Cytotechnology最新文献

{"title":"The protective role of baicalin regulation of autophagy in cancers.","authors":"Qi Zhang, Shiyun Guo, Hangwei Ge, Honggang Wang","doi":"10.1007/s10616-024-00689-0","DOIUrl":"https://doi.org/10.1007/s10616-024-00689-0","url":null,"abstract":"<p><p>Autophagy is a conservative process of self degradation, in which abnormal organelles, proteins and other macromolecules are encapsulated and transferred to lysosomes for subsequent degradation. It maintains the intracellular balance, and responds to cellular conditions such as hunger or stress. To date, there are mainly three types of autophagy: macroautophagy, microautophagy and chaperone-mediated autophagy. Autophagy plays a key role in regulating multiple physiological and pathological processes, such as cell metabolism, development, energy homeostasis, cell death and hunger adaptation, and so on. Increasing evidence indicates that autophagy dysfunction participates in many kinds of cancers, such as liver cancer, pancreatic cancer, prostate cancer, and so on. However, the relevant mechanisms are not yet fully understood. Baicalin is a natural flavonoid compound extracted from the traditional Chinese medicine <i>Scutellaria baicalensis</i>. The research has shown that after oral or intravenous administration of baicalin, it is delivered to various organs through the systemic circulation, with the highest volume in the kidneys and lungs. More and more evidence suggests that baicalin has antioxidant, anticancer, anti-inflammatory, anti-apoptotic, immunomodulatory and antiviral effects. Therefore, baicalin plays an important role in various diseases, such as cancers, lung diseases, liver diseases, cardiovascular diseases, ans so on. However, the relevant mechanisms have not yet been fully clear. Recently, increasing evidence indicates that baicalin participates in different cancer by regulating autophagy. Herein, we reviewed the current knowledge about the role and mechanism of baicalin regulation of autophagy in multiple types of cancers to lay the theoretical foundation for future related researches.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"33"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930631","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}

{"title":"LncRNA NORAD sponging to miR-26b-5p represses the progression of Alzheimer's disease in vitro by upregulating MME expression.","authors":"Lizhu Chen, Xiaoqiong Yan","doi":"10.1007/s10616-024-00691-6","DOIUrl":"10.1007/s10616-024-00691-6","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurological condition that causes brain shrinkage and cell death. This study aimed to identify the role of the NORAD/miR-26b-5p axis in AD. StarBase was used to examine the binding sequences of miR-26b-5p to LncRNA NORAD or its target genes, which were verified by a double luciferase reporter assay. PC12 cells were processed with Aβ_1-42 to construct an AD model in vitro, and LncRNA NORAD and miR-26b-5p levels in PC12 cells were identified by RT-qPCR. Cell viability and apoptosis were measured using the MTT assay and flow cytometry, respectively. LDH release and oxidative stress-related indicators (MDA, SOD, and CAT) were detected using the corresponding kits, and the levels of Bcl-2 and Bax were assessed by western blotting and RT-qPCR. Aβ_1-42 distinctly decreased LncRNA NORAD and membrane metalloendopeptidase (MME) levels in PC12 cells, while miR-26b-5p was generally increased. The LncRNA NORAD can adsorb miR-26b-5p, and the target gene of miR-26b-5p is neprilysin (MME). In the Aβ_1-42 induced AD model, PC12 cell activity decreased, LDH release and apoptosis increased, oxidative stress level increased, Bax expression increased, and Bcl-2 expression decreased. LncRNA NORAD plays a protective role in AD cell models by abrogating miR-26b-5p levels. Inhibition of MME expression eliminated the protective effects of the miR-26b-5p inhibitor in AD cell models. LncRNA NORAD inhibits AD progression in vitro by modulating the miR-26b-5p-MME signaling axis. The LncRNA NORAD/miR-26b-5p is expected to be a prospective therapeutic candidate for AD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00691-6.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"41"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969878","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}

