Molecular biomedicine最新文献_第7页

Single-cell transcriptomic profiling reveals decreased ER protein Reticulon3 drives the progression of renal fibrosis. 单细胞转录组分析显示，ER 蛋白 Reticulon3 的减少推动了肾脏纤维化的进展。

IF 6.3

Molecular biomedicine Pub Date : 2024-06-28 DOI: 10.1186/s43556-024-00187-x

Shuai Guo, Yi Dong, Ran Du, Yu-Xing Liu, Shu Liu, Qin Wang, Ji-Shi Liu, Hui Xu, Yu-Jie Jiang, Huang Hao, Liang-Liang Fan, Rong Xiang

{"title":"Single-cell transcriptomic profiling reveals decreased ER protein Reticulon3 drives the progression of renal fibrosis.","authors":"Shuai Guo, Yi Dong, Ran Du, Yu-Xing Liu, Shu Liu, Qin Wang, Ji-Shi Liu, Hui Xu, Yu-Jie Jiang, Huang Hao, Liang-Liang Fan, Rong Xiang","doi":"10.1186/s43556-024-00187-x","DOIUrl":"10.1186/s43556-024-00187-x","url":null,"abstract":"Chronic kidney disease (CKD) poses a significant global health dilemma, emerging from complex causes. Although our prior research has indicated that a deficiency in Reticulon-3 (RTN3) accelerates renal disease progression, a thorough examination of RTN3 on kidney function and pathology remains underexplored. To address this critical need, we generated Rtn3-null mice to study the consequences of RTN3 protein deficiency on CKD. Single-cell transcriptomic analyses were performed on 47,885 cells from the renal cortex of both healthy and Rtn3-null mice, enabling us to compare spatial architectures and expression profiles across 14 distinct cell types. Our analysis revealed that RTN3 deficiency leads to significant alterations in the spatial organization and gene expression profiles of renal cells, reflecting CKD pathology. Specifically, RTN3 deficiency was associated with Lars2 overexpression, which in turn caused mitochondrial dysfunction and increased reactive oxygen species levels. This shift induced a transition in renal epithelial cells from a functional state to a fibrogenic state, thus promoting renal fibrosis. Additionally, RTN3 deficiency was found to drive the endothelial-to-mesenchymal transition process and disrupt cell-cell communication, further exacerbating renal fibrosis. Immunohistochemistry and Western-Blot techniques were used to validate these observations, reinforcing the critical role of RTN3 in CKD pathogenesis. The deficiency of RTN3 protein in CKD leads to profound changes in cellular architecture and molecular profiles. Our work seeks to elevate the understanding of RTN3's role in CKD's narrative and position it as a promising therapeutic contender.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"24"},"PeriodicalIF":6.3,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11211315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141473295","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

Inhibition of cysteine-serine-rich nuclear protein 1 ameliorates ischemia-reperfusion injury during liver transplantation in an MAPK-dependent manner. 抑制富含半胱氨酸-丝氨酸的核蛋白 1 能以 MAPK 依赖性方式改善肝移植过程中的缺血再灌注损伤。

IF 6.3

Molecular biomedicine Pub Date : 2024-06-21 DOI: 10.1186/s43556-024-00185-z

Zhoucheng Wang, Wenwen Ge, Xinyang Zhong, Shizheng Tong, Shusen Zheng, Xiao Xu, Kai Wang

