Molecular and Cellular Biochemistry最新文献

{"title":"Interleukin-22 promotes endometrial carcinoma cell proliferation and cycle progression via ERK1/2 and p38 activation.","authors":"Shiqi Liu, Ruqian Zhao, Yuqin Zang, Pengzhu Huang, Qiaoling Zhang, Xiangqin Fan, Junyi Bai, Xingyu Zheng, Shuangshuang Zhao, Dan Kuai, Chao Gao, Yingmei Wang, Fengxia Xue","doi":"10.1007/s11010-024-05179-7","DOIUrl":"https://doi.org/10.1007/s11010-024-05179-7","url":null,"abstract":"<p><p>Endometrial carcinoma (EC) is one of the most common gynecological malignant tumors, but its underlying pathogenic mechanisms are largely obscure. Interleukin-22 (IL-22), one cytokine in the tumor immune microenvironment, was reported to be associated with carcinoma progression. Here, we aimed to investigate the regulation of IL-22 in endometrial carcinoma. Enzyme-linked immunosorbent assay (ELISA) analysis of IL-22 was done in 27 controls and 51 patients with EC. We examined the proliferative potential, cycle progression, and signaling pathways modulated by IL-22 in EC cells. Western blot analysis was performed to investigate the expression of proliferative and cycle-related proteins in EC cells. The effect of IL-22 mediated by interleukin-22 receptor alpha 1 (IL-22RA1) was examined using cell transfection with small interfering RNA (siRNA). In addition, a xenograft tumor model was performed to assess the effect of IL-22 in vivo. We demonstrated significant up-regulation of serum IL-22 concentrations in EC patients (42.59 ± 23.72 pg/mL) compared to the control group (27.47 ± 8.29 pg/mL). High levels of IL-22 concentrations appear to correlate with malignant clinicopathological features of EC. Treatment with IL-22 promoted cell proliferation and G1/S phase progression in Ishikawa and HEC-1B cells. Western blot analysis revealed that c-Myc, cyclin E1, cyclin-dependent kinase (CDK)2, cyclin D1, CDK4, CDK6, p-extracellular signal-regulated kinase1/2 (p-ERK1/2), and p-p38 were highly expressed in EC cells exposed to IL-22. Moreover, in the EC mice model, we found that giving exogenous IL-22 increased tumor volume and weight. Immunohistochemistry showed that intra-tumor Ki-67 expression was up-regulated upon IL-22 treatment. The IL-22-mediated changes in cell proliferation, cycle progression, and protein expression can be effectively inhibited by the ERK1/2 inhibitor U0126 and the p38 inhibitor SB202190. In addition, the role of IL-22 in EC is receptor-dependent. Our findings suggest that IL-22 promotes endometrial carcinoma cell proliferation and G1/S phase progression by activating ERK1/2 and p38 signaling. Therefore, IL-22 may represent a potential therapeutic target for the treatment of endometrial carcinoma.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Expression of Concern: Induction of HRR genes and inhibition of DNMT1 is associated with anthracycline anti-tumor antibiotic-tolerant breast carcinoma cells.","authors":"Hemantika Dasgupta, Md Saimul Islam, Neyaz Alam, Anup Roy, Susanta Roychoudhury, Chinmay Kumar Panda","doi":"10.1007/s11010-024-05182-y","DOIUrl":"https://doi.org/10.1007/s11010-024-05182-y","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune dysregulation of decidual NK cells mediated by GRIM19 downregulation contributes to the occurrence of recurrent pregnancy loss.","authors":"Ying Wang, Anliang Guo, Lin Yang, Xiaojuan Han, Qianni Li, Jin Liu, Yilong Han, Yang Yang, Lan Chao","doi":"10.1007/s11010-024-05181-z","DOIUrl":"https://doi.org/10.1007/s11010-024-05181-z","url":null,"abstract":"<p><p>In patients with recurrent pregnancy loss (RPL), excessive activation of decidual natural killer (dNK) cells has been widely observed, yet the precise underlying mechanisms remain to be elucidated. We collected decidual specimens from RPL patients and controls to assess GRIM19 expression, activation phenotype, cytotoxic function, inflammatory cytokine secretion, and mitochondrial homeostasis in dNK cells. Furthermore, we established a GRIM19-knockout NK-92MI cell line and a GRIM19 ± C57BL/6J mouse model to investigate the relationship between GRIM19 downregulation and dNK immune dysregulation, ultimately contributing to pregnancy loss. Decidual NK cells from