{"title":"Oxidative stress profile and auto-antibodies production in Tunisian patients with COVID-19.","authors":"Bochra Gargouri, Ichrak Ben Amor, Yosra Ramma, Riad Ben Mansour, Ahmed Bayoudh, Imen Kallel, Hammadi Attia","doi":"10.1007/s10616-024-00683-6","DOIUrl":"10.1007/s10616-024-00683-6","url":null,"abstract":"<p><p>The clinical evidence, complications and the pathogenesis of COVID-19 are not clearly understood. In COVID-19 patients, cellular immune response biomarkers and oxidative stress parameters have been used as gravity markers. Indeed, oxidative stress has been proposed to play an essential role in the genesis of COVID-19. In the present research, we investigated lipid peroxidation, protein oxidation, superoxide dismutase activity and the production of auto-antibodies against superoxide dismutase, in the blood of Tunisian patients with corona virus. To evaluate lipid peroxidation, plasma malondialdehyde and conjugated dienes, have been determined in 69 corona virus patients and 30 controls. To determine protein oxidation the thiol level was measured. Plasma superoxide dismutase activity has been measured in 30 corona virus patients and 30 controls on one hand. Utilizing a standard enzyme-linked immunosorbent assay, the level of immunoglobulin G (IgG), and M (IgM) directed against superoxide dismutase was evaluated. To investigate the implication of auto-antibody production in COVID-19 patients in the generation of oxidative stress, a correlation study between auto-antibodies production and oxidative stress parameters was performed. High levels of both malondialdehyde and conjugated dienes were found in the plasma of patients (p < 0.001, respectively). Protein oxidation was confirmed by the high level of thiol (p < 0.001). Superoxide dismutase activity was not significantly lower in COVID-19 patients (p > 0.05). The level of immunoglobulin G (IgG), and M (IgM) directed against superoxide dismutase is significantly higher in COVID-19 patients than in control group (p < 0.001 respectively). Statistical analyses have demonstrated a positive correlation between superoxide dismutase activity and IgM and IgG isotypes antibodies level against superoxide dismutase (p < 0.001). A strong positive correlation was observed between IgG and malondialdehyde level in all cases (r = 0.368; p ≤ 0.01). In addition, a significant positive correlation was noted between IgM and malondialdehyde (r = 0.290; p = 0.024). Similarly, two significant positive relationship was found between IgG / conjugated dienes (r = 0.356; p = 0.005) and between IgM / conjugated dienes (r = 0.285; p = 0.027).</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"22"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876634","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}

{"title":"Evaluating the impact of media and feed combinations on CHO cell culture performance and monoclonal antibody (trastuzumab) production.","authors":"Aron Gyorgypal, Antash Chaturvedi, Viki Chopda, Haoran Zhang, Shishir P S Chundawat","doi":"10.1007/s10616-024-00690-7","DOIUrl":"10.1007/s10616-024-00690-7","url":null,"abstract":"<p><p>The choice of media and feeds significantly influences the performance of Chinese Hamster Ovary (CHO) mammalian cell cultures in producing desired biologics like monoclonal antibodies (mAb). Sub-optimal nutrient feed/media composition can severely impact cell proliferation and the quality of the final mAb product. For instance, proper protein glycosylation, crucial for mAb stability, safety, and efficacy, heavily relies on cell culture conditions. Currently, starter CHO culture media and daily supplemental feeds used in industrial manufacturing consist of proprietary composition of nutrients critical for mAb production. Standardized optimal media/feed combinations necessary for different cell lines are often lacking, necessitating individualized optimization for each cell line and mAb product. Here, we focused on a CHO-K1 cell line engineered to produce a Trastuzumab biosimilar and evaluated the effects of fourteen commercially relevant basal media and seven feeds on cell culture parameters such as viable cell density, viability, nutrient consumption, metabolite production, mAb titer, and mAb N-glycosylation. Our findings demonstrate clearly that the compositions of the basal medium and feed play a pivotal role in enhancing cell growth and mAb production. This work offers valuable insights into strategies for optimizing feed/media composition for glycosylated monoclonal antibody production using CHO cells.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00690-7.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"40"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969860","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}

