Cytotechnology最新文献_第7页

Selective elimination of tumorigenic cells from mixed culture of normal and tumorigenic cells using hybrid liposomes aimed at realizing of cell therapy 利用旨在实现细胞疗法的混合脂质体，从正常细胞和致瘤细胞的混合培养液中选择性清除致瘤细胞

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-13 DOI: 10.1007/s10616-023-00613-y

{"title":"Selective elimination of tumorigenic cells from mixed culture of normal and tumorigenic cells using hybrid liposomes aimed at realizing of cell therapy","authors":"","doi":"10.1007/s10616-023-00613-y","DOIUrl":"https://doi.org/10.1007/s10616-023-00613-y","url":null,"abstract":"<h3>Abstract</h3> While induced pluripotent stem (iPS) cells are expected to be a cell source for regenerative medicine, they also have tumorigenic properties owing to their proliferative potential. During the manufacturing of regenerative medicine products, undifferentiated iPS cells and malignant transformed cells may be mixed in the cell culture population. Therefore, it is essential to eliminate tumorigenic cells selectively. In this study, a mixed culture of normal human fetal hepatocytes (Hc cells) and human hepatocellular carcinoma cells (HuH-7 cells) was used as a cell population model to be used as regenerative medicine products, and the selective elimination of HuH-7 cells by hybrid liposomes (HL) was analyzed. HL tended to fuse and accumulate more in HuH-7 cells due to larger fluidity of plasma membrane for HuH-7 cells than that for Hc cells. In a mixed culture of Hc and HuH-7 cells, HL selectively eliminated HuH-7 cells while allowing Hc cells to remain viable. In addition, HL treatment for the mixed culture of Hc and HuH-7 cells suppressed the tumorigenicity of HuH-7 cells. Therefore, HL selectively fused and accumulated in tumorigenic cells in a mixed cell culture of normal and tumorigenic cells, and eliminated tumorigenic cells while allowing normal cells to remain viable. The results of this study suggest the potential of HL in eliminating tumorigenic cells during the manufacturing of regenerative medicine products. Thus, HL could be expected to contribute to the development of safe regenerative medical products.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"13 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139762966","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}

引用次数: 0

Fructobacillus fructosus OS-1010 strain stimulates intestinal cells to secrete exosomes that activate muscle cells OS-1010 菌株能刺激肠道细胞分泌外泌体，从而激活肌肉细胞

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-01-26 DOI: 10.1007/s10616-023-00610-1

{"title":"Fructobacillus fructosus OS-1010 strain stimulates intestinal cells to secrete exosomes that activate muscle cells","authors":"","doi":"10.1007/s10616-023-00610-1","DOIUrl":"https://doi.org/10.1007/s10616-023-00610-1","url":null,"abstract":"<h3>Abstract</h3> Fructobacillus is a lactic-acid bacterium recently identified in fructose-rich environments. Fructobacillus is also known to exhibit unusual growth characteristics due to an incomplete gene encoding alcohol/acetaldehyde hydrogenase, which results in an imbalance in the nicotinamide adenine mononucleotide (NAD+)/NADN levels. Recently, the addition of d-fructose to the culture medium of Fructobacillus strains increased the intracellular nicotinamide mononucleotide (NMN) content. In the present study, we evaluated the functionality of Fructobacillus that produces high levels of NMN, using one substrain (Fructobacillus fructosus OS-1010). Therefore, in this study, we examined its functionality in the interaction between intestinal cells and muscle cells. The results showed that supernatant derived from intestinal epithelial cells (Caco-2 cells) treated with F. fructosus OS-1010 activated muscle cells (C2C12 cells). Further analysis revealed that Caco-2 cells treated with F. fructosus OS-1010 secreted exosomes known as extracellular vesicles, which activated the muscle cells. Furthermore, pathway analysis of the target genes of miRNA in exosomes revealed that pathways involved in muscle cell activation, including insulin signaling and cardiac muscle regulation, neurotrophic factors, longevity, and anti-aging, can be activated by exosomes. In other words, F. fructosus OS-1010 could activate various cells such as the skin and muscle cells, by secreting functional exosomes from the intestinal tract.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"224 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139588747","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}

引用次数: 0

Evodiamine ameliorates intervertebral disc degeneration through the Nrf2 and MAPK pathways 乙伏地明通过 Nrf2 和 MAPK 通路改善椎间盘退行性变

