Experimental cell research最新文献

{"title":"Long non-coding RNAs and their role in breast cancer pathogenesis and drug resistance: Navigating the non-coding landscape review","authors":"Tohada M. Al-Noshokaty ,&nbsp;Gharieb S. El-Sayyad ,&nbsp;Rehab Abdelhamid ,&nbsp;Abdallah Mansour ,&nbsp;Nourhan Abdellatif ,&nbsp;Ayat Alaaeldien ,&nbsp;Tasnim Reda ,&nbsp;David Gendi ,&nbsp;Nourhan M. Abdelmaksoud ,&nbsp;Shereen Saeid Elshaer ,&nbsp;Ahmed S. Doghish ,&nbsp;Osama A. Mohammed ,&nbsp;Ahmed I. Abulsoud","doi":"10.1016/j.yexcr.2024.114365","DOIUrl":"10.1016/j.yexcr.2024.114365","url":null,"abstract":"<div><div>Despite the progress made in the development of targeted therapies, breast cancer (BC) continues to pose a significant threat to the health of women. Transcriptomics has emerged due to the advancements in high-throughput sequencing technology. This provides crucial information about the role of non-coding RNAs (ncRNAs) in human cells, particularly long ncRNAs (lncRNAs), in disease development and function. When the control of these ncRNAs is disrupted, various illnesses emerge, including cancer. Numerous studies have produced empirical data on the function of lncRNAs in tumorigenesis and disease development. However, the roles and mechanisms of numerous lncRNAs remain unidentified at the molecular level because their regulatory role and the functional implications of abnormalities in cancer biology have yet to be thoroughly defined. The review gives an itemized summary of the most current developments in the role of lncRNA in BC, focusing on three main pathways, PI3K, MAPK, NF-kB, and hypoxia, and their resistance mechanisms.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114365"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767481","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":"Interactions between lncRNAs and cyclins/CDKs complexes; key players in determining cancer cell response to CDKs inhibitors","authors":"Bahaa Ibrahim Saeed ,&nbsp;Abhinav Kumar ,&nbsp;Enwa Felix Oghenemaro ,&nbsp;Layla A. Almutairi ,&nbsp;Rekha M. M ,&nbsp;Rohit Kumawat ,&nbsp;Subasini Uthirapathy ,&nbsp;Hanen Mahmod Hulail ,&nbsp;Shilpa Sharma ,&nbsp;M. Ravi Kumar","doi":"10.1016/j.yexcr.2025.114406","DOIUrl":"10.1016/j.yexcr.2025.114406","url":null,"abstract":"<div><div>Transcription takes place over a significant portion of the human genome. However, only a small portion of the transcriptome, roughly 1.2 %, consists of RNAs translated into proteins; the majority of transcripts, on the other hand, comprise a variety of RNA families with varying sizes and functions. A substantial portion of this diverse RNA universe consists of sequences longer than 200 bases, called the long non-coding RNA (lncRNA). The control of gene transcription, changes to DNA topology, nucleosome organization and structure, paraspeckle creation, and assistance for developing cellular organelles are only a few of the numerous tasks performed by lncRNA. The main focus of this study is on the function of lncRNA in controlling the levels and actions of cyclin-dependent kinase inhibitors (CDKIs). The enzymes required for the mitotic cycle's regulated progression are called cyclin-dependent kinases (CDKs). They have many degrees of regulation over their activities and interact with CDKIs as their crucial mechanisms. Interestingly, culminating evidence has clarified that lncRNAs are associated with several illnesses and use CDKI regulation to control cellular function. Nonetheless, despite the abundance of solid evidence in the literature, it still seems unlikely that lncRNA will have much of an impact on controlling cell proliferation or modulating CDKIs.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 2","pages":"Article 114406"},"PeriodicalIF":3.3,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046015","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":"Protective effects of tissue factor pathway inhibitor on mice with lipopolysaccharide-induced acute lung injury","authors":"Posum Wan ,&nbsp;Kaiheng Gao ,&nbsp;Feng Miao,&nbsp;Meng Shi,&nbsp;Xiaofeng Chen","doi":"10.1016/j.yexcr.2024.114357","DOIUrl":"10.1016/j.yexcr.2024.114357","url":null,"abstract":"<div><div>Acute lung injury (ALI) resulting from bacterial infection poses a significant risk, and its etiology involves the complex interplay of harmful immune responses and blood coagulation. Despite this understanding, the roles and mechanisms of tissue factor pathway inhibitor (TFPI) in LPS-induced ALI remain insufficiently elucidated. In this study, we aimed to explore the effects of TFPI in LPS-induced ALI. Our investigations revealed that TFPI exerts multiple beneficial effects in LPS-induced ALI. Specifically, TFPI reduces microvascular permeability, Myeloperoxidase (MPO) activity, and cytokine production while inhibiting blood coagulation. Moreover, TFPI demonstrates the capacity to promote proliferation and suppress