{"title":"The regulatory role of KIAA1429 in epithelial-mesenchymal transition in cervical cancer via mediating m6A modification of BTG2.","authors":"Mingyang Wang, Zhiliang Wang, Xiaofeng Zou, Danhe Yang, Ke Xu","doi":"10.1007/s10616-024-00694-3","DOIUrl":"https://doi.org/10.1007/s10616-024-00694-3","url":null,"abstract":"<p><p>Cervical cancer (CC) represents one of the important cancers affecting global female population worldwide. We sought to elucidate the roles and mechanisms of KIAA1429 in the malignant properties of CC cells and the epithelial-mesenchymal transition (EMT) process. KIAA1429 was predicted to be abnormally expressed in CC and correlate with shortened survival of CC patients by GEPIA2 and GSCA databases. High expression of KIAA1429 in human CC cell lines (SiHa, HT-3) was validated by RT-qPCR and Western blot assays. A series of small interfering (si)RNAs including si-KIAA1429-1, si-KIAA1429-2, si-YTHDF2, si-BTG2, and si-negative control (NC) were utilized to interfere the expression levels of KIAA1429, YTHDF2, and BTG2, respectively. Consequently, KIAA1429 silencing attenuated the proliferation, migratory, and invasive functions of CC cells and repressed EMT while promoting CC cell apoptosis. Mechanistically, KIAA1429 could affect N6-methyladenosine (m6A) modification to attenuate the stability of BTG2 mRNA and down-regulate its expression. Additionally, loss of BTG2 partly counteracted the effects of si-KIAA1429 on repressing the malignant activities of CC cells. The aforementioned results collectively demonstrated that KIAA1429-mediated m6A modification of BTG2 and contributed to malignant progression of CC in vitro.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00694-3.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"34"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930641","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}

{"title":"S-Sulfocysteine's toxic effects on HT-22 cells are not triggered by glutamate receptors, nor do they involve apoptotic or genotoxicity mechanisms.","authors":"Volkan Tekin, Fatih Altintas, Burak Oymak, Egem Burcu Unal, Melek Tunc-Ata, Levent Elmas, Vural Kucukatay","doi":"10.1007/s10616-024-00697-0","DOIUrl":"10.1007/s10616-024-00697-0","url":null,"abstract":"<p><p>S-Sulfocysteine (SSC) is a metabolite derived from the metabolism of sulfur-containing amino acids. It has been implicated in neurotoxicity observed in children with sulfite oxidase deficiency. The aim of our study was to confirm the neurotoxic effects of SSC using a mouse hippocampal cell line (HT-22) and to investigate the role of apoptosis in these effects, especially in terms of caspase-3 activation and genotoxicity. Based on the viability graph obtained following increasing concentrations of SSC, we determined the LC50 dose of SSC to be 125 µM by probit analysis. The cytotoxic effects of SSC were not reversed by glutamate receptor blocker administration. However, SSC treatment did not induce caspase-3 activation or induce DNA damage. Our results showed that SSC has a cytotoxic effect on neurons like glutamate, but glutamate receptor blockers reversed glutamate-induced toxicity, while these blockers did not protect neurons from SSC toxicity. The absence of caspase-3 activation and DNA fragmentation, which are indicative of apoptosis, in SSC-induced cell death suggests that alternative cell death pathways, such as necrosis and oxytosis may be implicated. Further research is necessary to fully elucidate SSC-induced cell death. The aim of our study was to confirm the neurotoxic effects of SSC using a mouse hippocampal cell line (HT-22) and to investigate the role of apoptosis in these effects, especially in terms of caspase-3 activation and genotoxicity.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"32"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11688261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920983","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}

