamous cell carcinoma cell lines.","authors":"Priyanka Joshi, Sanjay Bane, Pankaj Chaturvedi, Poonam Gera, Sanjeev K Waghmare","doi":"10.1007/s13577-025-01231-w","DOIUrl":"10.1007/s13577-025-01231-w","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is a common carcinoma in Indian population, wherein one-third of global OSCC cases are from India. The five-year survival rate is poor due to late diagnosis. Oral tongue squamous cell carcinoma (OTSCC) is the second-most common OSCC. An in vitro cell line model is a valuable tool to get a deeper understanding of the molecular mechanisms involved in therapy resistance and disease progression. We report establishment of three OTSCC cell lines from advanced stage treatment naïve Indian patient samples, such as ACOTSC120, ACOSTC132, and ACOTSC140. All three OTSCC cell lines showed epithelial morphology, which was confirmed by Keratin-14 staining. The cell lines showed in vitro spheroid-forming and in vivo tumorigenic potential. The STR of the cell lines ensured their human origin and novelty when compared to DSMZ cell line database. The karyotype of the cell lines showed aneuploidy and further confirmed their human origin. These cell lines showed the presence of cancer stem cell (CSCs) population, i.e., the ALDHbr/CD44+ population. These cell lines thus provide a model to help understand the biology of disease and its progression.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 4","pages":"102"},"PeriodicalIF":3.4,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12092557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 role of microglia in the development of diabetic retinopathy and its potential clinical application. 小胶质细胞在糖尿病视网膜病变发展中的作用及其潜在的临床应用。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-20 DOI: 10.1007/s13577-025-01226-7

Tingting Lu, Jiameng Shang, Shengdan Pu, Yuxin Xu, Xiaotong Sun, Xinyuan Gao

{"title":"The role of microglia in the development of diabetic retinopathy and its potential clinical application.","authors":"Tingting Lu, Jiameng Shang, Shengdan Pu, Yuxin Xu, Xiaotong Sun, Xinyuan Gao","doi":"10.1007/s13577-025-01226-7","DOIUrl":"https://doi.org/10.1007/s13577-025-01226-7","url":null,"abstract":"Lately, research on the function of microglia in diabetic retinopathy (DR) is becoming increasingly focused. Microglia are immune cells that dwell in the central nervous system and are crucial to the pathophysiology of DR. According to studies, a hyperglycemic environment can activate microglia, bringing them out of a resting state to an active state. This allows them to release a variety of inflammatory factors and chemokines, which can then cause retinal inflammatory reactions. When it comes to angiogenesis in DR, activated microglia release a variety of angiogenic substances, such as vascular endothelial growth factor (VEGF), to create aberrant new blood vessels. Moreover, microglia contribute to the retina's oxidative stress process by generating and releasing reactive oxygen and nitrogen-free radicals, which exacerbates retinal damage. Researchers have proposed a variety of strategies for the activation of microglia and the inflammatory response it triggers. By inhibiting the excessive activation of microglia and reducing the release of inflammatory factors, the inflammatory response and damage to the retina can be alleviated. Drugs that interfere with retinal microglia can also be used to regulate vascular damage and inhibit the formation of new blood vessels. In addition, antioxidants are used to remove reactive oxygen and free radicals, reduce oxidative stress levels, and protect retinal cells. These therapeutic strategies aim to achieve the purpose of treating DR by regulating the function of microglia. Thus, we highlight the possibility that therapy aimed at microglia could offer fresh ideas for treating DR.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 4","pages":"101"},"PeriodicalIF":3.4,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sunitinib-resistant renal cell carcinoma cell-derived exosomes promote facilitation of tumor progression via secretion of the lncRNA SNHG16. 舒尼替尼耐药肾细胞癌细胞源性外泌体通过分泌lncRNA SNHG16促进肿瘤进展。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-13 DOI: 10.1007/s13577-025-01228-5