IF 2.2 4区生物学

Cytotechnology Pub Date : 2023-12-27 DOI: 10.1007/s10616-023-00605-y

{"title":"Evodiamine ameliorates intervertebral disc degeneration through the Nrf2 and MAPK pathways","authors":"","doi":"10.1007/s10616-023-00605-y","DOIUrl":"https://doi.org/10.1007/s10616-023-00605-y","url":null,"abstract":"<h3>Abstract</h3> Degradation of extracellular matrix (ECM), reactive oxygen species (ROS) production, and inflammation are critical players in the pathogenesis of intervertebral disc degeneration (IDD). Evodiamine exerts functions in inhibiting inflammation and maintaining mitochondrial antioxidant functions. However, the biological functions of evodiamine and its related mechanisms in IDD progression remain unknown. The IDD-like conditions in vivo were stimulated via needle puncture. Hematoxylin and eosin staining, Safranin O/Fast Green staining and Alcian staining were performed to determine the degenerative status. The primary nucleus pulposus cells (NPCs) were isolated from Sprague–Dawley rats and then treated with tert-butyl peroxide (TBHP) to induce cellular senescence and oxidative stress. The cell viability was assessed by cell counting kit-8 assays. The mitochondria-derived ROS in NPCs was evaluated by MitoSOX staining. The mitochondrial membrane potential in NPCs was identified by JC-1 staining and flow cytometry. The expression of collagen II in NPCs was measured by immunofluorescence staining. The levels of mRNAs and proteins were measured by RT-qPCR and western blotting. The Nrf2 expression in rat nucleus pulposus tissues was measured by immunohistochemistry staining. Evodiamine alleviated TBHP-induced mitochondrial dysfunctions in NPCs. The enhancing effect of TBHP on the ECM degradation was reversed by evodiamine. The TBHP-stimulated inflammatory response was ameliorated by evodiamine. Evodiamine alleviated the IDD process in the puncture-induced rat model. Evodiamine promoted the activation of Nrf2 pathway and inactivated the MAPK pathway in NPCs. In conclusion, evodiamine ameliorates the progression of IDD by inhibiting mitochondrial dysfunctions, ECM degradation and inflammation via the Nrf2/HO-1 and MAPK pathways. ","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"10 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2023-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139056717","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}

引用次数: 0

Activation of the Nrf2/HO-1 axis by glutaredoxin 2 overexpression antagonizes vascular endothelial cell oxidative injury and inflammation under LPS exposure 过表达谷胱甘肽 2 激活 Nrf2/HO-1 轴可拮抗 LPS 暴露下的血管内皮细胞氧化损伤和炎症反应

IF 2.2 4区生物学

Cytotechnology Pub Date : 2023-12-11 DOI: 10.1007/s10616-023-00606-x

Yuna Liu, Jinlin Gong, Qing Wang, Na Wei, Lei Zhao, Zhenan Wu

{"title":"Activation of the Nrf2/HO-1 axis by glutaredoxin 2 overexpression antagonizes vascular endothelial cell oxidative injury and inflammation under LPS exposure","authors":"Yuna Liu, Jinlin Gong, Qing Wang, Na Wei, Lei Zhao, Zhenan Wu","doi":"10.1007/s10616-023-00606-x","DOIUrl":"https://doi.org/10.1007/s10616-023-00606-x","url":null,"abstract":"Atherosclerosis constitutes a proverbial pathogenic mechanism for cardio-cerebrovascular disease that accounts for the most common cause of disability and morbidity for human health worldwide. Endothelial dysfunction and inflammation are the key contributors to the progression of atherosclerosis. Glutaredoxin 2 (GLRX2) is abundantly existed in various tissues and possesses a range of pleiotropic efficacy including anti-oxidative and anti-inflammatory responses. However, its role in atherosclerosis is still undefined. Here, down-regulation of GLRX2 was validated in lipopolysaccha (LPS)-induced vascular endothelial cells (HUVECs). Moreover, elevation of GLRX2 reversed the inhibition of cell viability in LPS-treated HUVECs and decreased LPS-induced increases in cell apoptosis and caspase-3 activity. Additionally, enhancement of GLRX2 expression antagonized oxidative stress in HUVECs under LPS exposure by inhibiting ROS, lactate dehydrogenase and malondialdehyde production and increased activity of anti-oxidative stress superoxide dismutase. Notably, GLRX2 abrogated LPS-evoked transcripts and releases of pro-inflammatory cytokine (TNF-α, IL-6, and IL-1β), chemokine MCP-1 and adhesion molecule ICAM-1 expression. Furthermore, the activation of Nrf2/HO-1 signaling was demonstrated in LPS-stimulated HUVECs. Importantly, blockage of the Nrf2 pathway counteracted the protective roles of GLRX2 in LPS-triggered endothelial cell injury, oxidative stress and inflammatory response. Thus, these data reveal that GLRX2 may alleviate the progression of atherosclerosis by regulating vascular endothelial dysfunction and inflammation via the activation of the Nrf2 signaling, supporting a promising therapeutic approach for atherosclerosis and its complications.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"56 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2023-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138566338","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}

