Biocell最新文献

{"title":"Lovastatin modulation of YAP/TAZ signaling on cardiomyocyte autophagy and mitochondrial damage in myocardial I/R injury","authors":"KAITIAN ZHANG, MINGZHU LI, JIANPING ZHANG, Jinfeng Li, Ke-Di Li, HUANQIAN LU, JINYAN LV","doi":"10.32604/biocell.2024.053930","DOIUrl":"https://doi.org/10.32604/biocell.2024.053930","url":null,"abstract":"Objective: Studies have demonstrated that administering statins promptly following myocardial ischemia/reperfusion (MI/R) can confer cardioprotective benefits. This study investigates whether Lovastatin can modulate the Yes-... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 10","pages":"1489-1501"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147899477","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":"PKHD1L1 blocks the malignant behavior of lung adenocarcinoma cells and restricts tumor growth by regulating CBX7","authors":"KEWEI CHENG, Lei Shi, CAIWEN SHI, Shuanshuan Xie, CHANGHUI WANG","doi":"10.32604/biocell.2024.049626","DOIUrl":"https://doi.org/10.32604/biocell.2024.049626","url":null,"abstract":"<b>Objective:</b> To explore the role of polycystic kidney and hepatic disease 1-like 1 (PKHD1L1) in lung adenocarcinoma (LUAD). <b>Methods:</b> Bioinformatics tools were utilized to examine the clinical profile of PKHD1L1 and chromobox protein homolog 7 (CBX7) in LUAD. The Cell Counting Kit-8, colony formation, terminal deoxynucleotidyl transferase dUTP nick end labeling, Transwell, and wound-healing assays were carried out to assess the proliferative, apoptotic, invasive, and migrative capacities of the cells. Furthermore, the interrelation between PKHD1L1 and CBX7 was validated using a co-immunoprecipitation assay. A LUAD mice model was constructed by subcutaneous injection of A549 cells. Finally, immunohistochemical staining was performed to evaluate CBX7 and Ki67 expression. <b>Results:</b> PKHD1L1 was downregulated in LUAD and predicted dismal outcomes in patients with LUAD. PKHD1L1 upregulation repressed the proliferative, invasive, and migrative capabilities of A549 cells and exacerbated the apoptotic rate. Additionally, PKHD1L1 may bind to CBX7 and positively modulate CBX7 expression. CBX7 deletion partly abrogated the effects of PKHD1L1 upregulation on the cellular biological activities in A549 cells. Furthermore, the PKHD1L1/CBX7 axis regulates the Hippo signaling pathway in A549 cells. PKHD1L1 restricted tumor growth in LUAD xenograft mice; this was partly abolished by CBX7 knockdown. <b>Conclusion:</b> PKHD1L1 can hinder LUAD progression by regulating CBX7-mediated Hippo signaling.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 8","pages":"1209-1221"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://file.techscience.com/files/biocell/2024/TSP_BIOCELL-48-8/Biocell-48-08-49626/Biocell-48-49626.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892346","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":"Propofol suppressed cell proliferation through inhibition of SREBP1c-mediated &lt;i&gt;De novo&lt;/i&gt; lipogenesis in colorectal cancer cells","authors":"SHUANG YIN, YF Liu, YAJUN CAO, JIEXIAN ZHOU, YIDAN FANG","doi":"10.32604/biocell.2024.056374","DOIUrl":"https://doi.org/10.32604/biocell.2024.056374","url":null,"abstract":"Background: De novo lipogenesis (DNL) is a critical event for the development of tumors, in the present work, we revealed the role of propofol in colorectal cancer (CRC) cell proliferation. Methods: Western blotting (WB), Re... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 12","pages":"1773-1780"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://cdn.techscience.press/files/biocell/2024/TSP_BIOCELL-48-12/Biocell-48-12-56374/Biocell-48-56374.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147901321","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":"Knockdown of RCN1 contributes to the apoptosis of colorectal cancer via regulating IP3R1","authors":"XUAN SHI, YUFEN WANG, C.-Q. Li, WANGSHU FU, Xinyue Zhang, AIXIA GONG","doi":"10.32604/biocell.2024.048076","DOIUrl":"https://doi.org/10.32604/biocell.2024.048076","url":null,"abstract":"Background: The incidence of colorectal cancer (CRC) has been increasing in recent years. Thus, the discovery of factors that can assist in alleviating CRC is urgently warranted. Methods: To identify a potential factor involved in the development of CRC, we screened the upregulated genes in tumor tissues through four datasets from an online database. The expression of reticulocalbin 1 (RCN1), a Ca2+-binding protein, was upregulated in the four datasets. Based on loss-of-function experiments, the effect of RCN1 on cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. The regulatory effect of RCN1 on apoptosis was evaluated through Annexin V-fluorescein 5-isothiocyanate (FITC)/propidium iodide (PI) staining assay and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay in RKO and SW480 cells. Activation of endoplasmic reticulum (ER) stress signaling pathways was confirmed by estimating the phosphorylation and expression of PRKR-like ER kinase (PERK), inositol-requiring kinase-1 (IRE1), transcription factor 6 (ACT6), and CCAAT/enhancer-binding protein-homologous protein (CHOP). The intracellular Ca2+ homeostasis regulated by RCN1 was determined through the detection of Ca2+ concentration and mitochondrial membrane potential (MMP) measurement. Moreover, whether inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) was involved in the regulation of RCN1 in CRC was verified through the depletion of IP3R1 in RKO cells. Results: Knockdown of RCN1 reduced cell viability and facilitated apoptosis in RKO and SW480 cells. Phosphorylation of PERK and IRE1, activation of ATF6, and upregulation of CHOP were induced by the absence of RCN1, suggesting that the unfolded protein response (UPR) was activated in CRC cells. The concentration of Ca2+ in mitochondria was increased after RCN1 depletion, followed by reduction in the MMP and release of cytochrome c from mitochondria to the cytoplasm in RKO and SW480 cells. Moreover, it was demonstrated that IP3R1 mediates the effect of RCN1 on apoptosis induced by ER stress in CRC cells. The downregulation of IP3R1 restored the RCN1 loss-induced apoptosis and the increased Ca2+ concentration. Conclusion: Taken together, our results confirmed that silencing of RCN1 disrupted intracellular Ca2+ homeostasis and promoted cell apoptosis caused by TG-induced ER stress by regulating IP3R1 and activating the UPR signaling pathways.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 5","pages":"835-845"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20165/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902170","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":"Candidate oncogene placenta specific 8 affects cell growth and cell migration in non-small cell lung cancers","authors":"JINNI MA, MEILIN ZHOU, Xin Xu, XINYAO GAO, HAIXIA WANG, JINHUA SHEN, Lu Xue","doi":"10.32604/biocell.2023.045076","DOIUrl":"https://doi.org/10.32604/biocell.2023.045076","url":null,"abstract":"Background: Placenta specific 8 (PLAC8) is a candidate oncogene involved in the development and progression of solid tumors. However, the status of PLAC8 in lung cancer (LC), especially non-small cell lung cancer (NSCLC) is still not lucid. Methods: Tissue microarray analysis (TMA) was performed to detect the expression patterns of PLAC8 in LC tissues and cell lines. Then a series of cellular experiments were performed fto assess cell proliferation, cell cycle profiles, and cell motility to explore the role of PLAC8 in NSCLC-derived cell lines: H1299 and A549. Results: TMA results showed that PLAC8 played complex and even contradictory roles in different LC samples. Detailed cell-based experiments confirmed that PLAC8 could promote cell viability, alter the cell cycle, and accelerate cell mobility by regulating cell cyclins or cadherins, respectively. Conclusions: The study findings indicate that PLAC8 might participate in LC, especially NSCLC, by affecting cellular physiological processes. The outcomes also shed new light on the potential role of PLAC8 as a therapeutic biomarker in NSCLC.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 2","pages":"239-252"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19787/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907775","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":"Circular RNA circ_0003609 ameliorates hypertrophied ligamentum flavum by regulating the miR-155/SIRT1 axis","authors":"Guibin Zhong, SHURONG WANG, YUJIN HE, Daming Feng, Ke Wei, YANQIU YANG, Jianwei Chen, JUNLING CHEN","doi":"10.32604/biocell.2024.050294","DOIUrl":"https://doi.org/10.32604/biocell.2024.050294","url":null,"abstract":"Background: Hypertrophy of the ligamentum flavum (HLF) is a common contributor to spinal stenosis which results in significant neurological impairments. Circular RNA (circRNA) circ_0003609 has been linked to HLF; however, the exact mechanism by which it causes this disease is unclear. Methods: Circ_0003609 expressions were regulated in HLF cells by overexpression vectors and RNA interference. Cell proliferation and fibrosis-related gene expression were checked by the Cell Counting Kit-8 (CCK-8) assay and western blotting. CircBank’s prediction of the association between miR-155 and circ_0003609 was supported by a dual-luciferase reporter experiment. The function of the miR- 155/sirtuin 1 (SIRT1) axis in controlling HLF fibrosis was further examined. Results: Overexpression of circ_0003609 suppressed HLF cell propagation and fibrosis compared to its silencing. It was found that circ_0003609 served as the sponge for miR-155 and that the circ_0003609/miR-155 axis controlled the fibrosis of HLF cells. It was found that circ_0003609 acted as a sponge for miR-155, regulating the fibrosis of HLF cells. Further, miR-155 targets SIRT1, and the miR-155/SIRT1 axis promotes HLF cell fibrosis. Conclusion: Circ_0003609 ameliorates hypertrophied ligamentum flavum (LF) by modulating the miR-155/SIRT1 axis, indicating a potential treatment approach for HLF.