Frontiers in bioscience (Landmark edition)最新文献

{"title":"DLX5 Promotes Radioresistance in Renal Cell Carcinoma by Upregulating c-Myc Expression.","authors":"Danfei Hu, Mingyao Li, Xiaodong Chen","doi":"10.31083/j.fbl2911400","DOIUrl":"https://doi.org/10.31083/j.fbl2911400","url":null,"abstract":"<p><strong>Background: </strong>Renal cell carcinoma (RCC) is a prevalent and aggressive kidney cancer with notable metastatic potential. While radiotherapy is effective for treating metastatic RCC, the emergence of radioresistance presents a major challenge. This study explores the role of <i>DLX5</i>, previously identified as an oncogene in various cancers, in the development of radioresistance in RCC.</p><p><strong>Methods: </strong>Distal-less homeobox 5 (DLX5) expression was measured using western blot analysis. To study the effects of DLX5, its expression was knocked down in 786-O and Caki-1 RCC cell lines through si-DLX5 transfection, and the impact of DLX5 on RCC cell proliferation and radioresistance was assessed using cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) incorporation assay, flow cytometry, colony formation, immunofluorescence, and western blot assays. The underlying mechanisms were explored through western blot, colony formation, and CCK-8 assays. <i>In vivo</i> effects were examined using a xenograft mouse model.</p><p><strong>Results: </strong><i>In silico</i> results showed increased DLX5 levels in RCC tissues. Similarly, DLX5 expression was elevated in RCC cell lines. Silencing DLX5 reduced RCC cell proliferation and induced apoptosis <i>in vitro</i>. Additionally, DLX5 knockdown decreased radioresistance and increased DNA damage in RCC cells. Mechanistic studies revealed that DLX5 promotes radioresistance through the upregulation of c-Myc. <i>In vivo</i>, DLX5 silencing impeded tumor growth and reduced radioresistance.</p><p><strong>Conclusion: </strong>DLX5 contributes to RCC cell growth and radioresistance by upregulating c-Myc expression, highlighting its potential as a target for overcoming radioresistance in RCC.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"400"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Huang Y, <i>et al</i>. Sophocarpine inhibits the growth of gastric cancer cells via autophagy and apoptosis. Frontiers in Bioscience-Landmark. 2019; 24: 616-627.","authors":"Frontiers In Bioscience-Landmark Editorial Office","doi":"10.31083/j.fbl2911399","DOIUrl":"https://doi.org/10.31083/j.fbl2911399","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"399"},"PeriodicalIF":3.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142756008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CELF6 as an Oncogene in Colorectal Cancer: Targeting Stem-Cell-Like Properties Through Modulation of <i>HOXA5</i> mRNA Stability.","authors":"Zhiming Fu, Xiang Wang, Zhiju Chen, Baochun Wang, Weiwei Huang, Xin Liu","doi":"10.31083/j.fbl2911395","DOIUrl":"https://doi.org/10.31083/j.fbl2911395","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence indicates the essential role of cancer stem cells (CSCs) in the development and progression of various cancers, including colorectal cancer (CRC). CELF6, a member of the cytosine-uridine-guanine-binding protein (CUG-BP), Elav-like family (CELF), has been reported to be downregulated in CRC tissues. This study aims to elucidate the role and underlying mechanisms of CELF6 in CRC progression.</p><p><strong>Methods: </strong>The expression levels and prognostic significance of CELF6, along with its association with homeobox A5 (HOXA5), were analyzed using University of Alabama at Birmingham Cancer Data Analysis Portal (UALCAN), PrognoScan, and Tumor Immune Estimation Resource (TIMER) databases. The expression of CELF6 was further assessed through quantitative real-time polymerase chain reaction (qRT-PCR), immunoblotting, and immunohistochemistry. Both <i>in vitro</i> and <i>in vivo</i> experiments were conducted to investigate the effects of CELF6 on CRC cell proliferation, stemness and tumorigenesis, and to elucidate the molecular mechanisms.