Human Cell最新文献_第3页

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

Establishment and characterization of NCC-PS2-C1: a novel cell line of high-grade pleomorphic spindle cell sarcoma, most consistent with myxofibrosarcoma. NCC-PS2-C1：高级别多形性梭形细胞肉瘤的新细胞系的建立和表征，与黏液纤维肉瘤最一致。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-20 DOI: 10.1007/s13577-025-01217-8

Shuhei Iwata, Rei Noguchi, Julia Osaki, Yuki Adachi, Yomogi Shiota, Shuhei Osaki, Shogo Nishino, Akihiko Yoshida, Seiji Ohtori, Akira Kawai, Tadashi Kondo

{"title":"Establishment and characterization of NCC-PS2-C1: a novel cell line of high-grade pleomorphic spindle cell sarcoma, most consistent with myxofibrosarcoma.","authors":"Shuhei Iwata, Rei Noguchi, Julia Osaki, Yuki Adachi, Yomogi Shiota, Shuhei Osaki, Shogo Nishino, Akihiko Yoshida, Seiji Ohtori, Akira Kawai, Tadashi Kondo","doi":"10.1007/s13577-025-01217-8","DOIUrl":"https://doi.org/10.1007/s13577-025-01217-8","url":null,"abstract":"Pleomorphic sarcoma (PS) is a heterogeneous group of malignant mesenchymal tumors that lack specific histological differentiation. PS is characterized by genetic instability and diversity and unique histological features such as pronounced morphologic pleomorphism. PS is one of the most common soft tissue sarcomas. Complete surgical resection remains the only curative treatment and is often combined with neoadjuvant radiotherapy. Effective systemic chemotherapy is yet to be established, and PS frequently recurs locally and metastasizes to the lungs. Patient-derived cancer cell lines are invaluable tools for basic and preclinical research for developing novel chemotherapies. Herein, we report a high-grade pleomorphic spindle cell sarcoma, most consistent with myxofibrosarcoma cell line, NCC-PS2-C1, which was derived from a primary tumor specimen. NCC-PS2-C1 cells exhibited a range of copy number alterations. This cell line demonstrated consistent proliferation, spheroid formation, and invasive capabilities in vitro. Drug screening using NCC-PS2-C1 cells revealed that cobimetinib, crenolanib, and ixazomib were effective against PS. In conclusion, we established NCC-PS2-C1 cells from primary tumors of PS. This cell line is a valuable resource for developing novel chemotherapies.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"93"},"PeriodicalIF":3.4,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009489","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

Hyaluronic acid-modified milk exosomes carrying ZNF516 inhibit ABCC5 and contribute to pemetrexed sensitivity in lung adenocarcinoma. 携带ZNF516的透明质酸修饰的乳外泌体抑制ABCC5并有助于肺腺癌培美曲塞的敏感性。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-19 DOI: 10.1007/s13577-025-01219-6

Hui Li, Yanyan Sun, Jue Wang, Zhiwu Wang, Lan Wu, Jie Lei, Ying Gao

{"title":"Hyaluronic acid-modified milk exosomes carrying ZNF516 inhibit ABCC5 and contribute to pemetrexed sensitivity in lung adenocarcinoma.","authors":"Hui Li, Yanyan Sun, Jue Wang, Zhiwu Wang, Lan Wu, Jie Lei, Ying Gao","doi":"10.1007/s13577-025-01219-6","DOIUrl":"https://doi.org/10.1007/s13577-025-01219-6","url":null,"abstract":"Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Milk-derived exosomes (mEXOs) have critical roles in cancer treatment. This paper explores the effects of hyaluronic acid (HA)-modified mEXOs (HA-mEXOs) in LUAD. HA-mEXOs were isolated and prepared, and PMX-resistant cells were developed. CCK-8, colony formation, Transwell, flow apoptosis, xenograft tumor assay, immunohistochemistry, and TUNEL experiments were conducted to explore the impact of mEXOs and HA-mEXOs on malignant behaviors and PMX sensitivity. The role of ZNF516 and ABCC5 on malignant behaviors and PMX sensitivity was investigated by shRNA lentiviral infection. HA modification increased the uptake and affinity of LUAD cells for mEXOs. mEXOs induced PMX-resistant LUAD cell sensitivity and inhibited their malignant behaviors. mEXOs enhanced PMX sensitivity and inhibited tumor growth. HA-mEXOs had superior effects to mEXOs. ZNF516 was lowered in LUAD-resistant cells and upregulated by mEXOs. ZNF516 bound to the ABCC5 promoter and repressed its transcriptional activation. The combined knockdown of ZNF516 reversed the antitumor benefits of mEXOs. HA-mEXOs-carrying ZNF516 enhance ZNF516 levels in LUAD/PMX cells and repress ABCC5, which in turn induces cell sensitivity to PMX and inhibits LUAD progression.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"92"},"PeriodicalIF":3.4,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144058719","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