引用次数: 0

Deciphering variations in the endocytic uptake of a cell-penetrating peptide: the crucial role of cell culture protocols. 解读细胞穿透肽内吞摄取的变化：细胞培养方案的关键作用。

IF 2 4区生物学

Cytotechnology Pub Date : 2023-12-01 Epub Date: 2023-09-08 DOI: 10.1007/s10616-023-00591-1

Joshua Diaz, Jean-Philippe Pellois

{"title":"Deciphering variations in the endocytic uptake of a cell-penetrating peptide: the crucial role of cell culture protocols.","authors":"Joshua Diaz, Jean-Philippe Pellois","doi":"10.1007/s10616-023-00591-1","DOIUrl":"10.1007/s10616-023-00591-1","url":null,"abstract":"Delivery tools, including cell-penetrating peptides (CPPs), are often inefficient due to a combination of poor endocytosis and endosomal escape. Aspects that impact the delivery of CPPs are typically characterized using tissue culture models. One problem of using cell culture is that cell culture protocols have the potential to contribute to endosomal uptake and endosomal release of CPPs. Hence, a systematic study to identify which aspects of cell culturing techniques impact the endocytic uptake of a typical CPP, the TMR-TAT peptide (peptide sequence derived from HIV1-TAT with the N-terminus labeled with tetramethylrhodamine), was conducted. Aspects of cell culturing protocols previously found to generally modulate endocytosis, such as cell density, washing steps, and cell aging, did not affect TMR-TAT endocytosis. In contrast, cell dissociation methods, media, temperature, serum starvation, and media composition all contributed to changes in uptake. To establish a range of endocytosis achievable by different cell culture protocols, TMR-TAT uptake was compared among protocols. These protocols led to changes in uptake of more than 13-fold, indicating that differences in cell culturing techniques have a cumulative effect on CPP uptake. Taken together this study highlights how different protocols can influence the amount of endocytic uptake of TMR-TAT. Additionally, parameters that can be exploited to improve CPP accumulation in endosomes were identified. The protocols identified herein have the potential to be paired with other delivery enhancing strategies to improve overall delivery efficiency of CPPs.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-023-00591-1.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"75 6","pages":"473-490"},"PeriodicalIF":2.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10575844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233116","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}

引用次数: 0

Hypoxia-induced the upregulation of NDUFA4L2 promoted colon adenocarcinoma progression through ROS-mediated PI3K/AKT pathway. 缺氧诱导NDUFA4L2的上调通过ROS介导的PI3K/AKT途径促进结肠腺癌的进展。

IF 2 4区生物学

Cytotechnology Pub Date : 2023-12-01 Epub Date: 2023-09-19 DOI: 10.1007/s10616-023-00590-2

Nianyuan Ye, Yibo Wang, Peng Jiang, Huaji Jiang, Wei Ding, Zheng Zhang, Cheng Xi

{"title":"Hypoxia-induced the upregulation of NDUFA4L2 promoted colon adenocarcinoma progression through ROS-mediated PI3K/AKT pathway.","authors":"Nianyuan Ye, Yibo Wang, Peng Jiang, Huaji Jiang, Wei Ding, Zheng Zhang, Cheng Xi","doi":"10.1007/s10616-023-00590-2","DOIUrl":"10.1007/s10616-023-00590-2","url":null,"abstract":"The NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 4-like 2 (NDUFA4L2) gene has been reported to be upregulated in colorectal cancer (CRC) and is associated with worse prognosis. However, the specific function and underlying mechanism of NDUFA4L2 in colon adenocarcinoma (COAD) under hypoxia has never been investigated. Our study discovered that hypoxia promoted the viability, metastasis, and epithelial-mesenchymal transition (EMT) of COAD cells. Besides, hypoxia-induced HIF-1α upregulated the expression of NDUFA4L2 which served as an oncogene and an independent diagnostic and prognostic marker in COAD. Under hypoxic environment, NDUFA4L2 mediated the viability, metastasis, and epithelial-EMT of COAD cells. Additionally, the ROS-dependent PI3K/Akt signaling was activated by NDUFA4L2 in COAD in hypoxia and NDUFA4L2 facilitated the malignant behaviors of hypoxia-treated COAD cells by elevating ROS production. Collectively, abundant NDUFA4L2 expression induced by HIF-1α under hypoxia promoted the development of COAD through activation of the PI3K/AKT signaling in a ROS-dependent manner, indicating NDUFA4L2 as a promising target in COAD diagnosis and treatment.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"75 6","pages":"461-472"},"PeriodicalIF":2.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10575837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233118","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}

