Human Cell最新文献

{"title":"Fetal adnexa-derived allogeneic mesenchymal stem cells for cardiac regeneration: the future trend of cell-based therapy for age-related adverse conditions.","authors":"Fazel Gorjipour, Sepideh Bohloolighashghaei, Mohammadjavad Sotoudeheian, Hamidreza Pazoki Toroudi","doi":"10.1007/s13577-025-01190-2","DOIUrl":"10.1007/s13577-025-01190-2","url":null,"abstract":"<p><p>Heart failure is known as the leading cause of mortality and morbidity in adults, not only in USA but worldwide. Since the world's population is aging, the burden of cardiovascular disorders is increasing. Mesenchymal stem/stromal cells (MSCs) from a patient's bone marrow or other tissues have been widely used as the primary source of stem cells for cellular cardiomyoplasty. The incongruencies that exist between various cell-therapy approaches for cardiac diseases could be attributed to variations in cell processing methods, quality of the process, and cell donors. Off-the-shelf preparations of MSCs, enabled by batch processing of the cells and controlled cell processing factories in regulated facilities, may offer opportunities to overcome these problems. In this study, for the first time, we focused on the fetal membranes and childbirth byproducts as a promising source of cells for regenerative medicine. While many studies have described the advantages of cells derived from these organs, their advantage as a source of younger cells has not been sufficiently covered by the literature. Thus, herein, we highlight challenges that may arise from the impairment of the regenerative capacity of MSCs due to donor age and how allograft cells from fetal adnexa can be a promising substitute for the aged patients' stem cells for myocardial regeneration. Moreover, obstacles to the use of off-the-shelf cell-therapy preparations in regenerative medicine are briefly summarized here.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"61"},"PeriodicalIF":3.4,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143494381","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}

{"title":"β-Hydroxybutyrate mitigates the detrimental effects of high glucose in human retinal pigment epithelial ARPE-19 cells.","authors":"Francesca Argentino, Marta Mallardo, Ciro Costagliola, Aurora Daniele, Ersilia Nigro","doi":"10.1007/s13577-025-01187-x","DOIUrl":"10.1007/s13577-025-01187-x","url":null,"abstract":"<p><p>High glucose leads to cellular damage and dysfunction in the retina. Dietary interventions, including the use of ketogenic diets, have been explored for their potential to reduce the adverse effects of hyperglycemia. β-Hydroxybutyrate (BHB), a ketone body, has immune and anti-inflammatory properties. This study aims to investigate whether BHB ameliorates the harmful effects induced by high glucose in ARPE-19 cells, a model of retinal pigment epithelium. We investigated the effects induced by high glucose and/or BHB on viability, migration, colony-forming ability, cell cycle progression and cytokine production. Our data indicate that high glucose significantly reduces the viability of ARPE-19 cells with no significant changes in apoptosis or autophagy, while inducing cell cytostasis. On the other hand, BHB exerts a protective effect on ARPE-19 cells under hyperglycemic conditions improving cell viability and alleviating glucose-induced cell cycle arrest. Additionally, BHB treatment affects the expression of IL-8 and IL-17α, as well as of MCP-1, modulating the inflammatory response, cell migration and wound healing. In conclusion, this study highlights the potential protective role of BHB against the detrimental effects induced by high glucose on ARPE-19 cells. These findings support the use of ketone bodies in mitigating high glucose-induced cellular damage. Future research will be critical to translate these findings to the clinical practice for metabolic diseases.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"59"},"PeriodicalIF":3.4,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460299","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}

