JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献_第6页

Bazi Bushen attenuates osteoporosis in SAMP6 mice by regulating PI3K-AKT and apoptosis pathways 八子布神通过调节 PI3K-AKT 和细胞凋亡途径减轻 SAMP6 小鼠的骨质疏松症。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-29 DOI: 10.1111/jcmm.70161

Zhe Xu, Zeyu Zhang, Huifang Zhou, Shan Lin, Boyang Gong, Zhaodong Li, Shuwu Zhao, Yunlong Hou, Yanfei Peng, Yuhong Bian

{"title":"Bazi Bushen attenuates osteoporosis in SAMP6 mice by regulating PI3K-AKT and apoptosis pathways","authors":"Zhe Xu, Zeyu Zhang, Huifang Zhou, Shan Lin, Boyang Gong, Zhaodong Li, Shuwu Zhao, Yunlong Hou, Yanfei Peng, Yuhong Bian","doi":"10.1111/jcmm.70161","DOIUrl":"10.1111/jcmm.70161","url":null,"abstract":"Osteoporosis (OP), a systemic skeletal disease, is characterized by low bone mass, bone tissue degradation and bone microarchitecture disturbance. Bazi Bushen, a Chinese patented medicine, has been demonstrated to be effective in attenuating OP, but the pharmacological mechanism remains predominantly unclear. In this study, the senescence-accelerated mouse prone 6 (SAMP6) model was used to explore bone homeostasis and treated intragastrically for 9 weeks with Bazi Bushen. In vivo experiments showed that Bazi Bushen treatment not only upregulated the levels of bone mineral density and bone mineral content but also increased the content of RUNX2 and OSX. Furthermore, the primary culture of bone mesenchymal stem cells (BMSCs) in SAMP6 mice was used to verify the effects of Bazi Bushen on the balance of differentiation between osteoblasts and adipocytes, as well as ROS and aging levels. Finally, the pharmacological mechanism of Bazi Bushen in attenuating OP was investigated through network pharmacology and experimental verification, and we found that Bazi Bushen could significantly orchestrate bone homeostasis and attenuate the progression of OP by stimulating PI3K-Akt and inhibiting apoptosis. In summary, our work sheds light on the first evidence that Bazi Bushen attenuates OP by regulating PI3K-AKT and apoptosis pathways to orchestrate bone homeostasis.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70161","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exploring the prognostic value and potential therapeutic strategies of MS4A6A in glioblastoma: A comprehensive analysis of single-cell and multi-omics data 探索 MS4A6A 在胶质母细胞瘤中的预后价值和潜在治疗策略：单细胞和多组学数据的综合分析。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-29 DOI: 10.1111/jcmm.70177

Fangchao Wan, Yanling Li, Jianming Zhu, Dandan Yu, Hongjuan Liu, Bohong Hu

引用次数: 0

GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR-driven transcriptional activation GOLM1 通过与 PSMD1 相互作用并增强 AR 驱动的转录激活，促进前列腺癌的进展。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-29 DOI: 10.1111/jcmm.70186

Guang Yan, Tianhang Zhu, Jiawei Zhou, Xia Li, Zonghua Wen, Bahaerguli Miuhuitijiang, Zhiyong Zhang, Yuejun Du, Chengyao Li, Xiaojun Shi, Wanlong Tan

{"title":"GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR-driven transcriptional activation","authors":"Guang Yan, Tianhang Zhu, Jiawei Zhou, Xia Li, Zonghua Wen, Bahaerguli Miuhuitijiang, Zhiyong Zhang, Yuejun Du, Chengyao Li, Xiaojun Shi, Wanlong Tan","doi":"10.1111/jcmm.70186","DOIUrl":"10.1111/jcmm.70186","url":null,"abstract":"Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen-independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR-driven transcriptional activity in PCa progression. Utilizing local clinical data and TCGA data, we have established a robust association between GOLM1 and AR target genes, and further demonstrated that GOLM1 can enhance the expression of AR target genes. We discovered that GOLM1 interacts with PSMD1, a component of the 19S regulatory complex in the 26S proteasome, using mass spectrometry and Co-IP analysis. It is well known that ubiquitin-proteasome plays a vital role in AR expression and transcriptional regulation. Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR-driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR-driven transcriptional activation.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bone sialoprotein facilitates anoikis resistance in lung cancer by inhibiting miR-150-5p expression 骨硅蛋白通过抑制 miR-150-5p 的表达促进肺癌的抗肿瘤能力