LncRNA OLMALINC promotes osteosarcoma progression through USP1-mediated autophagy suppression. LncRNA OLMALINC通过usp1介导的自噬抑制促进骨肉瘤进展。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-18 DOI: 10.1007/s13577-025-01221-y

Jianping Li, Bo Yu, Zhaowen Xue, Yiping Liang, Shanchuang Chen, Tao Gui, Zitao Liu, Lei Zhang, Rui Peng

{"title":"LncRNA OLMALINC promotes osteosarcoma progression through USP1-mediated autophagy suppression.","authors":"Jianping Li, Bo Yu, Zhaowen Xue, Yiping Liang, Shanchuang Chen, Tao Gui, Zitao Liu, Lei Zhang, Rui Peng","doi":"10.1007/s13577-025-01221-y","DOIUrl":"https://doi.org/10.1007/s13577-025-01221-y","url":null,"abstract":"Osteosarcoma (OS) remains a challenging malignancy with poor prognosis, especially in metastatic or recurrent cases. Despite progress, the molecular mechanisms driving OS, particularly the regulation of autophagy, are not fully understood. Here, through integrated analysis of single-cell and transcriptomic data, we identify a novel long non-coding RNA (lncRNA), OLMALINC, as a critical autophagy regulator in OS. OLMALINC is significantly upregulated in OS tissues, with its expression correlating to poor clinical outcomes. Functional studies show that altering OLMALINC expression impacts OS cell progression and autophagy. Mechanistically, transcriptome analysis and RNA immunoprecipitation reveal Ubiquitin-Specific Peptidase 1 (USP1) as a direct downstream target of OLMALINC. The OLMALINC-USP1 axis inhibits autophagy and activates the hypoxia-inducible factor 1 (HIF-1α) pathway, promoting OS progression. Therapeutically, combining the USP1 inhibitor ML-323 with doxorubicin demonstrated synergistic anti-tumor effects in vitro and in vivo, enhancing autophagy and apoptosis while inhibiting tumor growth. These findings uncover a novel OLMALINC-USP1-HIF-1α axis in OS progression and highlight the potential of combining autophagy modulation with chemotherapy for improved therapeutic outcomes.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"91"},"PeriodicalIF":3.4,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045119","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

Clinical characteristics and induced pluripotent stem cells (iPSCs) disease model of Harel-Yoon syndrome caused by compound heterozygous ATAD3A variants. ATAD3A复合杂合变异体致Harel-Yoon综合征临床特征及诱导多能干细胞（iPSCs）疾病模型

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-17 DOI: 10.1007/s13577-025-01214-x

Ziyi Jiang, Hongyu Chen, Xianghong Zhang, Xiaoling Jiang, Zhengqing Tong, Jingjing Ye, Shanshan Shi, Xucong Shi, Fengxia Li, Weiqin Shao, Qiang Shu, Lan Yu