WeiLijiang Saimaiti, Jun Ma, Paluoke Dilimulati, Yujie Wang

{"title":"Sunitinib-resistant renal cell carcinoma cell-derived exosomes promote facilitation of tumor progression via secretion of the lncRNA SNHG16.","authors":"WeiLijiang Saimaiti, Jun Ma, Paluoke Dilimulati, Yujie Wang","doi":"10.1007/s13577-025-01228-5","DOIUrl":"https://doi.org/10.1007/s13577-025-01228-5","url":null,"abstract":"Renal cell carcinoma (RCC) is one of the most common tumors of high malignancy in the urological system. Sunitinib is commonly used to treat RCC, while drug resistance severely limited the therapeutic efficacy. Tumor-derived exosomes play important roles in facilitating cancer development. However, the role of drug-resistant tumor-derived exosomes in tumorigenesis and resistance of RCC has not been elucidated. Here we isolated sunitinib-sensitive/resistant RCC cells-derived exosomes, characterized by transmission electron microscopy (TEM) and western blot. Furthermore, co-culture experiments were performed and we found that sunitinib-resistant RCC cells-derived exosomes (R-exos) promoted cell proliferation and upregulated proliferation-related genes cyclin D1 (CCND1) and proliferating cell nuclear antigen (PCNA) expression, and inhibited apoptosis and the expression of Bax and Caspase-3 of sunitinib-resistant RCC (RCC/R) cells by delivering lncRNA small nuclear RNA host gene 16 (SNHG16). In resistant cell-derived xenograft (CDX-R) models, R-exos induced tumor growth in vivo, while knockdown of SNHG16 effectively diminished the tumorigenesis of RCC. Moreover, SNHG16 positively regulated the expression of trophinin associated protein (TROAP) by sponging miR-106a-5p in RCC cells, whereas inhibition of miR-106a-5p or overexpression of TROAP greatly reversed the suppression of tumorigenesis and sunitinib resistant by silencing SNHG16. R-exos lncRNA SNHG16 promoted sunitinib resistant and malignant progress by regulating the miR-106a-5p/TROAP axis, and targeting SNHG16/miR-106a-5p/TROAP axis may be a novel therapeutic approach for sunitinib-treated patients of RCC.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 4","pages":"100"},"PeriodicalIF":3.4,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Advanced glycation end products alter the structural integrity, increase the permeability and transform the biocompatibility of collagen within the peritoneal membrane. 晚期糖基化终产物改变了腹膜内胶原的结构完整性，增加了通透性并改变了其生物相容性。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-12 DOI: 10.1007/s13577-025-01229-4

Makoto Fukuda, Yusuke Chiwata, Takayuki Narita, Maki Yoshihara, Hiroyuki Morimoto, Ayako Takamori, Shota Shibuki, Rinko Hinami, Ayano Ishibashi, Akinori Nagashima, Motoaki Miyazono, Shigehisa Aoki

{"title":"Advanced glycation end products alter the structural integrity, increase the permeability and transform the biocompatibility of collagen within the peritoneal membrane.","authors":"Makoto Fukuda, Yusuke Chiwata, Takayuki Narita, Maki Yoshihara, Hiroyuki Morimoto, Ayako Takamori, Shota Shibuki, Rinko Hinami, Ayano Ishibashi, Akinori Nagashima, Motoaki Miyazono, Shigehisa Aoki","doi":"10.1007/s13577-025-01229-4","DOIUrl":"https://doi.org/10.1007/s13577-025-01229-4","url":null,"abstract":"In patients undergoing long-term peritoneal dialysis, the peritoneal accumulation of advanced glycation end-products (AGEs) due to the Maillard reaction has long been acknowledged as problematic, although the underlying mechanisms remain insufficiently understood. Recognizing collagen as both a principal substrate for AGEs deposition and a vital cellular scaffold, we developed an innovative procedure that induces the Maillard reaction in collagen at near-physiological temperatures, enabling systematic evaluations of its structural and functional modifications. Our findings reveal that Maillard reaction-treated collagen exhibits markedly increased permeability to small- and medium-sized molecules. Furthermore, this denatured collagen diminishes the proliferative capacity of adherent mesothelial cells, implicating glycation-induced alterations in collagen in the progressive deterioration of peritoneal membrane function during extended dialysis. By illuminating previously uncharacterized morphological and functional shifts in collagen triggered by the Maillard reaction, our model provides critical insights that will enhance the safety of peritoneal dialysis and inform the development of novel therapeutic strategies.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 4","pages":"99"},"PeriodicalIF":3.4,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Establishment and characterization of Cri Du Chat neuronal stem cells: a novel promising resource to study the syndrome. Cri Du Chat神经干细胞的建立和表征：研究该综合征的一个新的有前途的资源。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-09 DOI: 10.1007/s13577-025-01230-x