apoptosis in Human microvascular endothelial cells (HMEC-1) and Human umbilical vein endothelial cells (HUVEC) through the inhibition of the caspase pathway and mitochondrial apoptosis pathway. Furthermore, our findings indicate a correlation between tissue factor (TF) and TFPI expression, with TFPI regulation observed in HMEC-1 cells following LPS treatment. This novel insight suggests that TFPI plays a regulatory role in TF expression. Overall, the protective effect of TFPI on LPS-induced ALI is unveiled by its ability to enhance endothelial cell proliferation and inhibit apoptosis through the modulation of caspase and Bcl-2/Bax pathways. These results underscore the potential of TFPI as a promising therapeutic target for ALI treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114357"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738909","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":"COPS5 regulates osteosarcoma progression by upregulating KHSRP to promote Per2 mRNA decay","authors":"Jie Bu,&nbsp;Xuezheng Xu,&nbsp;Yi Luo,&nbsp;Jianfan Liu,&nbsp;Xinyu Yao","doi":"10.1016/j.yexcr.2024.114358","DOIUrl":"10.1016/j.yexcr.2024.114358","url":null,"abstract":"<div><div>Osteosarcoma (OS) is a common bone sarcoma that is often seen in children and adolescents. This study delves into the intricate regulatory network involving COP9 signalosome subunit 5 (COPS5), KH-type splicing regulatory protein (KHSRP), and Period circadian clock 2 (Per2) in the context of osteosarcoma cell malignant phenotype. CCK-8 assay was applied to assess cell proliferation. Wound healing or transwell assay was selected to evaluate cell migration or invasion. Apoptosis was determined employing flow cytometry assay. Co-IP and GST-pull down determined the interaction between COPS5 and KHSRP. The interaction relationship between KHSRP and Per2 mRNA was detected by RNA-pull down and RIP assays. We found that COPS5 knockdown repressed proliferation, migration, and invasion and facilitated apoptosis of OS cells. Knockdown of COPS5 also restrained the tumor growth in the nude mice tumor xenograft model. COPS5 interacted with KHSRP to maintain the protein stability of KHSRP. Furthermore, there was a binding relationship between KHSRP and Per2 mRNA. Besides, COPS5 promoted OS cell tumorigenesis by mediating the decay effect of KHSRP on Per2 mRNA. Collectively, COPS5 promoted the decay of Per2 mRNA via contacting and mediating KHSRP, thereby facilitating OS progression. Our study unveils COPS5 as a key modulator in OS.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114358"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142744083","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":"Exosomal noncoding RNA (ncRNA) in breast cancer pathogenesis and therapy; two sides of the same coin","authors":"Fatma Magdi Ibrahim ,&nbsp;Raed Obaid Saleh ,&nbsp;Herlina Uinarni ,&nbsp;Dmitry Olegovich Bokov ,&nbsp;Soumya V. Menon ,&nbsp;Khamdamov Baxtiyor Zarifovich ,&nbsp;Neeti Misra ,&nbsp;Mais Mazin Al-Hamdani ,&nbsp;Beneen Husseen ,&nbsp;Mohammed Abed Jawad","doi":"10.1016/j.yexcr.2024.114359","DOIUrl":"10.1016/j.yexcr.2024.114359","url":null,"abstract":"<div><div>Over the past few years, breast cancer has become the most prevalent type of cancer globally, with the primary cause of death from the disease being metastatic cancer. This has led to the development of early detection techniques, mainly using non-invasive biomarkers in a range of body fluids. Exosomes are unique extracellular vesicles (EVs) transmitting cellular signals over great distances via various cargo. They are readily apparent in physiological fluids due to release by breast cancer cells or breast cancer-tumor microenvironment (TME) cells. In light of this, numerous biological and functional facets of human tumours, such as breast cancer, are intimately associated with exosomal noncoding RNAs (ncRNAs), containing miRNAs (microRNAs), lncRNAs (long noncoding RNAs), and circRNAs (circular RNAs). Exosomal ncRNAs serve a critical role in various steps of breast cancer development, enabling the exchange of genetic information between cancer cells and other cells (e.g., immune cells), thus regulating tumour angiogenesis, growth, metastasis, immune responses and drug resistance. They interact with multiple regulatory complexes with dissimilar enzymatic actions, which, in turn, modify the chromatin sceneries, including nucleosome modifications, DNA methylation, and histone modifications. Herein, we look into the exosomes' underlying regulatory mechanisms in breast cancer. Furthermore, we inspect the existing understanding of the functions of exosomal miRNAs, lncRNAs, and circRNAs in breast cancer to authenticate their possible significance in identifying biomarkers, deciphering their role in immune escape and drug resistance, and finally, analyzing treatment practices.