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 6","pages":"1001-1008"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20498/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909317","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-30a-5p alleviates LPS-induced HPMEC injury through regulation of autophagy via Beclin-1","authors":"RAN PAN, JIAYAN MAO, Yueliang Zheng, Wei Chen, JUNPING GUO, Lijun Wang","doi":"10.32604/biocell.2023.046484","DOIUrl":"https://doi.org/10.32604/biocell.2023.046484","url":null,"abstract":"Background: Sepsis, a type of systemic disease, can impact nearly all organs, tissues and cells. Among them, endothelial cells are amongst the first to be affected and respond to the insult. In this study, we investigated the protective effects of microRNA-30a-5p (miR-30a-5p) on human pulmonary microvascular endothelial cells (HPMECs) treated with lipolysaccharide (LPS). Results: An in vitro model of sepsis was established in HPMECs with the use of LPS. Transfecting with different tools (mimetic and inhibitor) to modify miR-30a-5p expression. Cell viability, proliferation and apoptosis were detected by the CCK-8 assay, the EdU kit and fluorescence staining, respectively. The autophagy-related protein and mRNA expression, the number of autophagosomes were separately examined through Western blot analysis, qPT-PCR and confocal microscopy. TargetScan and the luciferase reporter assays were used to probe target genes interacting with miR-30a-5p. Results: LPS caused a reduction in the viability and proliferation of HPMECs, as well as an elevation in the number of apoptotic cells. Subsequently, we observed that miR-30a-5p might play a role in preventing LPS-induced inhibition of cell damage and decreasing HPMEC apoptosis, suggesting the potential function of miR-30a-5p in this injury process. Finally, we confirmed that miR-30a-5p exerts its protective effect by regulating cell autophagy, possibly by targeting Beclin-1. Conclusion: Our study provided evidence that autophagy is a crucial aspect in the protective role of miR-30a-5p against LPS-induced HPMEC injury, identifying a promising target for sepsis-related endothelial cell injury.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 3","pages":"431-441"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19985/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911632","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":"Gp78 regulates PMP22 and causes ER stress and autophagy in EV71-VP1-overexpressing mouse Schwann cells","authors":"DANPING ZHU, Guang‐Ming Liu, Kuan Feng, Suyun Li, Dandan Hu, Sida Yang, Peiqing Li","doi":"10.32604/biocell.2024.044856","DOIUrl":"https://doi.org/10.32604/biocell.2024.044856","url":null,"abstract":"Background: During Enterovirus type 71 (EV71) infection, the structural viral protein 1 (VP1) activates endoplasmic reticulum (ER) stress associated with peripheral myelin protein 22 (PMP22) accumulation and induces autophagy. However, the specific mechanism behind this process remains elusive. Methods: In this research, we used the VP1-overexpressing mouse Schwann cells (SCs) models co-transfected with a PMP22 silencing or Autocrine motility factor receptor (AMFR/gp78) overexpressing vector to explore the regulation of gp78 on PMP22 and its relationship with autophagy and apoptosis. Results: The activity of gp78 could be influenced by EV71-VP1, leading to a decrease in the ubiquitination and degradation of PMP22, resulting in PMP22 accumulation in ER. In VP1-overexpressing mouse SCs, all three ER stress sensors, including pancreatic endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6) and inositol-requiring enzyme 1 (IRE1) and the related downstream signals (C/EBP-homologous protein (CHOP) and Caspase 12) were activated, as well as the ER-resident chaperone Glucose-regulated protein 78 (GRP78). In addition, VP1 upregulated the autophagy marker Microtubule-associated protein 1 light chain 3 beta (LC3B), while PMP22 silencing or gp78 overexpression reversed the phenomenon. Meanwhile, PMP22 silencing or gp78 overexpression increased proliferation of EV71-VP1-transfected mouse SCs. Conclusion: Gp78 could regulate PMP22 accumulation through ubiquitination degradation and cause ER stress and autophagy in EV71-VP1-overexpressing mouse SCs. Therefore, the gp78/PMP22/ER stress axis might emerge as a promising therapeutic target for myelin and neuronal damage induced by EV71 infection.