引用次数: 0

MiR-224-5p inhibits osteoblast differentiation and impairs bone formation by targeting Runx2 and Sp7. MiR-224-5p通过靶向Runx2和Sp7抑制成骨细胞分化并损害骨形成。

IF 2 4区生物学

Cytotechnology Pub Date : 2023-12-01 Epub Date: 2023-09-05 DOI: 10.1007/s10616-023-00593-z

Siyang Ding, Yunfei Ma, Jiashu Yang, Yuting Tang, Yucui Jin, Lingyun Li, Changyan Ma

{"title":"MiR-224-5p inhibits osteoblast differentiation and impairs bone formation by targeting Runx2 and Sp7.","authors":"Siyang Ding, Yunfei Ma, Jiashu Yang, Yuting Tang, Yucui Jin, Lingyun Li, Changyan Ma","doi":"10.1007/s10616-023-00593-z","DOIUrl":"10.1007/s10616-023-00593-z","url":null,"abstract":"Osteoporosis is a complicated multifactorial disorder characterized by low bone mass and deteriorated bone microarchitecture with an elevated fracture risk. MicroRNAs play important roles in osteoblastic differentiation. In the present study, we found that miR-224-5p was markedly downregulated during the osteogenic differentiation of C2C12 cells. Overexpression of miR-224-5p in C2C12 cells inhibited osteoblast activity, as indicated by reduced ALP activity, matrix mineralization and the expression of osteogenic marker genes. Moreover, we demonstrated that Runx2 and Sp7 were direct targets of miR-224-5p. Furthermore, the specific inhibition of miR-224-5p by femoral bone marrow cavity injection with miR-224-5p antagomir prevented ovariectomy-induced bone loss. Finally, we found that the levels of miR-224-5p were markedly elevated in the sera of patients with osteoporosis. Collectively, this study revealed that miR-224-5p negatively regulates osteogenic differentiation by targeting Runx2 and Sp7. It also highlights the potential use of miR-224-5p as a therapeutic target and diagnostic biomarker for osteoporosis.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-023-00593-z.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"75 6","pages":"505-516"},"PeriodicalIF":2.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10575840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233119","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}

引用次数: 0

MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting IL10RA MiR-4763-3p通过靶向IL10RA加速脂多糖诱导的心肌细胞凋亡和炎症反应

IF 2.2 4区生物学

Cytotechnology Pub Date : 2023-12-01 DOI: 10.1007/s10616-023-00607-w

Lei Yang, Qian Dai, Xiaoming Bao, Wang Li, Jie Liu

{"title":"MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting IL10RA","authors":"Lei Yang, Qian Dai, Xiaoming Bao, Wang Li, Jie Liu","doi":"10.1007/s10616-023-00607-w","DOIUrl":"https://doi.org/10.1007/s10616-023-00607-w","url":null,"abstract":"In order to investigate miR-4763-3p and associated genes’ roles in myocarditis, AC16 cell line was divided into LPS + miR-4763-3p inhibitor, LPS + NC inhibitor, LPS + miR-4763-3p inhibitor + si-IL10RA and NC groups, and Q-PCR was used to find out whether miR-4763-3p was expressed; Targetscan, Genecards, and MiRDB were used to estimate the miR-4763-3p target; Targetscan was used to display binding sites. Western blot assay was undertaken to detect Bax, Bcl-2, and IL10RA expression. Proliferation and apoptosis were processed using CCK8 and the flow cytometry assay, respectively. Migration and invasion were confirmed utilizing Transwell test. ELISA assay was processed to show the content of IL-6, IL-1ß, IL-10 and TGF-ß in the cell culture supernatant. After being exposed to LPS, cardiomyocyte cells expressed more miR-4763-3p. MiR-4763-3p inhibitor accelerated proliferation, migration and invasion behavior, while it also decreased apoptosis rate in LPS-treated cardiomyocyte cells. MiR-4763-3p inhibitor attenuated the inflammatory response by up-regulating Bax expression and down-regulating Bcl-2 level in LPS-treated cardiomyocyte cells. In cardiomyocyte cells treated with LPS, MiR-4763-3p expression was elevated. si-IL10RA The miR-4763-3p inhibitor restored its effects. MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting IL10RA, which might be a potential target for myocarditis.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138530451","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}

