Cell Biology International最新文献

Erucic acid increases the potency of cisplatin-induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel. 芥酸通过上调 TRPM2 通道增加顺铂诱导的结直肠癌细胞死亡和氧化应激的效力。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-09-23 DOI: 10.1002/cbin.12248

Ayşenur Nazıroğlu, Ahmet Çarhan, Mustafa Nazıroğlu

{"title":"Erucic acid increases the potency of cisplatin-induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel.","authors":"Ayşenur Nazıroğlu, Ahmet Çarhan, Mustafa Nazıroğlu","doi":"10.1002/cbin.12248","DOIUrl":"10.1002/cbin.12248","url":null,"abstract":"Erucic acid (ErA) is a source of omega-9 monounsaturated fatty acids. ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells, with the exception of the HT-29 human colorectal cancer cell line. The apoptotic and Ca2+ signaling pathways in tumor cells are triggered when mitochondrial Ca2+ and Zn2+ accumulation produce reactive free oxygen species (ROS), which in turn activate TRPM2. ErA-induced ROS and TRPM2 stimulation may augment the anticancer action of cisplatin (CSP). We aimed to study the effects of ErA and CSP incubations on ROS, apoptosis, and cell death in the HT-29 cells by activating TRPM2. The cells were divided into five groups: control, ErA (200 µM for 48 h), CSP (25 µM for 24 h), and ErA + CSP + TRPM2 antagonists (200 µM carvacrol and 25 µM N-(p-amylcinnamoyl)anthranilic acid for 24 h). The TRPM2 antagonists reduced ErA plus CSP-induced increases in H2O2-induced intracellular free Ca2+ concentration ([Ca2+]c) and adenosine diphosphate-ribose-caused TRPM2 currents. ErA and CSP were found to cause apoptosis and cell death by raising the intracellular free Zn2+ concentration (Zn2+]c), caspase-3, -8, and -9, mitochondrial membrane dysfunction, and ROS, while lowering reduced glutathione, cell viability, and cell number. The oxidative, apoptotic, and tumor cell death effects of CSP in the cells were enhanced by the increase of ErA-mediated [Ca2+]c and Zn2+]c entering mitochondria through the activation of TRPM2. In conclusion, we observed that the combination of ErA and CSP was synergistic via TRPM2 activation for the treatment of HT-29 tumor cells.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prediction of clinical prognosis and drug sensitivity in hepatocellular carcinoma through the combination of multiple cell death pathways. 通过结合多种细胞死亡途径预测肝细胞癌的临床预后和药物敏感性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-08-27 DOI: 10.1002/cbin.12235

QingKun Chen, ChenGuang Zhang, Tao Meng, Ke Yang, QiLi Hu, Zhong Tong, XiaoGang Wang

{"title":"Prediction of clinical prognosis and drug sensitivity in hepatocellular carcinoma through the combination of multiple cell death pathways.","authors":"QingKun Chen, ChenGuang Zhang, Tao Meng, Ke Yang, QiLi Hu, Zhong Tong, XiaoGang Wang","doi":"10.1002/cbin.12235","DOIUrl":"10.1002/cbin.12235","url":null,"abstract":"Hepatocellular carcinoma (HCC) is the sixth most common malignant tumor, highlighting a significant need for reliable predictive models to assess clinical prognosis, disease progression, and drug sensitivity. Recent studies have highlighted the critical role of various programmed cell death pathways, including apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, entotic cell death, NETotic cell death, parthanatos, lysosome-dependent cell death, autophagy-dependent cell death, alkaliptosis, oxeiptosis, and disulfidptosis, in tumor development. Therefore, by investigating these pathways, we aimed to develop a predictive model for HCC prognosis and drug sensitivity. We analyzed transcriptome, single-cell transcriptome, genomic, and clinical information using data from the TCGA-LIHC, GSE14520, GSE45436, and GSE166635 datasets. Machine learning algorithms were used to establish a cell death index (CDI) with seven gene signatures, which was validated across three independent datasets, showing that high CDI correlates with poorer prognosis. Unsupervised clustering revealed three molecular subtypes of HCC with distinct biological processes. Furthermore, a nomogram integrating CDI and clinical information demonstrated good predictive performance. CDI was associated with immune checkpoint genes and tumor microenvironment components using single-cell transcriptome analysis. Drug sensitivity analysis indicated that patients with high CDI may be resistant to oxaliplatin and cisplatin but sensitive to axitinib and sorafenib. In summary, our model offers a precise prediction of clinical outcomes and drug sensitivity for patients with HCC, providing valuable insights for personalized treatment strategies.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Shikonin protects skin cells against oxidative stress and cellular dysfunction induced by fine particulate matter. Shikonin 可保护皮肤细胞免受微粒物质引起的氧化应激和细胞功能障碍的影响。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-08-21 DOI: 10.1002/cbin.12233