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 4","pages":"653-664"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20109/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903515","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":"3-Methyladenine potentiates paclitaxel-induced apoptosis and phosphorylation of cyclin-dependent kinase 1 at thr161 in nasopharyngeal carcinoma cell","authors":"XIAOQI WU, YECHUAN HE, Yeqin Yuan, XIAN TAN, Lin Zhu, D Wang, BINYUAN JIANG","doi":"10.32604/biocell.2024.048758","DOIUrl":"https://doi.org/10.32604/biocell.2024.048758","url":null,"abstract":"Background: Nasopharyngeal carcinoma (NPC) exhibits a significant prevalence in the southern regions of China, and paclitaxel (PTX) is frequently employed as a medication for managing advanced NPC. However, drug resistance is typically accompanied by a poor prognosis. Exploring the synergistic potential of combining multiple chemotherapeutic agents may represent a promising avenue for optimizing treatment efficacy. Methods: This study investigated whether 3-Methyladenine (3-MA) could potentiated the effect of PTX and its potential molecular mechanism. Samples were divided into the following categories: Negative control (NC) with the solvent dimethyl sulfoxide (DMSO, 0.5% v/v), PTX (400 nM), 3-MA (4 mM), and PTX (400 nM) + 3-MA (4 mM). The viability of NPC cells was assessed using both the cell counting kit-8 (CCK-8) assay and the colony formation assay. Microscopic observation was performed to identify morphological cell changes. Flow cytometry was used to assess cell cycle status, mitochondrial membrane potential (MMP), and apoptotic cells. Western blotting was conducted to quantify the protein expression. Results: 3-MA enhanced PTX-specific inhibition of NPC cell proliferation. PTX, either alone or in combination with 3-MA, caused cell cycle halt at the G2/M phase in the majority of NPC cells, and the combination treatment of PTX with 3-MA induced a higher rate of NPC cell death compared to PTX alone. Western blotting results revealed the combination of PTX with 3-MA heightened activation of cyclin-dependent kinase 1 (CDK1), a key molecule in shifting cells from mitotic arrest to apoptosis, led to a reduction in Myeloid Cell Leukemia 1 (MCL-1) expression and an increase in Poly (ADP-ribose) polymerase (PARP) cleavage. Conclusion: The concurrent administration of PTX with 3-MA effectively enhances PTX’s inhibitory impact on NPC and activates the apoptosis signal regulated by CDK1.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 5","pages":"861-872"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20263/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903701","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 lactylation index predicts the immune microenvironment and prognosis of pan-cancer patients","authors":"XUEJIA ZHAI, Jie Liu, Jin-wei Xiao, Tao Zhang, Jun Wang, Jianjun Li, S Z Yu","doi":"10.32604/biocell.2024.050803","DOIUrl":"https://doi.org/10.32604/biocell.2024.050803","url":null,"abstract":"<b>Background:</b> Protein lactylation is a new way for the “metabolic waste” lactic acid to perform novel functions. Nevertheless, our understanding of the contribution of protein lactylation to both tumor progression and therapeutic interventions remains imited. The construction of a scoring system for lactylation to predict the prognosis of pan-cancer patients and to evaluate the tumor immune microenvironment (TIME) would improve our understanding of the clinical significance of lactylation. <b>Methods:</b> Consensus clustering analysis of lactylation-related genes was used to cluster 177 pancreatic adenocarcinoma (PAAD) patients. Subsequently, a scoring system was developed using the least absolute shrinkage and selection operator (LASSO) regression. Internal validation and external validation were both conducted to assess and confirm the predictive accuracy of the scoring system. Finally, leucine rich repeat containing 1 (LRRC1), a newly discovered lactylation-related gene, was analyzed in PAAD <i>in vitro</i>. <b>Results:</b> Utilizing the profiles of 332 lactylation-related genes, a total of 177 patients with PAAD were segregated into two distinct groups. LacCluster^high patients had a poorer prognosis than LacCluster^low patients. Through the differential analysis between the LacCluster^high and LacCluster^low groups, we identified additional genes associated with lactylation. These genes were then integrated to construct the LacCluster-enhanced system, which enabled more accurate prognosis prediction for patients with PAAD. Then, a lactylation index containing three genes (LacI-3) was constructed using LASSO regression. This was done to enhance the usability of the LacCluster-enhanced system in the clinic. Compared to those in the LacI-3^high subgroup, patients in the LacI-3^low subgroup exhibited increased expression of immune checkpoint-related genes, more immune cell infiltration, lower tumor mutation burdens, and better prognoses, indicating a “hot tumor” phenotype. Moreover, knocking down the expression of LRRC1, the hub gene in the LacI-3 scoring system, inhibited PAAD cell invasion, migration, and proliferation <i>in vitro</i>. Ultimately, the significance of LacI-3 across cancers was confirmed. <b>Conclusion:</b> Our findings strongly imply that protein lactylation may represent a new approach to diagnosing and treating malignant tumors.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 8","pages":"1223-1239"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://file.techscience.com/files/biocell/2024/TSP_BIOCELL-48-8/Biocell-48-08-50803/Biocell-48-50803.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903841","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}