</p><p><strong>Results: </strong>CELF6 was found to be downregulated in CRC and was associated with poor prognosis. Functional studies revealed that overexpression of CELF6 resulted in decreased CRC cell proliferation and stemness <i>in vitro</i>, reduced tumor growth <i>in vivo</i>, and induced G1 phase cell cycle arrest. Mechanistically, CELF6 regulated the expression of HOXA5 by modulating its mRNA stability. Furthermore, the knockdown of HOXA5 reversed the inhibitory effects of CELF6 on CRC cell proliferation and stemness, demonstrating that silencing HOXA5 counteracted the suppressive effects of CELF6.</p><p><strong>Conclusions: </strong>This study is the first to identify CELF6 as a suppressor of stemness and a modulator of CRC progression. These findings provide new insights into the role of CELF6 in CRC and highlight its potential as a novel therapeutic target.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"395"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Arginine Vasopressin on Hippocampal Myelination in an Autism Rat Model: A RNA-seq and Mendelian Randomization Analysis.","authors":"Xingxing Bao, Bo Zhou, Min Wen","doi":"10.31083/j.fbl2911394","DOIUrl":"https://doi.org/10.31083/j.fbl2911394","url":null,"abstract":"<p><strong>Background: </strong>To explore the therapeutic role of arginine vasopressin (AVP) and its possible mechanisms in autism.</p><p><strong>Methods: </strong>Mid-trimester pregnant rats treated with valproate on embryonic day 12.5 and their offspring were selected as autism model. The autism rats were randomly assigned to autism group and AVP treatment group that given AVP by inhalation per day from postnatal days 21 to 42. The changes in social behavior and the hippocampus transcriptome were compared, and the hub genes were confirmed by quantitative real-time polymerase chain reaction (qPCR) and Mendelian randomization (MR).</p><p><strong>Results: </strong>403 genes were found to be differentially expressed in the autism model, with the majority of these genes being involved in oligodendrocyte development and myelination. Only 11 genes associated with myelination exhibited statistically significant alterations following AVP treatment when compared to the autism group. Gene set enrichment, expression patterns, and weighted gene co-expression network analysis (WGCNA) analysis consistently indicated that the biological processes of oligodendrocyte development and myelination were markedly enriched in the autism group and exhibited improvement following treatment. The variation trend of various nerve cells demonstrated a notable increase in the proportion of oligodendrocytes and oligodendrocyte precursor cells in the autism group, which subsequently exhibited a significant decline following treatment. Five hub genes (<i>MBP, PLIP, CNP, GFAP,</i> and <i>TAOK1</i>) were verified by qPCR. Finally, MR studies have confirmed a causal relationship between hippocampal myelination-related gene expression and the risk of autism.</p><p><strong>Conclusions: </strong>AVP could markedly enhance social interaction abilities in the autism rat model, possibly due to the significantly improved hippocampus oligodendrocytes development and myelination.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"394"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SENP1 Promotes Caspase-11 Inflammasome Activation and Aggravates Inflammatory Response in Murine Acute Lung Injury Induced by Lipopolysaccharide.","authors":"Mingjun Du, Wenhan Wang, Shaoyuan Zhang, Jianmin Gu, Chunbing Zhang, Hai Zhang","doi":"10.31083/j.fbl2911397","DOIUrl":"https://doi.org/10.31083/j.fbl2911397","url":null,"abstract":"<p><strong>Background: </strong>Infection is the leading cause of acute lung injury (ALI). Macrophages, which are pivotal innate immune cells, play a critical role in mediating inflammatory processes. Intracellular lipopolysaccharide (LPS) from invasive Gram-negative bacteria can activate the caspase-11 inflammasome, leading to the induction of pyroptosis in macrophages. This process subsequently triggers the release of inflammatory cytokines and damage-associated molecular patterns from pyroptotic macrophages, thereby exacerbating inflammatory progression in ALI. However, the precise regulatory mechanisms governing caspase-11 activation is still unclear. Sentrin-specific proteases (SENPs) have been identified as notable targets for their anti-inflammatory properties. Nevertheless, the specific role of SENPs in macrophage pyroptosis during the pathogenesis of ALI remains unknown.