{"title":"Etomidate suppresses proliferation, migration, invasion, and glycolysis in esophageal cancer cells via PI3K/AKT pathway inhibition.","authors":"Xiangchao Zhang, Zhengjun Li, Tao Wang","doi":"10.1007/s10616-024-00661-y","DOIUrl":"10.1007/s10616-024-00661-y","url":null,"abstract":"<p><p>Esophageal cancer remains a formidable challenge in oncology, characterized by its poor prognosis and limited therapeutic options. Recent investigations have unveiled the potential of repurposing existing drugs for cancer treatment. Notably, etomidate, an anesthetic agent traditionally used for inducing general anesthesia, has emerged as a promising candidate demonstrating significant anticancer properties across various tumor types. The present study aims to investigate the effects of etomidate on esophageal carcinoma cells, with a specific focus on its ability to modulate the PI3K/AKT signaling pathway and inhibit tumor proliferation. This study employed both in vitro and in vivo methodologies to assess the effects of etomidate on esophageal cancer cells. In vitro experiments evaluated the effects of etomidate on cell proliferation, migration, invasion, and glycolytic processes. An in vivo xenograft mouse model was established to investigate the therapeutic potential of etomidate on tumor growth and assess its impact on the PI3K/AKT signaling pathway in a physiologically relevant context. Etomidate demonstrated a significant inhibitory effect on the proliferation, migration, invasion, and glycolytic capacity of esophageal cancer cells. This multifaceted suppression of tumorigenic properties was closely associated with the inhibition of the PI3K/AKT pathway, as evidenced by reduced phosphorylation levels of PI3K and AKT. In vivo studies using a murine model of esophageal cancer corroborated these findings. Etomidate administration resulted in a substantial reduction in tumor volume and mass, accompanied by increased apoptotic activity and the inhibition of the PI3K/AKT pathway within the tumor tissue. This study demonstrates etomidate's potent inhibition of esophageal cancer progression through suppression of the PI3K/AKT pathway. These promising results warrant further clinical investigation of etomidate as a potential therapeutic strategy for esophageal cancer.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00661-y.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"4"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11579264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709400","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}

{"title":"Docetaxel treatment together with CTLA-4 knockdown enhances reduction of cell viability and amplifies apoptosis stimulation of MCF-7 breast cancer cells.","authors":"Negar Hosseinkhani, Shiva Alipour, Amir Ghaffari Jolfayi, Leili Aghebati-Maleki, Elham Baghbani, Nazila Alizadeh, Vahid Khaze, Behzad Baradaran","doi":"10.1007/s10616-024-00677-4","DOIUrl":"10.1007/s10616-024-00677-4","url":null,"abstract":"<p><p>Breast cancer is the most frequent cancer in women with a 20% mortality rate. The fate of patients suffering from breast cancer can be influenced by immune cells and tumor cells interaction in the tumor microenvironment (TME). Immune checkpoints such as Cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) are regulators of the immune system and defend normal tissues from immune cell attacks but they can be expressed in breast cancer tissue and facilitate immune evasion of tumoral cells. Based on this, here we studied the role of CTLA-4 silencing by specific siRNA in MCF-7 breast cancer cell line together with Docetaxel treatment which is one of the robust chemotherapy agents to demonstrate the significance of combining chemotherapy with efficient targeted therapy in tumor regression. The MCF-7 breast cancer cell line was transfected with CTLA-4-siRNA through the electroporation method, then received an appropriate dose of Docetaxel determined by MTT assay. Flow cytometry was utilized to investigate the consequence of simultaneous CTLA-4 gene silencing and Docetaxel treatment on the apoptosis and cell cycle of MCF-7 cells. The expression levels of Bax and Bcl-2 were also investigated using quantitative real-time PCR. Compared to control groups, CTLA-4-suppressed and Docetaxel-treated cells became more susceptible to apoptosis and cell cycle arrest at the G2-M phase. The additive effect of CTLA-4 knockdown together with Docetaxel treatment significantly downregulated BCL-2 level and upregulated BAX expression. Our findings support the idea that combining chemotherapy such as Docetaxel with efficient targeted therapy against inhibitory immune checkpoints can be a promising strategy in cancer treatment.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"19"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11638433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827603","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}