RPL patients exhibited significantly lower GRIM19 expression, accompanied by abnormal hyperactivation, enhanced cytotoxicity, and abnormal mitochondrial activation. In vitro experiments confirmed that reduced GRIM19 expression significantly potentiated the cytotoxicity and pro-inflammatory cytokine secretion of NK-92MI cells, while also promoting mitochondrial homeostasis imbalance. Mouse model studies corroborated that GRIM19 downregulation triggers NK cell homeostasis imbalance, contributing to the occurrence of pregnancy loss. Downregulation of GRIM19 in dNK cells contributes to RPL through hyperactivation and disruption of mitochondrial homeostasis, emphasizing its potential as a diagnostic and therapeutic target.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activated TREM1-mediated MAPK signaling in endothelial cells caused by highly expressed STAT1 is associated with intracranial aneurysms occurrence and rupture.","authors":"Hao Zhu, Ge Gao, Yingang Wu, Yang Wang, Yu Chen, Chaoshi Niu","doi":"10.1007/s11010-024-05173-z","DOIUrl":"https://doi.org/10.1007/s11010-024-05173-z","url":null,"abstract":"<p><p>Intracranial aneurysm (IA) poses significant health risks, yet the specific mRNA profiles and regulatory mechanisms distinguishing unruptured IA (UIA) from ruptured IA (RIA) remain unclear. This study aimed to elucidate these differences through comprehensive mRNA analysis. We employed RNA sequencing to compare mRNA expression patterns among control individuals, UIA patients, and RIA patients. Differential expression analysis identified triggering receptor expressed on myeloid cells 1 (TREM1) as a potential biomarker for IA occurrence and rupture, which was validated in an expanded cohort. In vitro experiments revealed that TREM1 overexpression in human umbilical vein endothelial cells (HUVECs) inhibited proliferation, angiogenesis, and migration while promoting apoptosis and inflammation. Bioinformatic predictions and subsequent chromatin immunoprecipitation assays confirmed signal transducer and activator of transcription 1 (STAT1) as a transcriptional regulator of TREM1. STAT1 overexpression in HUVECs activated the MAPK signaling pathway and mimicked the effects of TREM1 overexpression, which were reversible by TREM1 inhibition. Conversely, P38 MAPK inhibition produced opposite effects, which were negated by STAT1 overexpression. This study identifies TREM1 as a potential biomarker for IA occurrence and rupture, likely regulated by STAT1, offering new avenues for non-invasive IA intervention strategies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Downregulation of Hyaluronic acid-CD44 signaling pathway in cervical cancer cell by natural polyphenols Plumbagin, Pongapin and Karanjin.","authors":"Rituparna Roy, Suvra Mandal, Jayanta Chakrabarti, Prosenjit Saha, Chinmay Kumar Panda","doi":"10.1007/s11010-024-05183-x","DOIUrl":"https://doi.org/10.1007/s11010-024-05183-x","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of biomarkers and imaging techniques for the diagnosis of traumatic brain injury: challenges and opportunities.","authors":"James Duerksen, Rhea Carina T Lopez, Paramjit S Tappia, Bram Ramjiawan, Behzad Mansouri","doi":"10.1007/s11010-024-05176-w","DOIUrl":"https://doi.org/10.1007/s11010-024-05176-w","url":null,"abstract":"<p><p>Concussion is a pervasive health issue in the present day. Increased prevalence in recent years has indicated a need to improve the current understanding of minor traumatic brain injury (mTBI). Effort has been devoted to understanding the underlying pathophysiology of TBIs, but some mechanisms remain unknown. Potentially lethal secondary effects of concussion include second impact syndrome and chronic traumatic encephalopathy (CTE), introducing long-term considerations for the management of mTBI. Post-concussion syndrome is another long-term consequence of concussion and may be influenced by both neuroinflammation and hormonal imbalances resulting from head trauma. Genetically mutated apolipoprotein E may also contribute to the severity and persistence of concussion symptoms, perhaps even acting as a risk factor for CTE. As it stands, the diagnosis of concussion is nuanced, depending