引用次数: 0

Effective methods for immobilization of non-adherent Pv11 cells while maintaining their desiccation tolerance. 固定非粘附性Pv11细胞同时保持其干燥耐受性的有效方法。

IF 2 4区生物学

Cytotechnology Pub Date : 2023-12-01 Epub Date: 2023-10-06 DOI: 10.1007/s10616-023-00592-0

Hiroto Fuse, Takahiro Kikawada, Richard Cornette

{"title":"Effective methods for immobilization of non-adherent Pv11 cells while maintaining their desiccation tolerance.","authors":"Hiroto Fuse, Takahiro Kikawada, Richard Cornette","doi":"10.1007/s10616-023-00592-0","DOIUrl":"10.1007/s10616-023-00592-0","url":null,"abstract":"Pv11 was derived from embryos of the sleeping chironomid Polypedilum vanderplanki, which displays an extreme form of desiccation tolerance known as anhydrobiosis. Pre-treatment with a high concentration of trehalose allows Pv11 cells to enter anhydrobiosis. In the dry state, Pv11 cells preserve transgenic luciferase while retaining its activity. Thus, these cells could be utilized for dry-preserving antibodies, enzymes, signaling proteins or other valuable biological materials without denaturation. However, Pv11 cells grow in suspension, which limits their applicability; for instance, they cannot be integrated into microfluidic devices or used in devices such as sensor chips. Therefore, in this paper, we developed an effective immobilization system for Pv11 cells that, crucially, allows them to maintain their anhydrobiotic potential even when immobilized. Pv11 cells exhibited a very high adhesion rate with both biocompatible anchor for membrane (BAM) and Cell-Tak coatings, which have been reported to be effective on other cultured cells. We also found that Pv11 cells immobilized well to uncoated glass if handled in serum-free medium. Interestingly, Pv11 cells showed desiccation tolerance when trehalose treatment was done prior to immobilization of the cells. In contrast, trehalose treatment after immobilization of Pv11 cells resulted in a significant decrease in desiccation tolerance. Thus, it is important to induce anhydrobiosis before immobilization. In summary, we report the successful development of a protocol for the dry preservation of immobilized Pv11 cells.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-023-00592-0.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"75 6","pages":"491-503"},"PeriodicalIF":2.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10575823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233117","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}

引用次数: 0

The m6A reader IGF2BP1 manipulates BUB1B expression to affect malignant behaviors, stem cell properties, and immune resistance of non-small-cell lung cancer stem cells. m6A阅读器IGF2BP1操纵BUB1B表达，以影响非小细胞肺癌癌症干细胞的恶性行为、干细胞特性和免疫抵抗。

IF 2 4区生物学

Cytotechnology Pub Date : 2023-12-01 Epub Date: 2023-09-21 DOI: 10.1007/s10616-023-00594-y

Shuo Hu, Xi Yan, Wen Bian, Bin Ni

{"title":"The m6A reader IGF2BP1 manipulates BUB1B expression to affect malignant behaviors, stem cell properties, and immune resistance of non-small-cell lung cancer stem cells.","authors":"Shuo Hu, Xi Yan, Wen Bian, Bin Ni","doi":"10.1007/s10616-023-00594-y","DOIUrl":"10.1007/s10616-023-00594-y","url":null,"abstract":"N6-methyladenosine (m6A) modification is the most common internal modification in eukaryotic mRNA and an important mechanism for post-transcriptional regulation of genes. This study focuses on the role of the m6A reader insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) in the malignant behaviors of non-small-cell lung cancer (NSCLC) cells and especially the cancer stem cells (CSCs). We obtained IGF2BP1 as an aberrantly upregulated gene linking to poor survival of patients with NSCLC by bioinformatics, and then confirmed increased IGF2BP1 expression in NSCLC tissues and cells, especially in the enriched CSCs. Knockdown of IGF2BP1 suppressed proliferation, mobility and epithelial-mesenchymal transition activity of NSCLC cells and CSCs, and it reduced stemness, self-renewal ability, xenograft tumorigenesis and immune resistance of the CSCs. IGF2BP1 was predicted to have a positive correlation with BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B), and it upregulated BUB1B expression through m6A modification. Further overexpression of BUB1B in CSCs counteracted the effects of IGF2BP1 silencing and restored the malignant phenotype, self-renewal, and immune resistance of CSCs in vitro and in vivo. Taken together, this work demonstrates that IGF2BP1 manipulates BUB1B expression to affect malignant behaviors, stem cell properties and immune resistance of NSCLC stem cells.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"75 6","pages":"517-532"},"PeriodicalIF":2.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10575838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233120","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}

引用次数: 0