</p><p><strong>Methods: </strong>We used LPS as an endotoxin to induce ALI. We analyzed the expression and location of sentrin-specific protease 1 (SENP1), pulmonary impairment, macrophage infiltration, caspase-11 inflammasome expression and activation, caspase-11 SUMOylation, and inflammatory cytokine secretion.</p><p><strong>Results: </strong>Upregulated expression of SENP1 in lung tissue and macrophages was observed following LPS stimulation. SENP1 mediates de-SUMOylation and activation of caspase-11 inflammasome in macrophages. Moreover, pharmacological inhibition or genetic deficiency of SENP1 in macrophages significantly improved ALI-related histological damage by reducing the secretion of inflammatory cytokines and suppressing caspase-11-dependent pyroptosis.</p><p><strong>Conclusions: </strong>Collectively, our findings highlight the involvement of SENP1 in caspase-11 activation and inflammatory progression in macrophages, thereby establishing a scientific foundation for the exploration of novel therapeutic strategies aimed at treating ALI.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"397"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay of Reactive Oxygen Species (ROS) and Epigenetic Remodelling in Cardiovascular Diseases Pathogenesis: A Contemporary Perspective.","authors":"Amin Al-Awar, Shafaat Hussain","doi":"10.31083/j.fbl2911398","DOIUrl":"https://doi.org/10.31083/j.fbl2911398","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) continue to be the leading cause of mortality worldwide, necessitating the development of novel therapies. Despite therapeutic advancements, the underlying mechanisms remain elusive. Reactive oxygen species (ROS) show detrimental effects at high concentrations but act as essential signalling molecules at physiological levels, playing a critical role in the pathophysiology of CVD. However, the link between pathologically elevated ROS and CVDs pathogenesis remains poorly understood. Recent research has highlighted the remodelling of the epigenetic landscape as a crucial factor in CVD pathologies. Epigenetic changes encompass alterations in DNA methylation, post-translational histone modifications, adenosine triphosphate (ATP)-dependent chromatin modifications, and noncoding RNA transcripts. Unravelling the intricate link between ROS and epigenetic changes in CVD is challenging due to the complexity of epigenetic signals in gene regulation. This review aims to provide insights into the role of ROS in modulating the epigenetic landscape within the cardiovascular system. Understanding these interactions may offer novel therapeutic strategies for managing CVD by targeting ROS-induced epigenetic changes. It has been widely accepted that epigenetic modifications are established during development and remain fixed once the lineage-specific gene expression pattern is achieved. However, emerging evidence has unveiled its remarkable dynamism. Consequently, it is now increasingly recognized that epigenetic modifications may serve as a crucial link between ROS and the underlying mechanisms implicated in CVD.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"398"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HDL Cholesterol-Associated Shifts in the Expression of Preselected Genes Reveal both Pro-Atherogenic and Atheroprotective Effects of HDL in Coronary Artery Disease.","authors":"Alexander D Dergunov, Elena V Nosova, Alexandra V Rozhkova, Margarita A Vinogradina, Veronika B Baserova, Mikhail A Popov, Svetlana A Limborska, Liudmila V Dergunova","doi":"10.31083/j.fbl2911396","DOIUrl":"https://doi.org/10.31083/j.fbl2911396","url":null,"abstract":"<p><strong>Background: </strong>The associations of high-density lipoprotein (HDL) level and functionality with lipid metabolism, inflammation, and innate immunity in coronary artery disease (CAD) remain controversial. The differential expression of a set of genes related to HDL metabolism (24 genes) and atherogenesis (41 genes) in peripheral blood mononuclear cells (PBMC) from CAD and control patients with varied HDL cholesterol (HDL-C) levels was compared.</p><p><strong>Methods: </strong>76 male patients 40-60 years old with CAD diagnosed by angiography and 63 control patients were divided into three groups with low, normal (1.0-1.4 mM), and increased HDL-C levels. Transcript levels were measured by real-time PCR. The differentially expressed genes (DEGs) and associated metabolic pathways were analyzed for three groups, with prevalent CAD as an outcome.