Giovanna Piovani, Rosalba Monica Ferraro, Silvia Clara Giliani

{"title":"Establishment and characterization of Cri Du Chat neuronal stem cells: a novel promising resource to study the syndrome.","authors":"Giovanna Piovani, Rosalba Monica Ferraro, Silvia Clara Giliani","doi":"10.1007/s13577-025-01230-x","DOIUrl":"https://doi.org/10.1007/s13577-025-01230-x","url":null,"abstract":"The Cri Du Chat (CdC) Syndrome is a rare chromosome disease condition resulting from variable size deletion occurring on the short arm of one of the chromosomes 5. This disorder, which affects one in 50,000 births, is responsible for developmental retardation, the mechanism of which has remained unexplained. TERT, SEMA5 A, CTNND2, TPPP, mapped in chromosome 5 short arm, are known to be expressed in the brain, and to play a role in the development of the nervous system, oligodentrocytes and in the regulation of glutamatergic and dopaminergic synaptic transmission. It is critical to understand how their haploinsufficiency might affect the development and presentation of the disease. In the absence of an animal model and of significant accessible, human tissue, human pluripotent stem cells (iPSC) directly reprogrammed from patient somatic cells open a new area of disease modeling as they can virtually be differentiated into any cell type. Our study reports, for the first time, the generation of neuronal stem cells (NSCs) from CdC-iPSCs line and in addition, subsequent differentiation into a heterogeneous population of neurons. Gene expression of the mentioned and single copy deleted genes was also evaluated by comparing their expression level in iPSC, NSCs and neuron lines. The present research represents the first and the most innovative approach, to create an in vitro CdC neuronal model to have a new translational framework to study the pathologic processes.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 4","pages":"98"},"PeriodicalIF":3.4,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12064636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Screening of pivotal oncogenes modulated by DNA methylation in hepatocellular carcinoma and identification of atractylenolide I as an anti-cancer drug. 肝癌DNA甲基化调控的关键癌基因筛选及白术内酯I抗癌药物的鉴定。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-05-05 DOI: 10.1007/s13577-025-01224-9

Yang Zhi, Tong Qiaoyun

{"title":"Screening of pivotal oncogenes modulated by DNA methylation in hepatocellular carcinoma and identification of atractylenolide I as an anti-cancer drug.","authors":"Yang Zhi, Tong Qiaoyun","doi":"10.1007/s13577-025-01224-9","DOIUrl":"https://doi.org/10.1007/s13577-025-01224-9","url":null,"abstract":"This study was performed to identify crucial oncogenes modulated by DNA methylation in hepatocellular carcinoma (HCC) and look for new drugs for HCC treatment. The data of TCGA-LIHC cohort were obtained from UCSC database. Weighted gene co-expression network analysis and multiple machine learning algorithms were applied to screen the crucial prognosis-related genes in HCC. Then these genes were further screened by DNA methylation status. Ten-eleven translocation 1 (TET1) was overexpressed in HCC cell lines, and its biological functions and regulatory effects on the oncogenes were explored by qPCR, methylation-specific polymerase chain reaction, cell viability assay, Western blot, etc. Molecular docking was applied to evaluate the binding affinity between atractylenolide I (AT-I) and TET1, and the tumor-suppressive functions of AT-I were examined with both in vitro and in vivo models. In this work, 12 crucial genes related to HCC prognosis were obtained, among which six genes were with differential methylation status in HCC tissues, including AKR1B10, ALPK3, NQO1, NT5DC2, SFN, and SPP1. The expression levels of ALPK3 and NT5DC2 were positively regulated by TET1, the crucial mediator of demethylation. TET1 overexpression increased the viability and stemness of HCC cells. AT-I had good binding affinity with TET1, and repressed its activity. AT-I promoted the methylation of ALPK3 and NT5DC2 promoter regions, and reduced their expression, and repressed the growth of HCC cells. In summary, DNA methylation contributes to HCC progression, and AT-I represses the malignancy of HCC cells by inhibiting TET1-mediated abnormal DNA demethylation.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 4","pages":"97"},"PeriodicalIF":3.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Deficiency of synaptotagmin-1 aggravates pressure overload-induced cardiac hypertrophy and dysfunction via the p38 MAPK signaling pathway in mice. synaptotagmin-1缺乏可通过p38 MAPK信号通路加重小鼠压力过载诱导的心脏肥厚和功能障碍。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-25 DOI: 10.1007/s13577-025-01220-z