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-28 DOI: 10.1111/jcmm.70155

Le Huynh Hoai Thuong, Chang-Lun Huang, Yi-Chin Fong, Chun-Lin Liu, Jeng-Hung Guo, Chih-Ying Wu, Po-I Liu, Chih-Hsin Tang

{"title":"Bone sialoprotein facilitates anoikis resistance in lung cancer by inhibiting miR-150-5p expression","authors":"Le Huynh Hoai Thuong, Chang-Lun Huang, Yi-Chin Fong, Chun-Lin Liu, Jeng-Hung Guo, Chih-Ying Wu, Po-I Liu, Chih-Hsin Tang","doi":"10.1111/jcmm.70155","DOIUrl":"10.1111/jcmm.70155","url":null,"abstract":"Metastatic lung cancer is a highly prevalent cancer with a very low chance of long-term survival. Metastasis at secondary sites requires that cancer cells develop anoikis resistance to survive during circulation. High levels of bone sialoprotein (BSP), a member of the small integrin-binding ligand N-linked glycoproteins (SIBLINGs), have been shown to promote the spread of lung cancer cells; however, the effects of BSP in anoikis resistance are largely unknown. In this study, we determined that BSP promotes anoikis resistance in lung cancer cells. BSP was also shown to promote the expression of E-cadherin and vimentin (epithelial-to-mesenchymal transition markers, which have been utilized as indicators of anoikis resistance). It appears that BSP facilitates MMP-14-dependent anoikis resistance by inhibiting the synthesis of miR-150-5p and activating the ERK signalling pathway. Knockdown of BSP expression was shown to block lung cancer metastasis by lowering anoikis resistance in vivo. These results indicate that BSP is a promising target to deal with anoikis resistance and metastasis in human lung cancers.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70155","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of E2 on the IDO1-mediated metabolic KYN pathway in OVX female mice E2 对 OVX 雌性小鼠体内 IDO1 介导的 KYN 代谢途径的影响。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-28 DOI: 10.1111/jcmm.70179

Xi Jiang, Xuefeng Yu, Shuran Hu, Huidan Dai, Hanqin Zhang, Yuyang Hang, Xupei Xie, Yubo Yang, Fan Wu

{"title":"Effects of E2 on the IDO1-mediated metabolic KYN pathway in OVX female mice","authors":"Xi Jiang, Xuefeng Yu, Shuran Hu, Huidan Dai, Hanqin Zhang, Yuyang Hang, Xupei Xie, Yubo Yang, Fan Wu","doi":"10.1111/jcmm.70179","DOIUrl":"10.1111/jcmm.70179","url":null,"abstract":"The aim of this study was to investigate the role of 17β-estradiol (E2)-mediated oestrogen receptor (ER) in modulating the depressive-like behaviours of ovariectomy (OVX) mice and the associated mechanisms. E2 was administrated in OVX mice. The behaviour and physiological changes of OVX mice including immobility time in tail suspension test (TST) and forced swimming test (FST), levels of serum E2, inflammatory mediators, oxidative stress factors, indoleamine2,3-dioxygenase 1 (IDO1) and the neurotransmitters mediated by IDO1 activation were then recorded. Cell injury models established by lipopolysaccharide (LPS) or H2O2 stimulation in HT22 and BV2 cells were employed to further explore the mechanisms of E2's function. E2 treatment improved OVX-induced increase of immobility time in FST and TST. Meanwhile, E2 ameliorated the changes of inflammatory factors (NF-κB, TNF-α and IL-6), IDO1, IDO1-mediated TRP/KYN pathway and oxidative stress factors (iNOS, MDA, GSH and SOD) in the hippocampus of OVX mice. Interestingly, ERβ inhibitor abolished E2's inhibitory effects on the inflammation and IDO1-mediated TRP/KYN pathway; ERβ inhibitor also abolished E2's anti-oxidative stress effect. In cell experiments, ERβ small interfering RNA (siRNA) pretreatment reversed E2's anti-inflammatory effect on LPS-treated HT22 and BV2 cells and E2's inhibitory effect on IDO1 expression in LPS-treated BV2 cells. ERβ siRNA pretreatment also reversed E2's anti-oxidation effect on H2O2-treated HT22 cells. E2 exert the antidepressant function in OVX mice via ERβ-modulated suppression of NF-κB-mediated inflammatory pathway, oxidative stress factors and IDO1-mediated TRP/KYN pathway in the hippocampus.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70179","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to ‘Acacetin exerts antioxidant potential against atherosclerosis through Nrf2 pathway in apoE−/− mice’ 对 "Acacetin 通过 Nrf2 通路在 apoE-/- 小鼠体内发挥抗氧化潜力，防止动脉粥样硬化 "的更正。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-28 DOI: 10.1111/jcmm.70145