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114359"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142744082","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":"The cystogenic effects of ouabain in autosomal dominant polycystic kidney disease require cell caveolae","authors":"Jordan Trant,&nbsp;Gladis Sanchez,&nbsp;Jeffery P. McDermott,&nbsp;Gustavo Blanco","doi":"10.1016/j.yexcr.2024.114356","DOIUrl":"10.1016/j.yexcr.2024.114356","url":null,"abstract":"<div><div>We have previously shown that the hormone ouabain is a circulating factor which can accelerate the progression of autosomal dominant polycystic kidney disease (ADPKD). At physiologic concentrations, ouabain increases cyst area and fibrosis in kidneys from ADPKD but not wildtype mice. These effects are due to an increased affinity for ouabain by its receptor, Na,K-ATPase (NKA), in the kidneys of ADPKD mice which leads to over-activation of NKA signaling function. Previous studies suggested that ouabain's stimulation of NKA signal transduction is mediated by NKA located within cell caveolae. Here, we determined whether caveolae are involved in the ouabain-induced progression of ADPKD cysts. We generated an ADPKD mouse with a global knockout of the main structural component of caveolae, caveolin-1 (CAV1), which we confirmed lacks caveolae in the kidney. When given physiological amounts of ouabain for 5 months, <em>Pkd1</em>^{<em>RC/RC</em>}<em>Cav1</em>^{<em>−/−</em>} mice did not exhibit any changes in cyst progression, contrasting with the <em>Pkd1</em>^{<em>RC/RC</em>} mice which showed a significant increase in cystic area and kidney fibrosis. Also, measures of ouabain-induced cell proliferation, including the number of Ki67-positive nuclei and phosphorylation of the extracellular regulated kinase (ERK) and protein kinase B (Akt), did not increase in the <em>Pkd1</em>^{<em>RC/RC</em>}<em>Cav1</em>^{<em>−/−</em>} mice compared with the <em>Pkd1</em>^{<em>RC/RC</em>} mice. Moreover, the abnormally increased affinity for ouabain of NKA in <em>Pkd1</em>^{<em>RC/RC</em>} mice was restored to wildtype levels in the <em>Pkd1</em>^{<em>RC/RC</em>}<em>Cav1</em>^{<em>−/−</em>} mice. This work highlights the role of caveolae in ouabain-induced NKA signaling and ADPKD cyst progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114356"},"PeriodicalIF":3.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715879","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":"Fbxo11 maintains mitochondrial function and prevents podocyte injury in adriamycin-induced nephropathy by mediating the ubiquitin degradation of Fosl2","authors":"Yanhua Jin,&nbsp;Huan Wang,&nbsp;Yu Xin,&nbsp;Yanning Zhang","doi":"10.1016/j.yexcr.2024.114345","DOIUrl":"10.1016/j.yexcr.2024.114345","url":null,"abstract":"<div><div>Mitochondrial dysfunction is a pivotal factor in the onset of podocyte damage, which is a central component in the pathogenesis of nephrotic syndrome (NS). However, the precise mechanisms underlying the changes in podocyte mitochondria remain elusive. Our study aims to clarify the potential mechanisms involved in the role of F-box protein 11 (Fbxo11) in NS, specifically concentrating on its impact on mitochondrial function. A mouse model was established by tail vein injection of adriamycin (ADR, 10 mg/kg) and was infected with lentivirus overexpressing Fbxo11 (lenti-Fbxo11-OE). Mouse podocytes (MPC-5) were infected with lenti-Fbxo11-OE, followed by treatment with 0.4 μg/mL of ADR. We identified the decreased expression of Fbxo11 in mouse renal tissues and MPC-5 cells induced by ADR. Lenti-Fbxo11-OE intervention relieved ADR-induced glomerular lesion, podocyte injury, and mitochondrial dysfunction. In vitro, overexpression of Fbxo11 in mouse podocytes improved mitochondrial function and reduced podocyte damage, thereby inhibiting podocyte apoptosis. Mechanistically, Fbxo11 decreased the protein expression of Fosl2 through ubiquitin-dependent proteasomal degradation. Rescue experiments revealed that overexpression of Fosl2 abolished the protective effects of Fbxo11 overexpression on mitochondrial damage and podocyte injury. Importantly, the regulatory effects of the Fbxo11/Fosl2 axis were reversed when treated with the mitochondrial fission inhibitor mdivi-1. Taken together, our results demonstrated that Fbxo11-mediated protein degradation of Fosl2 is critical for maintaining mitochondrial function and preventing podocyte injury during NS.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114345"},"PeriodicalIF":3.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709147","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":"MOTS-c relieves hepatocellular carcinoma resistance to TRAIL-induced apoptosis under hypoxic conditions by activating MEF2A","authors":"Haiying Shen ,&nbsp;Junjie Nie ,&nbsp;Xiaojun Wang ,&nbsp;Guangqing Li ,&nbsp;Liwei Zhao ,&nbsp;Yuji Jin ,&nbsp;Lianhai Jin","doi":"10.1016/j.yexcr.2024.114354","DOIUrl":"10.1016/j.yexcr.2024.114354","url":null,"abstract":"<div><h3>Background</h3><div>Mitochondrial ORF of the 12S rRNA type-c (MOTS-c) as an AMPK agonist can regulate the expression of adaptive nuclear genes to promote cell homeostasis. However, the investigation of MOTS-c in hepatocellular carcinoma (HCC) is insufficient. This study aims to reveal the role of MOTS-c on HCC cell apoptosis.