Jing Shen, Junqiu Miao, Lifei Wu, Deping Wang, Guang Li, Haixiong Wang, Jimin Cao

{"title":"Deficiency of synaptotagmin-1 aggravates pressure overload-induced cardiac hypertrophy and dysfunction via the p38 MAPK signaling pathway in mice.","authors":"Jing Shen, Junqiu Miao, Lifei Wu, Deping Wang, Guang Li, Haixiong Wang, Jimin Cao","doi":"10.1007/s13577-025-01220-z","DOIUrl":"https://doi.org/10.1007/s13577-025-01220-z","url":null,"abstract":"Cardiac hypertrophy is a major risk factor for heart failure and sudden cardiac death, but its molecular mechanisms have not been well clarified. Synaptotagmin-1 (SYT1) is an important regulator of exocytosis and apoptosis and has been found expressed in the myocardium, while its functions in heart diseases have rarely been studied. Here, we investigated the role and mechanism of SYT1 in pressure overload-induced cardiac hypertrophy. Transverse aortic constriction (TAC) surgeries were performed to induce cardiac hypertrophy in global Syt1 knockout (Syt1+/-) mice and C57BL/6J wild-type (WT) littermates in vivo, with respective sham mice as negative controls. Cardiomyocyte hypertrophy was induced by angiotensin II (Ang II) in H9C2 cells in vitro. The results showed that SYT1 expression was significantly upregulated in WT-TAC mice and in Ang II-treated H9C2 cells. Blocking angiotensin receptor by losartan decreased SYT1 expression in Ang II-treated H9C2 cells. Syt1+/- mice showed significantly exacerbated cardiac hypertrophy, dysfunction, fibrosis, apoptosis and phosphorylation of myocardial p38 MAPK in response to TAC compared to WT mice. Knocking down SYT1 using siRNA in H9C2 cells aggravated Ang II-induced cell hypertrophy and apoptosis, and also enhanced p38 MAPK phosphorylation. Inhibition of p38 MAPK by SB203580 significantly alleviated the hypertrophy and apoptosis in Ang II-treated H9C2 cells. We conclude that deficiency of SYT1 aggravates pressure overload-induced cardiac hypertrophy via the p38 MAPK signaling pathway. The study elucidates a novel role of SYT1 in cardiac remodeling.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"96"},"PeriodicalIF":3.4,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12031904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Generation of human induced pluripotent stem cell lines derived from a patient carrying an intragenic deletion in the NFIA gene. 从携带NFIA基因基因内缺失的患者身上衍生的人类诱导多能干细胞系。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-23 DOI: 10.1007/s13577-025-01222-x

Ning Zhou, Shengnan Zhang, Chunli Wang, Bixia Zheng, Aihua Zhang, Wei Zhou

引用次数: 0

Retraction Note: RCC2 contributes to tumor invasion and chemoresistance to cisplatin in hepatocellular carcinoma. 注：在肝细胞癌中，RCC2参与肿瘤侵袭和顺铂化疗耐药。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-22 DOI: 10.1007/s13577-025-01223-w

Qingmin Chen, Peiqiang Jiang, Baoxing Jia, Yahui Liu, Ze Zhang

引用次数: 0