{"title":"Clinical characteristics and induced pluripotent stem cells (iPSCs) disease model of Harel-Yoon syndrome caused by compound heterozygous ATAD3A variants.","authors":"Ziyi Jiang, Hongyu Chen, Xianghong Zhang, Xiaoling Jiang, Zhengqing Tong, Jingjing Ye, Shanshan Shi, Xucong Shi, Fengxia Li, Weiqin Shao, Qiang Shu, Lan Yu","doi":"10.1007/s13577-025-01214-x","DOIUrl":"https://doi.org/10.1007/s13577-025-01214-x","url":null,"abstract":"ATPase family AAA-domain-containing protein 3 A (ATAD3A) is enriched on the mitochondrial membrane and is essential to the maintenance of mitochondrial structure and function. Variants of the ATAD3A gene can lead to Harel-Yoon syndrome (HAYOS), a developmental defect in neurological, cardiovascular, and other systems. This study aims to develop induced pluripotent stem cells (iPSCs) from the somatic cells of a patient (ZJUCHYLi001-A) and a negative control (ZJUCHYLi002-A) as effective tools for further investigations into the etiology of ATAD3A variant-related disease. We described and analyzed the clinical manifestations of the proband and her family members. Somatic cells from the proband and a negative control were collected and reprogrammed into iPSCs. Furthermore, we measured the ATAD3A expression levels in the iPSCs to confirm the validity of these cell lines. The proband and her elder sister were both critically ill and harbored compound heterozygous ATAD3A variants (F459S/T498 Nfs* 13). Their parents were carriers of these variants without any clinical manifestations. Both variants are located on the ATPase domain of the ATAD3A protein. Cell lines ZJUCHYLi001-A and ZJUCHYLi002-A presented typical features of pluripotent stem cells. The ATAD3A expression levels of ZJUCHYLi001-A were significantly reduced compared with ZJUCHYLi002-A. This study generated iPSCs from a patient with compound heterozygous variants of ATAD3A and a negative control as valuable tools for clarifying the molecular mechanisms underlying ATAD3A variant-related diseases.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"90"},"PeriodicalIF":3.4,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144054305","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

The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential. MICAL2在癌症进展中的作用：机制、挑战和治疗潜力。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-16 DOI: 10.1007/s13577-025-01212-z

Ruiying Wang, Zhijuan Hou, Xiao Gao, Binyan Wu, Huizheng Hu, Hongpei Wu

{"title":"The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.","authors":"Ruiying Wang, Zhijuan Hou, Xiao Gao, Binyan Wu, Huizheng Hu, Hongpei Wu","doi":"10.1007/s13577-025-01212-z","DOIUrl":"https://doi.org/10.1007/s13577-025-01212-z","url":null,"abstract":"Cancer is the greatest threat to public health worldwide and a major cause of human death. Compared with conventional chemotherapy, agents targeting key oncogenic drivers and signaling mechanisms are becoming an attractive treatment strategy. Molecule interacting with CasL 2 (MICAL2) is a flavin protein monooxygenase family protein that interacts with CasL2 and is involved in cytoskeletal redox regulation, axon-directed regulation, cell transport, and apoptosis. MICAL2 induces F-actin depolymerization through REDOX modification, thereby promoting the expression of epithelial-mesenchymal transition (EMT)-related proteins and inducing cancer cell invasion and proliferation. Mechanistically, MICAL2 induces EMT by regulating the serum response factor (SRF)/myocardin-related transcription factor A (MRTF-A) signaling pathway, and the semaphorin/plexin pathway and inducing reactive oxygen species (ROS) production. Recent studies have shown that MICAL2 is highly expressed in tumors, accelerates tumor progression, and is a novel tumor-promoting factor. This article summarizes recent research findings to review the biological functions of MICAL2, the potential mechanisms related to cancer progression, and discusses the challenges and prospects in this area, providing a new theoretical basis for clinical molecular targeted therapy for cancer.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"89"},"PeriodicalIF":3.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022266","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

SIX1 enhances aerobic glycolysis and progression in cervical cancer through ENO1. SIX1通过ENO1促进子宫颈癌的有氧糖酵解和进展。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-15 DOI: 10.1007/s13577-025-01215-w

Xuelian Liu, Hang Ren, Anjin Wang, Ziyan Liang, Su Min, Shijie Yao, Shimeng Wan, Yang Gao, Hua Wang, Hongbing Cai