</p><p><strong>Results: </strong>The common feature was the increased odds ratio values for liver X receptor (LXR) gene expression for three patient groups. CAD patients with low HDL-C possessed 24 DEGs with lower expression of genes involved in cholesterol efflux, and down-regulated <i>SREBF1</i> and <i>ABCG1</i> are suggested as gene signatures. CAD patients with normal HDL-C possessed nine DEGs with down-regulated <i>ITGAM</i> and <i>ALB</i> as gene signatures. CAD patients with increased HDL-C possessed 19 DEGs with down-regulated <i>APOA1</i> and <i>HMGCR</i> as gene signatures. With gene expression signatures, one standard deviation higher average gene expressions were associated with 5.1-, 48.8-, and 38.9-fold fewer CAD cases for three patient groups. As HDL-C increased in CAD patients, the expression of <i>ABCG1</i>, <i>CUBN</i>, and <i>HDLBP</i> genes increased, while the expression of <i>HMGCR</i> and <i>NPC2</i> genes, involved in cholesterol synthesis and trafficking, decreased. The expression of <i>CD14</i>, <i>CD36</i>, <i>S100A8</i>, <i>S100A9</i>, <i>S100A12</i>, <i>TLR5</i>, <i>TLR8</i>, and <i>VEGFA</i> genes, involved in angiogenesis and inflammation mainly via nuclear factor-κB (NF-κB), decreased.</p><p><strong>Conclusions: </strong>The increased accumulation of cholesteryl ester in PBMC from patients with low HDL-C was suggested. This assumption contrasts with the suggested accumulation of free cholesterol in PBMC from patients with increased HDL-C, concomitant with suppression of cholesterol synthesis and traffic to the plasma membrane, and with an inflammatory state controlled by depressed CD36-mediated and upregulated apoE-mediated immunometabolic signaling. Gene signatures may be used for the diagnosis, prognosis, and treatment of CAD in dependence on HDL-C levels.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"396"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective Role of Vitamin D Receptor in Cerebral Ischemia/Reperfusion Injury <i>In Vitro</i> and <i>In Vivo</i> Model.","authors":"Jie Dai, Haiyan Huang, Liucheng Wu, Mei Ding, Xiangyang Zhu","doi":"10.31083/j.fbl2911389","DOIUrl":"https://doi.org/10.31083/j.fbl2911389","url":null,"abstract":"<p><strong>Background: </strong>Vitamin D receptor (VDR) can prevent myocardial ischemia reperfusion injury (MIRI). Hence, we aimed to illuminate the effect of VDR on cerebral ischemia/reperfusion injury (CIRI).</p><p><strong>Methods: </strong>C57BL/6 mice and SK-N-SH cells were utilized to establish CIRI and cellular oxygen deprivation/reoxygenation (OGD/R) models. Mice were injected with 1 μg/kg Calcitriol or 1 μg/kg Paricalcitol (PC) and adenovirus-mediated VDR overexpression or knockdown plasmids. 2,3,5-triphenyl-tetrazolium chloride (TTC) and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were performed to measure the brain infarct volume and the apoptosis of cerebral cells. SK-N-SH cells were treated with 5 mM N-acetyl-L-cysteine (NAC) and transfected with VDR knockdown plasmid. Flow cytometry and Cell Counting Kit-8 (CCK-8) assays were employed to assess the apoptosis and cell viability. Enzyme-Linked Immunosorbent Assay (ELISA), quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) and Western blot were exploited to quantify the levels of reactive species oxygen (ROS), other oxidative stress-related factors, VDR and apoptosis-related factors.</p><p><strong>Results: </strong>The level of VDR in mouse cerebral tissue was elevated by CIRI (<i>p</i> < 0.001). CIRI-induced cerebral infarction (<i>p</i> < 0.001) and the apoptosis of cerebral cells (<i>p</i> < 0.001) in mice were mitigated by the activation of VDR. VDR overexpression abrogated while VDR silencing enhanced CIRI-induced infarction, oxidative stress and apoptosis of cerebral cells (<i>p</i> < 0.05). Furthermore, VDR silencing aggravated the oxidative stress and apoptosis in OGD/R-treated SK-N-SH cells (<i>p</i> < 0.05). NAC, a scavenger of oxidative stress, could reverse the effects of VDR silencing on apoptosis and oxidative stress in OGD/R-treated SK-N-SH cells (<i>p</i> < 0.01).</p><p><strong>Conclusion: </strong>VDR alleviates the oxidative stress to protect against CIRI.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"389"},"PeriodicalIF":3.