primarily on subjective diagnostic tools that incorporate patient-reported symptoms and neurocognitive tests. Diagnostic tools provide some assistance in concussion diagnosis, but still lack accuracy and inherently leave room for uncertainty. To mitigate some of this uncertainty, considerable research has been devoted to the development of methods to diagnose concussions objectively. Biomarkers such as S100 calcium binding protein B (S100B), glial fibrillary acidic protein (GFAP), neurofilament light protein (Nf-L), interleukin-6 (IL-6) and microRNAs (miRNAs) as well as imaging techniques including diffusion tensor imaging (DTI) and blood-oxygen level dependent functional magnetic resonance imaging (BOLD-fMRI) show great promise in this regard. This review aims to compile the relevant literature in these areas in the hopes of being used as a reference point for future research regarding concussions.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of breast cancer metastasis: the role of extracellular matrix.","authors":"Rui Chen, Ranqi Zhang, Famin Ke, Xiurong Guo, Fancai Zeng, Qiuyu Liu","doi":"10.1007/s11010-024-05175-x","DOIUrl":"https://doi.org/10.1007/s11010-024-05175-x","url":null,"abstract":"<p><p>The components of the extracellular matrix (ECM) are dynamic, and they mediate mechanical signals that modulate cellular behaviors. Disruption of the ECM can induce the migration and invasion of cancer cells via specific signaling pathways and cytokines. Metastasis is a leading cause of high mortality in malignancies, and early intervention can improve survival rates. However, breast cancer is frequently diagnosed subsequent to metastasis, resulting in poor prognosis and distant metastasis poses substantial hurdles in therapy. In breast cancer, there is notable tissue remodeling of ECM proteins, with several identified as essential components for metastasis. Moreover, specific ECM molecules, receptors, enzymes, and various signaling pathways play crucial roles in breast cancer metastasis, drug treatment, and resistance. The in-depth consideration of these elements could provide potential therapeutic targets to enhance the survival rates and quality of life for breast cancer patients. This review explores the mechanisms by which alterations in the ECM contribute to breast cancer metastasis and discusses current clinical applications targeting ECM in breast cancer treatment, offering valuable perspectives for future ECM-based therapies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autophagy-related gene BECN1 single nucleotide polymorphisms in diseases.","authors":"Sargeet Kaur, Jitendraa Vashistt, Ajay Kumar, Jyoti Parkash, Harish Changotra","doi":"10.1007/s11010-024-05177-9","DOIUrl":"10.1007/s11010-024-05177-9","url":null,"abstract":"<p><p>Autophagy is a cytoprotective process that operates within a cell to maintain cellular homeostasis. An array of multiple proteins is involved to mediate this conserved cellular process. Among these, Beclin 1 protein encoded by BECN1 gene plays a crucial role during the initiation of autophagy. It acts as a molecular platform onto which multiple proteins interact to mediate autophagy initiation. The functioning of such proteins has reportedly been influenced by the molecular markers such as Single Nucleotide Polymorphisms (SNPs) present within the encoding gene. The SNPs within the autophagy gene have been known to influence the functioning of autophagy proteins which further is involved in various diseases. Studies have reported that the SNPs within the BECN1 are involved in various diseases. This report outlines the findings of all the existing research on the role of SNPs within BECN1.