{"title":"Extrachromosomal circular DNA: a double-edged sword in cancer progression and age-related diseases.","authors":"Shadira Anindieta Irdianto, Astari Dwiranti, Anom Bowolaksono","doi":"10.1007/s13577-025-01178-y","DOIUrl":"10.1007/s13577-025-01178-y","url":null,"abstract":"<p><p>Extrachromosomal circular DNA (eccDNA) is a fascinating form of genetic material found outside the usual chromosomal DNA in eukaryotic cells, including humans. Since its discovery in the 1960s, eccDNA has been linked to critical roles in cancer progression and age-related diseases. This review thoroughly explores eccDNA, covering its types, how it forms, and its significant impact on diseases, particularly cancer. EccDNA, especially in its extrachromosomal DNA (ecDNA) form, contributes to the genetic diversity of tumour cells, helping them evolve quickly and resist treatments. Beyond cancer, eccDNA is also connected to age-related conditions like Werner syndrome, amyotrophic lateral sclerosis (ALS), and type 2 diabetes mellitus (T2DM), where it may affect genomic stability and disease development. The potential of eccDNA as a biomarker for predicting disease outcomes and as a target for new treatments is also highlighted. This review aims to deepen our understanding of eccDNA and inspire further research into its roles in human health and disease, paving the way for innovative diagnostic and therapeutic approaches.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"58"},"PeriodicalIF":3.4,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143450568","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}

{"title":"Relevance of mitochondrial morphological changes in keratoconus patients undergoing collagen cross-linking and deep anterior lamellar keratoplasty.","authors":"Shivam Sharma, Lata Singh, Tapas Chandra Nag, Seema Kashyap, Seema Sen, Chanda Panwar, Mithalesh Kumar Singh, Namrata Sharma","doi":"10.1007/s13577-025-01184-0","DOIUrl":"10.1007/s13577-025-01184-0","url":null,"abstract":"<p><p>Keratoconus (KC) is characterised by corneal stromal thinning and irregular astigmatism, resulting in diminution of vision. Underlying aetiology remains poorly understood. Recent evidence suggests dysregulation of oxidative balance and mitochondrial function in KC corneas. Therefore, this study aims to investigate the morphology of mitochondria in the corneal tissues. Twenty patients each diagnosed with KC and age-matched healthy controls were enrolled in this study. Demographic and clinical details were recorded. Corneal tissues were collected and analyzed using hematoxylin and eosin staining and transmission electron microscopy (TEM). Patients were followed up for 6 months. There was a male preponderance (75%) with an average age of 23.05 ± 6.92 years in KC patients. The clinical findings showed a history of eye atopy (65%), frequent eye rubbing (65%), and characteristic KC signs such as Munson's sign (60%) and Vogt striae (60%). The TEM analysis revealed that KC corneal epithelium exhibited numerous degraded mitochondria with dissolved cristae and heterogenous morphology, while healthy controls displayed intact mitochondrial structures. Similarly, the stroma of KC patients showed very few mitochondria with altered morphology, necrotic keratocytes, and loosely packed collagen fibrils. All the cases showed no disease progression on follow up. This is the first study providing the novel insights into the ultrastructural changes of mitochondria in epithelium and stromal layers of moderate and advanced cases of KC. This emphasises the significant mitochondrial degradation and morphological abnormalities in the corneal tissues of KC patients, indicating a pivotal role of mitochondrial dysfunction in the pathophysiology of keratoconus.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"56"},"PeriodicalIF":3.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442444","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}