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The PLCG2 Inhibits Tumor Progression and Mediates Angiogenesis by VEGF Signaling Pathway in Clear Cell Renal Cell Carcinoma.","authors":"Chuanyi Zhao, Daojia Miao, Diaoyi Tan, Jian Shi, Qingyang Lv, Zhiyong Xiong, Xiaoping Zhang","doi":"10.31083/j.fbl2911390","DOIUrl":"https://doi.org/10.31083/j.fbl2911390","url":null,"abstract":"<p><strong>Background: </strong>Clear cell renal cell carcinoma (ccRCC) represents the most prevalent form of renal cell carcinoma. The management of early-stage ccRCC has a better prognosis, while patients with metastatic ccRCC have a lower five-year survival rate. Angiogenesis serves as the fundamental process underlying tumor metastasis. Therefore, it is crucial to discover new targets for angiogenesis to improve patient survival rates.</p><p><strong>Methods: </strong>The Cancer Genome Atlas database, International Cancer Genome Consortium database, Clinical Proteomic Tumor Analysis Consortium database, and a gene set of the vascular endothelial growth factor (VEGF) signaling pathway were utilized to identify differentially expressed genes. Western blot (WB), quantitative real-time polymerase chain reaction, and immunohistochemistry were employed to validate the downregulation of phospholipase C gamma 2 (PLCG2) in ccRCC tissues and cells. Cell Counting Kit-8 (CCK-8) assays, transwell assays, tube formation assays, and oil-red staining were performed to elucidate the biological functions of PLCG2 in tumor cells. Gene set enrichment analysis was applied to explore the downstream pathway. Subcutaneous tumor models and live small animal fluorescent imaging assay were utilized for <i>in vivo</i> investigation of the roles played by PLCG2.</p><p><strong>Results: </strong>Our study has identified a novel biomarker, PLCG2, for ccRCC. <i>PLCG2</i> is a central gene in regulating angiogenesis in ccRCC, as validated by bioinformatics analysis. The findings revealed a diminished expression of PLCG2 in both ccRCC tissues and cells. Further experiments <i>in vivo</i> and <i>in vitro</i> have demonstrated the significant roles of PLCG2 in tumor proliferation, invasion, migration, and lipid accumulation. Results of tube formation assays and WB support the role of PLCG2 in regulating VEGFA expression and angiogenesis.</p><p><strong>Conclusions: </strong>Our results show that PLCG2 functions as a potential biomarker and an independent prognostic indicator for ccRCC. PLCG2 may modulate angiogenesis by influencing the expression of VEGFA. Therefore, targeting PLCG2 could potentially lead to drug discovery and improved cancer treatment strategies.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"390"},"PeriodicalIF":3.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual Role of Lysosome in Cancer Development and Progression.","authors":"Xiao-Qiong Chen, Quan Yang, Wei-Min Chen, Zi-Wei Chen, Guang-Hui Guo, Xuan Zhang, Xiao-Ming Sun, Tao Shen, Fu-Hui Xiao, Yun-Feng Li","doi":"10.31083/j.fbl2911393","DOIUrl":"https://doi.org/10.31083/j.fbl2911393","url":null,"abstract":"<p><p>Lysosomes are essential intracellular catabolic organelles that contain digestive enzymes involved in the degradation and recycle of damaged proteins, organelles, etc. Thus, they play an important role in various biological processes, including autophagy regulation, ion homeostasis, cell death, cell senescence. A myriad of studies has shown that the dysfunction of lysosome is implicated in human aging and various age-related diseases, including cancer. However, what is noteworthy is that the modulation of lysosome-based signaling and degradation has both the cancer-suppressive and cancer-promotive functions in diverse cancers depending on stage, biology, or tumor microenvironment. This dual role limits their application as targets in cancer therapy. In this review, we provide an overview of lysosome and autophagy-lysosomal pathway and outline their critical roles in many cellular processes, including cell death. We highlight the different functions of autophagy-lysosomal pathway in cancer development and progression, underscoring its potential as a target for effective cancer therapies.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"393"},"PeriodicalIF":3.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}