Kristina Shilnikova, Kyoung Ah Kang, Mei Jing Piao, Herath Mudiyanselage Udari Lakmini Herath, Pincha Devage Sameera Madushan Fernando, Hye-Jin Boo, Sang Pil Yoon, Jin Won Hyun

{"title":"Shikonin protects skin cells against oxidative stress and cellular dysfunction induced by fine particulate matter.","authors":"Kristina Shilnikova, Kyoung Ah Kang, Mei Jing Piao, Herath Mudiyanselage Udari Lakmini Herath, Pincha Devage Sameera Madushan Fernando, Hye-Jin Boo, Sang Pil Yoon, Jin Won Hyun","doi":"10.1002/cbin.12233","DOIUrl":"10.1002/cbin.12233","url":null,"abstract":"Shikonin, an herbal naphthoquinone, demonstrates a broad spectrum of pharmacological properties. Owing to increasingly adverse environmental conditions, human skin is vulnerable to harmful influences from dust particles. This study explored the antioxidant capabilities of shikonin and its ability to protect human keratinocytes from oxidative stress induced by fine particulate matter (PM2.5). We found that shikonin at a concentration of 3 µM was nontoxic to human keratinocytes and effectively scavenged reactive oxygen species (ROS) while increasing the production of reduced glutathione (GSH). Furthermore, shikonin enhanced GSH level by upregulating glutamate-cysteine ligase catalytic subunit and glutathione synthetase mediated by nuclear factor-erythroid 2-related factor. Shikonin reduced ROS levels induced by PM2.5, leading to recovering PM2.5-impaired cellular biomolecules and cell viability. Shikonin restored the GSH level in PM2.5-exposed keratinocytes via enhancing the expression of GSH-synthesizing enzymes. Notably, buthionine sulphoximine, an inhibitor of GSH synthesis, diminished effect of shikonin against PM2.5-induced cell damage, confirming the role of GSH in shikonin-induced cytoprotection. Collectively, these findings indicated that shikonin could provide substantial cytoprotection against the adverse effects of PM2.5 through direct ROS scavenging and modulation of cellular antioxidant system.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oxidative stress disrupts vascular microenvironmental homeostasis affecting the development of atherosclerosis. 氧化应激破坏血管微环境稳态，影响动脉粥样硬化的发展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-10-06 DOI: 10.1002/cbin.12239

Ruifei Shao, Rui Chen, Qiang Zheng, Mengyu Yao, Kunlin Li, Yu Cao, Lihong Jiang

{"title":"Oxidative stress disrupts vascular microenvironmental homeostasis affecting the development of atherosclerosis.","authors":"Ruifei Shao, Rui Chen, Qiang Zheng, Mengyu Yao, Kunlin Li, Yu Cao, Lihong Jiang","doi":"10.1002/cbin.12239","DOIUrl":"10.1002/cbin.12239","url":null,"abstract":"Atherosclerosis is primarily an inflammatory reaction of the cardiovascular system caused by endothelial damage, leading to progressive thickening and hardening of the vessel walls, as well as extensive necrosis and fibrosis of the surrounding tissues, the most necessary pathological process causing cardiovascular disease. When the body responds to harmful internal and external stimuli, excess oxygen free radicals are produced causing oxidative stress to occur in cells and tissues. Simultaneously, the activation of inflammatory immunological processes is followed by an elevation in oxygen free radicals, which directly initiates the release of cytokines and chemokines, resulting in a detrimental cycle of vascular homeostasis abnormalities. Oxidative stress contributes to the harm inflicted upon vascular endothelial cells and the decrease in nitric oxide levels. Nitric oxide is crucial for maintaining vascular homeostasis and is implicated in the development of atherosclerosis. This study examines the influence of oxidative stress on the formation of atherosclerosis, which is facilitated by the vascular milieu. It also provides an overview of the pertinent targets and pharmaceutical approaches for treating this condition.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of concern: "CXCR4 positive cell-derived Pdx1-high/Shh-low cells originated from embryonic stem cells improve the repair of pancreatic injury in mice". 表达关切："源自胚胎干细胞的 CXCR4 阳性细胞衍生 Pdx1 高/Shh 低细胞可改善小鼠胰腺损伤的修复"。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-10-17 DOI: 10.1002/cbin.12254