{"title":"SIX1 enhances aerobic glycolysis and progression in cervical cancer through ENO1.","authors":"Xuelian Liu, Hang Ren, Anjin Wang, Ziyan Liang, Su Min, Shijie Yao, Shimeng Wan, Yang Gao, Hua Wang, Hongbing Cai","doi":"10.1007/s13577-025-01215-w","DOIUrl":"https://doi.org/10.1007/s13577-025-01215-w","url":null,"abstract":"Cervical cancer is a significant threat to women's health, and its incidence in China has been increasing in recent years. Treating advanced and recurrent cervical cancer has become increasingly challenging, highlighting the urgent need to identify new therapeutic targets for this disease. SIX1 is associated with cell proliferation, metastasis, and chemoresistance in various human malignancies. SIX1 overexpression in cervical cancer tissues has been linked to increased clinical stage and lymph node metastasis; however, the regulatory function of SIX1 in cervical cancer remains largely unexplored. In this study, we found that SIX1 promotes cervical cancer cell proliferation, invasion, and migration by enhancing glucose metabolism. Additionally, SIX1 was shown to influence the glycolytic process in cervical cancer by upregulating GLUT1, PFK1, PGK1, ENO1, and PKM2 expression. Furthermore, we identified a binding site for SIX1 in the ENO1 promoter region, demonstrating that SIX1 has a regulatory effect. These results suggest that SIX1 regulates proliferation and glucose metabolism in cervical cancer cells by promoting the transcription of key glycolytic enzymes, such as ENO1. Understanding this regulatory mechanism is crucial for identifying potential therapeutic targets for cervical cancer.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"88"},"PeriodicalIF":3.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051682","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

The influence of cell source on the senescence of human mesenchymal stem/stromal cells. 细胞来源对人间充质干细胞/基质细胞衰老的影响。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-12 DOI: 10.1007/s13577-025-01213-y

Seyed Mehdi Hoseini, Fateme Montazeri

引用次数: 0

RFX5 promotes the progression of triple-negative breast cancer through transcriptional activation of JAG1. RFX5通过转录激活JAG1促进三阴性乳腺癌的进展。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-12 DOI: 10.1007/s13577-025-01216-9

Chenhao Li, Xin Wang, Dongliang Shi, Meng Yang, Wenhua Yang, Liang Chen

{"title":"RFX5 promotes the progression of triple-negative breast cancer through transcriptional activation of JAG1.","authors":"Chenhao Li, Xin Wang, Dongliang Shi, Meng Yang, Wenhua Yang, Liang Chen","doi":"10.1007/s13577-025-01216-9","DOIUrl":"https://doi.org/10.1007/s13577-025-01216-9","url":null,"abstract":"Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by high recurrence rates, low survival rates, and a lack of therapeutic targets. Regulatory Factor X5 (RFX5) is a critical transcription factor during tumor progression. However, the role of RFX5 involving breast cancer or TNBC has not been studied. This study obtained 60 tumor samples of TNBC for analysis and ascertained that RFX5 is linked with the severe stage. We constructed RFX5 knockdown and overexpression models involving TNBC cells. RFX5 overexpression enhanced TNBC cell proliferation by detecting cell vitality and replication of DNA and analyzing cell cycle data. RFX5 facilitated cell migration and invasion, which were determined by wound healing and Transwell assays. The anti-apoptotic RFX5 properties were confirmed with Hoechst staining and Annexin V/PI apoptosis assays. The Notch pathway was activated in TNBC, and Jagged canonical Notch ligand 1 (JAG1) could enhance TNBC growth and metastasis. RFX5 upregulation elevated JAG1 mRNA and protein levels. Chromatin immunoprecipitation and luciferase reporter assays indicated that RFX5 promoted the transcriptional activation of JAG1 by binding the promoter (- 1890/+ 15 or - 1359/+ 15 area). JAG1 knockdown reduced RFX5-induced expression of Notch signaling-related factors Notch1, NICD, and Hes1. This paper indicated that RFX5 is a transcription factor for JAG1 and established that RFX5 could activate the Notch pathway via transcriptional activation of JAG1 and promote TNBC progression. Targeting RFX5 could be a promising therapeutic approach against TNBC.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 3","pages":"86"},"PeriodicalIF":3.4,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023909","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

Ovarian Leydig cells and neural crests. 卵巢间质细胞和神经嵴。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-04-12 DOI: 10.1007/s13577-025-01210-1

José-Luis Carrasco-Juan, Olga Tapia, Miriam González-Gómez, Abian Vega-Falcón, Sonia García-Hernández, Alexis Rufino-Gómez, Rafael Méndez-Medina, Hugo Álvarez-Arguelles Cabrera

引用次数: 0