{"title":"Effect of pH on antitumor activity of Chinese cobra (Naja atra) cytotoxin-XII.","authors":"Xiancai Su, Jiayi Zhou, Mingyuan Zhang, Xiaoping Kang, Dongli Lu, Yanling Chen, Qing Lin, Cailing Yan, Yunlu Xu","doi":"10.1007/s10616-024-00681-8","DOIUrl":"10.1007/s10616-024-00681-8","url":null,"abstract":"<p><p>Cytotoxins (CTXs), proteins found in cobra venom, selectively inhibit tumor cell proliferation. Herein, we selected CTX-XII because of its potent antitumor activity to investigate the effect of solution pH on its response. MTT assay results showed significantly higher inhibition rates for CTX-XII at pH 5.72 (75.79 ± 3.48%) than that at pH 7.32 (50.75 ± 3.8%). Flow cytometry demonstrated that apoptosis rates in B16F10 cells induced by CTX-XII were also higher at pH 5.72 (44.92 ± 7.94%) and 4.12 (42.87 ± 1.89%) than at pH 7.32 (23.5 ± 4.02%). Confocal laser scanning microscopy images showed that red fluorescence, representing CTX-XII concentration, was more intense around tumor cells at pH 5.72, with higher levels in the cytoplasm, than at pH 7.32. In the murine melanoma model, tumor weight in the pH 5.72 CTX-XII group (0.45 ± 0.19 g) was significantly lower than that in the pH 7.32 CTX-XII group (0.84 ± 0.42 g). These results indicate that pH has a strong influence on the antitumor activity of CTX-XII, likely due to pH-dependent ionization changes in CTX-XII that increase its affinity for and penetration into tumor cell membranes. This study provides new insights into the antitumor effects of CTXs and factors influencing their activity.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00681-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"21"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11645386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827608","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}

{"title":"miR-141-3p inhibited BPA-induced proliferation and migration of lung cancer cells through PTGER4.","authors":"Feng Ling, Wenbo Xie, Xiang Kui, Yuyin Cai, Meng He, Jianqiang Ma","doi":"10.1007/s10616-024-00692-5","DOIUrl":"10.1007/s10616-024-00692-5","url":null,"abstract":"<p><p>The chemical substance bisphenol A (BPA) is widely used in household products, and its effect on human health has frequently been the focus of research. The aim of this study was to explore the potential molecular regulatory mechanism of BPA on the proliferation and migration of lung cancer cells. In this study, the H1299 and A549 lung cancer cell lines were selected as the study objects. The cells were treated with different concentrations of BPA (0, 0.1, 1, or 10 μM), and cell viability, proliferation, and migration were evaluated by CCK-8, EdU, clonogenic, and scratch test assays. Western blotting and RT‒qPCR were used to detect the expression of related proteins and genes. Our findings indicated that BPA markedly enhanced both the proliferation and migration capacities of lung cancer cells. In BPA-treated lung cancer cells, the level of miR-141-3p was decreased, PTGER4 expression was significantly increased, and PTGER4 knockdown reduced BPA-induced lung cancer cell proliferation and migration. In addition, miR-141-3p can target and negatively regulate the expression of PTGER4 and further inhibit PI3K/AKT signaling pathway activation and MMPs expression. Moreover, PTGER4 overexpression weakened the inhibitory effect of the miR-141-3p mimic on the proliferation and migration of lung cancer cells. In conclusion, miR-141-3p can inhibit the proliferation and migration of BPA-induced lung cancer cells by downregulating PTGER4, providing a new potential target for the treatment and prevention of lung cancer.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00692-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"28"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913887","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}