{"title":"Exploring the therapeutic potential of MOTS-c in age-related macular degeneration: from cellular responses to patient-derived cybrids.","authors":"Zahra Mohtashami, Kevin Schneider, Reza Azimi, Shari Atilano, Marilyn Chwa, M Cristina Kenney, Mithalesh Kumar Singh","doi":"10.1007/s13577-025-01188-w","DOIUrl":"10.1007/s13577-025-01188-w","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD), the leading cause of irreversible vision loss in the US, is on the rise among the elderly. Uncontrolled mitochondria-derived peptide production from mtDNA disruption and 16S or 12S rRNA damage could worsen AMD. Our previous work has shown that Humanin G possesses cytoprotective effects in retinal pigment epithelial (RPE) cells. However, MOTS-c, a highly efficient mitochondrial peptide, has yet to be evaluated on retinal cell survival. In this study, we show that there are differences in effects between wild-type (wt-) and differentiated ARPE19 cells (diff-ARPE19), implying that the cellular differentiation status may influence how cells respond to MOTS-c. MOTS-c has dose-dependent effects on apoptosis, inflammation, and mitochondrial biogenesis in diff-ARPE19 cells. Lower doses (500 nM) have more significant impacts than 5 µM concentrations. In diff-ARPE19 cells, a lower dose of MOTS-c can reduce the negative impact of hypoxia on cellular survival and gene expression, including apoptosis (CASP3, CASP9), mitochondrial biogenesis (TFAM, PGC-1α), and metabolic sensor (AMPK). However, it had no significant effect on ROS levels or NRF1 expression, regardless of MOTS-c dose. Exposing diff-ARPE19 cells to varied MOTS-c dosages before and after therapy in a chemically induced hypoxic environment yields no extra benefits as compared to MOTS-c treatment alone. MOTS-c had different effects on the expression of genes linked with apoptosis, mitochondrial biogenesis, and antioxidant activity in AMD patients versus age-matched control cybrids. The MOTS-c peptide appears to enhance cellular metabolism and regulate gene expression, which could potentially provide therapeutic benefits in AMD.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"57"},"PeriodicalIF":3.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442173","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}

{"title":"Immunomodulatory role of exosome-derived content in pediatric medulloblastoma: a molecular subgroup perspective.","authors":"Jessica Oliveira de Santis, Graziella Ribeiro de Sousa, Rosane Gomes de Paula Queiroz, Marina Ferreira Cândido, Fausto Almeida, Caroline Patini de Rezende, Patricia Cassia de Ruy, Gabriel Santos Arini, Beth Coyle, Philippa Wade, María Sol Brassesco, Carlos Alberto Scrideli, Luiz Gonzaga Tone, Elvis Terci Valera","doi":"10.1007/s13577-025-01181-3","DOIUrl":"10.1007/s13577-025-01181-3","url":null,"abstract":"<p><p>Medulloblastoma (MB) is the most common malignant brain tumor in children, comprising four distinct subgroups: wingless (WNT), sonic hedgehog (SHH), Group 3, and Group 4. MYC amplification and metastatic dissemination are challenges in clinical management, and tumor-associated macrophages (TAMs) play an essential role in these intricate molecular processes. However, the influence of immune cells in MB metastasis and MYC-amp is unclear. Secretion of extracellular vesicles (EVs) has emerged as a pivotal mediator facilitating communication within the tumor microenvironment, orchestrating coordinated responses among immune cells during tumor initiation, progression, and tumor dissemination. Here, we sought to elucidate the role of exosome-derived MBs in promoting specific patterns of TAM polarization across different molecular subgroups of MB cell lines. CIBERSORTx analysis using a single-cell RNA dataset revealed an increase in M0 macrophages and a decreased proportion of M2 macrophages in MB patients with tumor dissemination in the central nervous system (CNS). Cell-derived exosomes were found to secrete high levels of IL-4, IL-10, and TGF-β, indicative of a protumor M2-profile pattern. Moreover, EVs from SHH TP53-mutated, Group 3/4, and MYC-amplified MBs induced dissimilar patterns of TNF-α and/or IL-1β overexpression. This study demonstrates that exosomes from pediatric MBs promote a predominant M2-macrophage phenotype and Group 3, Group 4, SHH TP53-mutated, and MYC-amplified MBs induced a mixed M1/M2 response pattern. These findings shed light on the pivotal role of exosomes in modulating the immune response, potentially contributing to immune escape in this malignant neoplasm.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"55"},"PeriodicalIF":3.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442237","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}