引用次数: 0

Deciphering the cellular landscape and potential targets of nasopharyngeal and oral cancers using single-cell RNA sequencing. 利用单细胞 RNA 测序破解鼻咽癌和口腔癌的细胞图谱和潜在靶点。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-08-29 DOI: 10.1002/cbin.12236

Yanfei Zhang, Xiaoyu Qin, Weihua Lou, Liang Wang, Wuhao Lu, Changhui Gao, Shousen Hu

{"title":"Deciphering the cellular landscape and potential targets of nasopharyngeal and oral cancers using single-cell RNA sequencing.","authors":"Yanfei Zhang, Xiaoyu Qin, Weihua Lou, Liang Wang, Wuhao Lu, Changhui Gao, Shousen Hu","doi":"10.1002/cbin.12236","DOIUrl":"10.1002/cbin.12236","url":null,"abstract":"Cellular heterogeneity in nasopharyngeal cancer (NPC) and oral cancer remains unclear. In the current study, using single-cell RNA sequencing techniques, we investigated the cellular landscape in NPC and oral cancers. We identified a diverse range of cell types within the tumor microenvironment (TME) and variations in cell infiltration between NPC and oral cancer. In oral cancer, we observed a predominant infiltration of epithelial cells, fibroblasts, and endothelial cells (ECs), while T cells were the main infiltrating cell population in NPCs. We further classified these infiltrating cells into subclusters. Additionally, we observed complex interactions among cells that led to distinct trajectories. In particular, a unique epithelial subcluster with high expression of major histocompatibility complex class II (MHC-II) molecules was correlated with a favorable outcome and infiltration of CD4+ T cells. In addition, MHC-II+ epithelial cells inhibited mouse tumor growth and promoted T-cell infiltration. Consequently, our findings provide a deep understanding of the TME showing a significant prognostic value and therapeutic potential.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pax6 expressing neuroectodermal and ocular stem cells: Its role from a developmental biology perspective. 表达 Pax6 的神经外胚层和眼干细胞：从发育生物学角度看其作用

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-09-23 DOI: 10.1002/cbin.12246

Shubhangi More, Sumit Mallick, Sudheer Shenoy P, Bipasha Bose

{"title":"Pax6 expressing neuroectodermal and ocular stem cells: Its role from a developmental biology perspective.","authors":"Shubhangi More, Sumit Mallick, Sudheer Shenoy P, Bipasha Bose","doi":"10.1002/cbin.12246","DOIUrl":"10.1002/cbin.12246","url":null,"abstract":"Pax-6 emerges as a critical transcription factor that guides the fate of stem cells towards neural lineages. Its expression influences the differentiation of neural progenitors into diverse neuronal subtypes, glial cells, and other neural cell types. Pax-6 operates with other regulatory factors to ensure the precise patterning and organization of the developing nervous system. The intricate interplay between Pax-6 and other signaling pathways, transcription factors, and epigenetic modifiers underpins the complicated balance between stem cell maintenance, proliferation, and differentiation in neuroectodermal and ocular contexts. Dysfunction of Pax-6 can lead to a spectrum of developmental anomalies, underscoring its importance in these processes. This review highlights the essential role of Pax-6 expression in neuroectodermal and ocular stem cells, shedding light on its significance in orchestrating the intricate journey from stem cell fate determination to the emergence of diverse neural and ocular cell types. The comprehensive understanding of Pax-6 function gained from a developmental biology perspective offers valuable insights into normal development and potential therapeutic avenues for neuroectodermal and ocular disorders.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to "The Hippo-YAP pathway regulates the proliferation of alveolar epithelial progenitors after acute lung injury". 对 "急性肺损伤后肺泡上皮祖细胞的增殖受 Hippo-YAP 通路调控 "的更正。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 Epub Date: 2024-11-06 DOI: 10.1002/cbin.12247