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salidroside overcomes cisplatin resistance in ovarian cancer via the inhibition of CRNDE-mediated autophagy.","authors":"Ge Yu, Abiyasi Nanding","doi":"10.1007/s11010-024-05168-w","DOIUrl":"https://doi.org/10.1007/s11010-024-05168-w","url":null,"abstract":"<p><p>Cisplatin (DDP) resistance significantly affects the survival rate of patients with ovarian cancer (OC). Autophagy is recognized as a common cause of resistance to DDP. This study aimed to investigate the impact of salidroside on OC progression and explore its potential regulatory effects on DDP resistance and autophagy. A DDP-resistant A2780 (A2780/DDP) cell line was induced by exposure to increasing DDP concentrations. The protein levels of autophagy proteins (p62, Beclin-1, ATG5, and LC3 II/LC3 I), apoptosis proteins (cleaved caspase-3 and cleaved caspase-9), and PI3K/AKT/mTOR pathway were determined by western blotting. Autophagic vacuoles in cells were observed with LC3 dyeing with confocal fluorescent microscopy. Cell viability and apoptosis were evaluated by cell counting kit-8 assays and flow cytometry. RT-qPCR was conducted to measure the relative levels of various lncRNAs in A2780 or A2780/DDP cells. A xenograft model was established by subcutaneous injection of 1 × 10⁷ A2780 cells into the posterior flank of nude mice. Tumor size and weight were recorded. The expression of Ki67, cleaved caspase-3 and LC3 in tumor tissues was assessed by immunohistochemistry staining. The biodistribution of DDP in organs and blood of normal nude mice and tumors of tumor-bearing mice was detected using the ICP-MS. Hematoxylin-eosin staining was used to assess the histopathological changes of kidney, liver, and spleen sections. For in vitro analysis, autophagy was enhanced in DDP-resistant A2780 cells. Additionally, salidroside inhibits DDP resistance to A2780 cells via autophagy inhibition. Mechanistically, salidroside downregulated CRNDE in DDP-resistant A2780 cells. CRNDE knockdown inhibited autophagy, while CRNDE overexpression reversed the protective effects of salidroside. Additionally, salidroside activated the PI3K/AKT/mTOR pathway in DDP-resistant A2780 cells, and inhibition of PI3K reversed the effect of salidroside on inhibiting autophagy and apoptosis of A2780/DDP cells. For in vivo analysis, salidroside inhibited tumor growth, autophagy, and nephrotoxicity of DDP. Additionally, salidroside downregulated CRNDE and activated PI3K/AKT/mTOR signaling in vivo. Salidroside prevents autophagy-mediated DDP resistance in OC by downregulating lncRNA CRNDE and activating the PI3K/AKT/mTOR pathway.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of astragaloside IV against zinc oxide nanoparticles induced human neuroblastoma SH-SY5Y cell death: a focus on mitochondrial quality control.","authors":"Liwei Wang, Lu Zhang, Yang Yun, Tingting Liang, Chaoqun Yan, Zhuoya Mao, Jingfang Zhang, Baoshe Liu, Jian Zhang, Taigang Liang","doi":"10.1007/s11010-024-05172-0","DOIUrl":"https://doi.org/10.1007/s11010-024-05172-0","url":null,"abstract":"<p><p>Occupational and unintentional exposure of zinc oxide nanoparticles (ZnONPs) raises concerns regarding their neurotoxic potential and there is an urgent need for the development of effective agents to protect against the toxic effects of ZnONPs. Astragalus memeranaceus (AM), a famous Traditional Chinese Medicine, as well as its bioactive components, showing a potential neuroprotective function. This study aims to investigate the neuroprotective effects of bioactive components of AM against ZnONPs-induced toxicity in human neuroblastoma SH-SY5Y cells and its underlying mechanisms. The cell apoptosis, ROS generation, MMP changes, mitochondrial fission/fusion, biogenesis, and mitophagy were assessed. In this study, AM treatment inhibited ZnONPs-induced cell apoptosis and ROS overproduction in SH-SY5Y cells. And astragaloside IV (ASIV) played a dominant role in the attenuation of cytotoxicity after ZnONPs exposure, rather than flavonoids and polysaccharides. ASIV treatment significantly reduced ROS generation and MMP collapse in ZnONPs-exposed cells. Furthermore, the protein expressions of mitochondrial biogenesis (PGC-1α), fusion (Mfn1 and Mfn2), and fission (Drp1) were markedly increased. Meanwhile, the PINK1/Parkin-mediated mitophagy was activated after ASIV administration, which ameliorated ZnONPs-induced SH-SY5Y cell death. Collectively, ASIV administration mitigated ZnONPs-induced cytotoxicity in SH-SY5Y cells through restoring mitochondrial quality control process, which hinted the protective role of ASIV in ZnONPs-induced neurotoxicity.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}