{"title":"Long noncoding RNA SNHG4 promotes glioma progression via regulating miR-367-3p/MYO1B axis in zebrafish xenografts.","authors":"Yueqing Zhang, Yongjin Wang, Yang Yang, Chunming Sun","doi":"10.1007/s13577-025-01183-1","DOIUrl":"10.1007/s13577-025-01183-1","url":null,"abstract":"<p><p>Glioma is one of the most malignancy and prevalent tumor in the human central nervous system, which is associated with severe morbidity and high mortality. Numerous studies have explained the clear correlation between abnormal expression of lncRNA and progression of Glioma. LncRNA small nucleolar RNA host gene 4 (SNHG4) have been proved to play oncogenesis roles in various tumors, however, the underlying mechanism remains to be explored deeply. In this study, by analysis of the public database, we found that SNHG4 was upregulated in multiple cancer tissues, including glioma. Subsequently, the functional roles of SNHG4 were investigated, and we found that knockdown of SNHG4 remarkedly inhibited cell proliferation, migration. While, overexpression of SNHG4 enhanced these functions of glioma cells in vitro. Meanwhile, as the in vivo tool, zebrafish xenograft model was used to verify the functions of SNHG4 in glioma cells. Mechanically, we identified that SNHG4 or MYO1B could bind with miR-367-3p by the luciferase reporter assays. Furthermore, the rescue experiments showed that the inhibition of miR-367-3p or the expression of MYO1B partially rescue the inhibition effects of SNHG4 in glioma cells. Our study reveals that SNHG4 promotes the proliferation, migration of glioma via regulating miR-367-3p/MYO1B axis.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"53"},"PeriodicalIF":3.4,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11828807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415870","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}

{"title":"Derivation of hiPSC line (ICADRB2i007-A-3) from an individual with osteoporosis linked to ADRB2: c.46G > A.","authors":"O Krasnova, P Semenova, A Kovaleva, J Sopova, V Turilova, T Yakovleva, O Bystrova, M Martynova, I Neganova","doi":"10.1007/s13577-025-01180-4","DOIUrl":"10.1007/s13577-025-01180-4","url":null,"abstract":"<p><p>Osteoporosis is a complex multifactorial bone disease with a strong genetic component. Among the various genes implicated in the progression of osteoporosis, those encoding G-protein-coupled receptors (GPCRs) play a crucial role in its pathogenesis. This superfamily of membrane receptors regulates myriad of cellular events including physiological and pathological processes in bone tissue. Beta-2-adrenergic receptor (a member of the GPCR superfamily) mediates cues from sympathetic nervous system to the bone tissue being expressed on both types of bone cells osteoblasts and osteoclasts. While the impact of this receptor typically investigated using animal models, the human gene ADRB2 coding beta-2-adrenergic receptor harbors numerous non-synonymous single-nucleotide polymorphisms (SNPs) that alter the activity of the receptor. One of the most prevalent SNP is c.46G > A; however, its impact on bone homeostasis has only been explored in epidemiological studies with results showing considerable variability. In this study, we generated for the first time induced pluripotent stem cells (iPSCs) line from the patient with osteoporosis carrying c.46G > A in ADRB2. This new cell line exhibits hallmarks of pluripotency, normal karyotype, and ability to differentiate into three-germ layers. Furthermore, we conducted a comparative analysis of ADRB2 expression between newly obtained iPSCs and those derived from healthy donors. This comparison extended to mesenchymal stem cells (iMSCs) derived from these iPSC lines, assessing both basal and osteogenic conditions at the mRNA and protein levels. Our findings revealed that iMSCs from an osteoporotic patient with the c.46G > A in ADRB2 exhibited decreased ADRB2 expression, which correlated with a diminished potential for osteogenic differentiation. Newly obtained iPSCs line represents a promising cell source for in vitro osteoporosis model and offers the possibility to study in-depth the specific impact of c.46G > A in ADRB2 on osteoporosis pathogenesis.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"54"},"PeriodicalIF":3.4,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426535","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}