</div></div><div><h3>Methods</h3><div>Huh7 and HCCLM3 cells were incubated with MOTS-c under a hypoxic condition. MOTS-c levels were quantified by enzyme-linked immunosorbent assay in the peripheral blood of HCC patients and healthy controls. Cell viability was detected by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell apoptosis was investigated by flow cytometry and Tunel assay. Protein expression was detected by western blotting or immunohistochemistry assay. Dual-luciferase reporter assay and chromatin immunoprecipitation assay were performed to identify the association among myocyte enhancer factor 2A (MEF2A), death receptor 4 (DR4) and DR5. A tumor-bearing nude mouse model was conducted to assess the effect of MOTS-c on HCC tumor formation <em>in vivo</em>.</div></div><div><h3>Results</h3><div>MOTS-c levels in the peripheral blood of HCC patients were significantly lower compared to healthy individuals. MOTS-c promoted HCC cell apoptosis under hypoxia conditions. Hypoxia stimulation decreased the protein expression of MEF2A, DR4, DR5, fas-associating via death domain (FADD) and caspase-8, while these effects were attenuated after MOTS-c treatment. MOTS-c induced TRAIL-induced apoptosis of HCC cells by activating MEF2A through the phosphorylation of AMPK under hypoxia treatment. In addition, MEF2A transcriptionally up-regulated DR4 and DR5. MOTS-c activated MEF2A to regulate DR4 and DR5 expression, further mediating TRAIL-induced apoptosis. Further, MOTS-c treatment relieved hypoxia-induced tumor growth <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div>MOTS-c relieved hypoxia-induced HCC cell resistance to TRAIL-caused apoptosis by activating MEF2A.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114354"},"PeriodicalIF":3.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709197","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":"DDX18 influences chemotherapy sensitivity in colorectal cancer by regulating genomic stability","authors":"Wenchao Zhao ,&nbsp;Qingqing Luo ,&nbsp;Han Zhan ,&nbsp;Zhen Du ,&nbsp;Tan Deng ,&nbsp;Huaxin Duan","doi":"10.1016/j.yexcr.2024.114344","DOIUrl":"10.1016/j.yexcr.2024.114344","url":null,"abstract":"<div><div>Chromosomal Instability (CIN) encompasses approximately 65 %–70 % of colorectal cancer (CRC) patients, playing a pivotal role in tumor progression. However, controversies persist regarding the molecular characteristics and treatment strategies associated with these patients. Integrative colorectal cancer proteogenomic analysis identified DDX18 in colorectal cancer. We investigated the molecular mechanisms underlying the regulation of colorectal cancer by the R-loop binding protein DDX18 using colon cancer tissues, cell lines and patient-derived organoids. Our findings revealed that DDX18 expression positively correlates with the expression of genomic instability marker R-loops. Moreover, heightened DDX18 expression delays the completion of DNA damage repair, leading to an increase in double-strand DNA breaks, thereby promoting genomic instability. Notably, the upregulation of DDX18 enhances sensitivity to DNA-damaging. This study elucidated DDX18 beyond participating in fundamental physiological functions, may play a crucial role in the regulation of genomic stability, and also provides a powerful resource for further functional exploration of DDX18 in cancer progression and therapeutic application.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114344"},"PeriodicalIF":3.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692853","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":"Seven Theorems of Joseph G. Gall","authors":"Ji-Long Liu","doi":"10.1016/j.yexcr.2024.114343","DOIUrl":"10.1016/j.yexcr.2024.114343","url":null,"abstract":"<div><div>On June 30, 2020, Professor Joseph Grafton Gall announced his retirement at 92. On August 13, 2020, Joe's former trainees and colleagues held a retirement celebration online to celebrate Joe's “Remarkable Career with Astonishing Discoveries”, covering Joe's nearly 70 years of education and research. As a representative of Joe's trainees in the 2000s, I gave a speech titled “Seven Theorems of Joe”. On September 12, 2024, Joe passed away peacefully, at 96. In memoriam, here I expand and update my previous speech and explain the “Seven Theorems of Joseph G. Gall”, a scientists' scientist.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114343"},"PeriodicalIF":3.3,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681152","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}