引用次数: 0

Immortalized mesenchymal stromal cells overexpressing alpha-1 antitrypsin protect acinar cells from apoptotic and ferroptotic cell death 过表达α-1抗胰蛋白酶的永久化间充质基质细胞可保护胰腺细胞免于凋亡和铁细胞死亡。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-28 DOI: 10.1111/jcmm.70093

Sara Shoeibi, Erica Green, Hua Wei, Wenyu Gou, Charlie Strange, Hongjun Wang

{"title":"Immortalized mesenchymal stromal cells overexpressing alpha-1 antitrypsin protect acinar cells from apoptotic and ferroptotic cell death","authors":"Sara Shoeibi, Erica Green, Hua Wei, Wenyu Gou, Charlie Strange, Hongjun Wang","doi":"10.1111/jcmm.70093","DOIUrl":"10.1111/jcmm.70093","url":null,"abstract":"Chronic pancreatitis (CP) is a progressive inflammatory disorder that impairs endocrine and exocrine function. Our previous work showed that mesenchymal stem/stromal cells (MSCs) and MSCs overexpressing alpha-1 antitrypsin (AAT-MSCs) could be therapeutic tools for CP. However, primary MSCs are predisposed to undergo senescence during culture expansion, which limits their therapeutic applications. We generated and characterized immortalized human MSCs (iMSCs) and AAT-MSCs (iAAT-MSCs) and tested their protective effect on 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced acinar cell death in an in vitro cell culture system. Primary MSCs were immortalized by transduction with simian virus 40 large T antigen (SV40LT), and the resulting iMSC and iAAT-MSC lines were analysed for proliferation, senescence, phenotype and multi-differentiation potential. Subsequently, apoptosis and ferroptosis pathways were investigated by assessing changes before and after TNBS treatment. Coculture of iMSCs and iAAT-MSCs with acinar cell lines inhibited early cell death induced by TNBS, reduced ER stress and reversed TNBS-induced protein reduction at tight junctions. Additionally, iMSCs and iAAT-MSCs exerted such protection by regulating mitochondrial respiration, ATP content and ROS production in TNBS-induced acinar cells. Furthermore, iMSCs and iAAT-MSCs ameliorated TNBS-induced ferroptosis by modulating iron generation and ROS production and regulating the ferritin heavy chain 1 (FTH1)/protein disulfide isomerase (PDI)/glutathione peroxide 4 (GPX4) signalling pathways in acinar cells. These findings identify ferroptosis as an unrecognized mechanism that leads to TNBS-induced cell death and offer mechanistic insights relevant to using stem cell therapy to treat acinar cell death associated with CP.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhancing osteogenic differentiation of diabetic tendon stem/progenitor cells through hyperoxia: Unveiling ROS/HIF-1α signalling axis 通过高氧增强糖尿病肌腱干/祖细胞的成骨分化：揭示 ROS/HIF-1α 信号轴

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-28 DOI: 10.1111/jcmm.70127

Ming Zhang, Guan-Chun Dai, Yuan-Wei Zhang, Pan-Pan Lu, Hao Wang, Ying-Juan Li, Yun-Feng Rui