引用次数: 0

ZNF655 involved in the progression of multiple myeloma via the activation of AKT. ZNF655 通过激活 AKT 参与多发性骨髓瘤的进展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-03 DOI: 10.1002/cbin.12256

Haiming Kou, Shuqin Jiang, Xueqiong Wu, Changhua Jing, Xinxin Xu, Jiaju Wang, Cui Zhang, Wenting Liu, Yan Gao, Qian Men, Ping Lu, Zhenhui Lv

{"title":"ZNF655 involved in the progression of multiple myeloma via the activation of AKT.","authors":"Haiming Kou, Shuqin Jiang, Xueqiong Wu, Changhua Jing, Xinxin Xu, Jiaju Wang, Cui Zhang, Wenting Liu, Yan Gao, Qian Men, Ping Lu, Zhenhui Lv","doi":"10.1002/cbin.12256","DOIUrl":"https://doi.org/10.1002/cbin.12256","url":null,"abstract":"Multiple myeloma (MM) is an incurable hematological malignancy, and the number of MM patients is increasing year by year. Zinc finger protein 655 (ZNF655) has been shown to regulate various biological processes and is implicated in the progression of many diseases. However, the roles of ZNF655 in MM progression remains unclear. In this study, we aimed to explore the effects of ZNF655 on progression by detecting the alteration of the phenotypes and tumorigenesis induced by ZNF655 knockdown in MM. The expression level of ZNF655 in MM was clarified by real-time quantitative polymerase chain reaction assays. Furthermore, loss-of-function assays in vitro and in vivo was investigated the biological functions of ZNF655 in MM. These findings revealed that ZNF655 depletion remarkably inhibited MM cell proliferation, arrested cell cycle, and induced cell apoptosis. Mechanistically, ZNF655 was found to regulate AKT in MM. In conclusion, this study indicated that ZNF655 regulated the progression of MM via AKT activation and downregulation of ZNF655 may be a promising antitumor strategy in MM.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MARCHF1 promotes breast cancer through accelerating REST ubiquitylation and following TFAM transcription. MARCHF1 通过加速 REST 泛素化和跟随 TFAM 转录来促进乳腺癌的发生。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-10-20 DOI: 10.1002/cbin.12255

Jutao Li, Zhenming Gao

{"title":"MARCHF1 promotes breast cancer through accelerating REST ubiquitylation and following TFAM transcription.","authors":"Jutao Li, Zhenming Gao","doi":"10.1002/cbin.12255","DOIUrl":"https://doi.org/10.1002/cbin.12255","url":null,"abstract":"Breast cancer has become the leading cause of death in women. Membrane associated ring-CH-type finger 1 (MARCHF1) is associated with the development of various types of cancer, but the exact role of MARCHF1 in breast cancer remains unclear. In our study, the higher MARCHF1 expression was observed in tumor samples of patients with breast cancer and then the role of MARCHF1 in breast cancer was further evaluated. Overexpression of MARCHF1 contributed to proliferation of cancer cells and inhibition of oxidative stress. Knockdown of MARCHF1 reduced breast cancer cell proliferation, increased mitochondrial dysfunction induced by oxidative stress, eventually aggravating cell death. In vivo, MARCHF1 promoted the tumor growth and oppositely, MARCHF1 silencing suppressed the tumor development. Moreover, MARCHF1 interacted with repressor Element-1 silencing transcription factor (REST) and facilitated its ubiquitylation and degradation. Subsequently, REST negatively regulated the transcription of mitochondrial transcription factor A (TFAM). The subcutaneous tumor formation assay in nude mice also supported these conclusions. In details, knockdown of MARCHF1 upregulated the protein expression of REST and downregulated the mRNA level of TFAM. On the contrary, MARCHF1 overexpression exhibited opposite effects. Thus, MARCHF1 is conducive to the progression of breast cancer via promoting the ubiquitylation and degradation of RSET and then the transcription of TFAM. Downregulating MARCHF1 could provide a novel direction for treating breast cancer.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0