{"title":"Differentiation of human hyalocytes from induced pluripotent stem cells through ascorbic acid treatment.","authors":"Elena Laura Mazzoldi, Gabriele Benini, Rosalba Monica Ferraro, Moira Micheletti, Giovanni Martellosio, Viola Balduchelli, Piergiuseppe Sacristani, Daniele Lussignoli, Francesco Semeraro, Sara Rezzola, Marco Presta, Loredana Bergandi, Alessandro Meduri, Silvia Clara Giliani","doi":"10.1007/s13577-025-01182-2","DOIUrl":"10.1007/s13577-025-01182-2","url":null,"abstract":"<p><p>Hyalocytes are macrophage-like cells residing in the eye vitreous cortex. Even though hyalocytes have been firstly described in the mid-Nineteenth century, they have been poorly explored. Recent researches highlighted hyalocyte involvement in both physiological and pathological processes of the vitreoretinal interface. Nonetheless, the majority of works involving hyalocyte cultures were carried out in animals, while fewer studies were performed on humans because their isolation requires vitrectomy. The aim of this study was to differentiate human induced pluripotent stem cells (iPSCs) into hyalocytes as a non-invasive method to continuously obtain cells. iPSCs were first differentiated into hematopoietic stem/progenitor cells (HSPCs) and then into macrophages. Macrophages were either left untreated (NT) or treated with ascorbic acid (AA) alone or combined with bFGF and/or TGF-β1. Additionally, macrophages were cultured in the presence of a pool of vitreous bodies from vitrectomies. Cells were analyzed for morphology and then for gene and protein expression through qRT-PCR, immunofluorescence, Western Blot, and flow cytometry. Similar to cells treated with the vitreous body, macrophages treated with AA alone or in combination with bFGF exhibited a more elongated shape compared to NT or cells treated with TGF-β1. Additionally, these treatments resulted in gene expression downregulation for S100A4, S100A10, S100B, and CX3CR1, while upregulating COL6A1, HLA-DRA, and CD74. At the protein level, S100B, CD14, and CD49d were downregulated with all treatments, while collagen VI and HLA-DR were upregulated. This work demonstrates that hyalocytes can be differentiated by treatment of iPSC-derived macrophages with ascorbic acid for a period of 21 days.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"52"},"PeriodicalIF":3.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11821750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400446","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}

{"title":"The miR-1305/KLF5 negative regulatory loop affects pancreatic cancer cell proliferation and apoptosis.","authors":"Yufu Zhou, Yulin Tang, Feizhou Huang, Zhichao Wang, Zhengbin Wen, Qi Fang, Changfa Wang","doi":"10.1007/s13577-025-01173-3","DOIUrl":"10.1007/s13577-025-01173-3","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is characterized by a high relapse rate and unfavorable prognosis. Currently, the optimal treatment for PC is complete resection followed by adjuvant systemic chemotherapy. Nevertheless, tumor cell repopulation and subsequent tumor relapse and metastasis after chemotherapy result in a poor prognosis. Therefore, it is of great value to explore the potential molecular mechanisms underlying PC for developing novel treatment strategies. Herein, we aimed to investigate the potential regulatory mechanism of miR-1305 upon aerobic proliferation, metastasis, and apoptosis in PC. miR-1305 was downregulated in PC tissues and cell lines. miR-1305 overexpression prominently inhibited PC cell proliferation and metastasis promoted cell apoptosis in vitro, and alleviated PC formation in vivo. As predicted, KLF5 could directly bind to miR-1305. Silencing of KLF5 or KLF5 inhibitor (ML264) suppressed PC cell viability and cell invasion, and enhanced cell apoptosis. KLF5 restrained miR-1305 transcription and expression by binding to its promoter region. miR-1305 exerted a suppressive effect on PC cell proliferation and apoptosis via regulation of the KLF5-ERBB2 axis; KLF5 gene is a transcriptional regulator of miR-1305, promising to be a new target for the diagnosis and treatment of PC.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"51"},"PeriodicalIF":3.4,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374835","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}