{"title":"Enhancing osteogenic differentiation of diabetic tendon stem/progenitor cells through hyperoxia: Unveiling ROS/HIF-1α signalling axis","authors":"Ming Zhang, Guan-Chun Dai, Yuan-Wei Zhang, Pan-Pan Lu, Hao Wang, Ying-Juan Li, Yun-Feng Rui","doi":"10.1111/jcmm.70127","DOIUrl":"10.1111/jcmm.70127","url":null,"abstract":"Diabetic calcific tendinopathy is the leading cause of chronic pain, mobility restriction, and tendon rupture in patients with diabetes. Tendon stem/progenitor cells (TSPCs) have been implicated in the development of diabetic calcified tendinopathy, but the molecular mechanisms remain unclear. This study found that diabetic tendons have a hyperoxic environment, characterized by increased oxygen delivery channels and carriers. In hyperoxic environment, TSPCs showed enhanced osteogenic differentiation and increased levels of reactive oxygen species (ROS). Additionally, hypoxia-inducible factor-1a (HIF-1a), a protein involved in regulating cellular responses to hyperoxia, was decreased in TSPCs by the ubiquitin-proteasome system. By intervening with antioxidant N-acetyl-L-cysteine (NAC) and overexpressing HIF-1a, we discovered that blocking the ROS/HIF-1a signalling axis significantly inhibited the osteogenic differentiation ability of TSPCs. Animal experiments further confirmed that hyperoxic environment could cause calcification in the Achilles tendon tissue of rats, while NAC intervention prevented calcification. These findings demonstrate that hyperoxia in diabetic tendons promotes osteogenic differentiation of TSPCs through the ROS/HIF-1a signalling axis. This study provides a new theoretical basis and research target for preventing and treating diabetic calcified tendinopathy.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

KRAS mutation promotes the colonization of Fusobacterium nucleatum in colorectal cancer by down-regulating SERTAD4 KRAS 基因突变通过下调 SERTAD4 促进核酸镰刀菌在结直肠癌中的定植。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-27 DOI: 10.1111/jcmm.70182

Yizhen Chen, Yuanyuan Zheng, Shaolin Liu

{"title":"KRAS mutation promotes the colonization of Fusobacterium nucleatum in colorectal cancer by down-regulating SERTAD4","authors":"Yizhen Chen, Yuanyuan Zheng, Shaolin Liu","doi":"10.1111/jcmm.70182","DOIUrl":"10.1111/jcmm.70182","url":null,"abstract":"This study explores and verifies potential molecular targets through which KRAS mutations regulate the colonization of Fusobacterium nucleatum (FN) in colorectal cancer (CRC). This study combined multiple bioinformatics methods and biological assays. Through The Cancer Genome Atlas, Gene Expression Omnibus, Human Protein Atlas, immunohistochemistry, and co-culture assays, we further confirmed the differential expression of SERTAD4 in CRC. We delved deeper into examining how expression of SERTAD4 is linked with immune cell infiltration and the enrichment of potential pathways. Lastly, through bacterial phenotypic assays, we validated the function of SERTAD4. As a molecule associated with KRAS mutations and FN infection, the expression levels of SERTAD4 were downregulated in CRC. The diagnostic efficacy of SERTAD4 for CRC is not inferior to that of CEA. Low expression of SERTAD4 is associated with poorer overall survival in CRC. Correlation analysis found that increased expression of SERTAD4 is associated with various immune cell infiltrations and immune checkpoint genes. Finally, bacterial adhesion and invasion assays verify that SERTAD4 inhibits the adhesion and invasion abilities of FN in CRC. This study demonstrates that SERTAD4 exerts a protective role in CRC by inhibiting the colonization of FN.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 20","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11512757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Old disease—New reflections: Gaucher, immunity, and inflammation 老疾病-新思考：戈谢病、免疫和炎症

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2024-10-27 DOI: 10.1111/jcmm.70087

Can Veysel Şoroğlu, Ezgi Gizem Berkay

引用次数: 0