{"title":"Inhibition of cysteine-serine-rich nuclear protein 1 ameliorates ischemia-reperfusion injury during liver transplantation in an MAPK-dependent manner.","authors":"Zhoucheng Wang, Wenwen Ge, Xinyang Zhong, Shizheng Tong, Shusen Zheng, Xiao Xu, Kai Wang","doi":"10.1186/s43556-024-00185-z","DOIUrl":"10.1186/s43556-024-00185-z","url":null,"abstract":"Hepatic ischemia-reperfusion injury (HIRI) is a critical pathophysiological process during liver transplantation (LT). Multiple genes and signal pathways are dysregulated during HIRI. This study aims to identify genes as potential therapeutic targets for ameliorating HIRI. Datasets containing samples from the human donor liver (GSE151648) and mouse HIRI model (GSE117066) were analyzed to determine differentially expressed genes (DEGs). The selected DEGs were confirmed by real-time PCR and western blot in the hepatocyte hypoxia-reoxygenation (HR) model, mouse HIRI model, and human liver samples after transplantation. Genetic inhibition was used to further clarify the underlying mechanism of the gene in vitro and in vivo. Among the DEGs, CSRNP1 was significantly upregulated (|log FC|= 2.08, P < 0.001), and was positively correlated with the MAPK signal pathway (R = 0.67, P < 0.001). CSRNP1 inhibition by siRNA significantly suppressed apoptosis in the AML-12 cell line after HR (mean Annexin+ ratio = 60.62% vs 42.47%, P = 0.0019), but the protective effect was eliminated with an additional MAPK activator. Knocking down CSRNP1 gene expression by intravenous injection of AAV-shRNA markedly reduced liver injury in mouse HIRI model (ALT: AAV-NC vs AAV-shCsrnp1 = 26,673.5 ± 2761.2 vs 3839.7 ± 1432.8, P < 0.001; AST: AAV-NC vs AAV-shCsrnp1 = 8640.5 ± 1450.3 vs 1786.8 ± 518.3, P < 0.001). Liver-targeted delivery of siRNA by nanoparticles effectively inhibited intra-hepatic genetic expression of Csrnp1 and alleviated IRI by reducing tissue inflammation and hepatocyte apoptosis. Furthermore, CSRNP1 inhibition was associated with reduced activation of the MAPK pathway both in vitro and in vivo. In conclusion, our results demonstrated that CSRNP1 could be a potential therapeutic target to ameliorate HIRI in an MAPK-dependent manner.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"22"},"PeriodicalIF":6.3,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11189853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141433533","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

Ckip-1 3'UTR alleviates prolonged sleep deprivation induced cardiac dysfunction by activating CaMKK2/AMPK/cTNI pathway. Ckip-1 3'UTR通过激活CaMKK2/AMPK/cTNI通路缓解长期睡眠剥夺诱发的心功能障碍。

IF 6.3

Molecular biomedicine Pub Date : 2024-06-14 DOI: 10.1186/s43556-024-00186-y

Beilei Dong, Rui Xue, Jianwei Li, Shukuan Ling, Wenjuan Xing, Zizhong Liu, Xinxin Yuan, Junjie Pan, Ruikai Du, Xinming Shen, Jingwen Zhang, Youzhi Zhang, Yingxian Li, Guohui Zhong

{"title":"Ckip-1 3'UTR alleviates prolonged sleep deprivation induced cardiac dysfunction by activating CaMKK2/AMPK/cTNI pathway.","authors":"Beilei Dong, Rui Xue, Jianwei Li, Shukuan Ling, Wenjuan Xing, Zizhong Liu, Xinxin Yuan, Junjie Pan, Ruikai Du, Xinming Shen, Jingwen Zhang, Youzhi Zhang, Yingxian Li, Guohui Zhong","doi":"10.1186/s43556-024-00186-y","DOIUrl":"10.1186/s43556-024-00186-y","url":null,"abstract":"Sleep deprivation (SD) has emerged as a critical concern impacting human health, leading to significant damage to the cardiovascular system. However, the underlying mechanisms are still unclear, and the development of targeted drugs is lagging. Here, we used mice to explore the effects of prolonged SD on cardiac structure and function. Echocardiography analysis revealed that cardiac function was significantly decreased in mice after five weeks of SD. Real-time quantitative PCR (RT-q-PCR) and Masson staining analysis showed that cardiac remodeling marker gene Anp (atrial natriuretic peptide) and fibrosis were increased, Elisa assay of serum showed that the levels of creatine kinase (CK), creatine kinase-MB (CK-MB), ANP, brain natriuretic peptide (BNP) and cardiac troponin T (cTn-T) were increased after SD, suggesting that cardiac remodeling and injury occurred. Transcript sequencing analysis indicated that genes involved in the regulation of calcium signaling pathway, dilated cardiomyopathy, and cardiac muscle contraction were changed after SD. Accordingly, Western blotting analysis demonstrated that the cardiac-contraction associated CaMKK2/AMPK/cTNI pathway was inhibited. Since our preliminary research has confirmed the vital role of Casein Kinase-2 -Interacting Protein-1 (CKIP-1, also known as PLEKHO1) in cardiac remodeling regulation. Here, we found the levels of the 3' untranslated region of Ckip-1 (Ckip-1 3'UTR) decreased, while the coding sequence of Ckip-1 (Ckip-1 CDS) remained unchanged after SD. Significantly, adenovirus-mediated overexpression of Ckip-1 3'UTR alleviated SD-induced cardiac dysfunction and remodeling by activating CaMKK2/AMPK/cTNI pathway, which proposed the therapeutic potential of Ckip-1 3'UTR in treating SD-induced heart disease.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"23"},"PeriodicalIF":6.3,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141319180","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

Signaling pathways in colorectal cancer implications for the target therapies. 结直肠癌信号通路对靶向疗法的影响。

IF 6.3

Molecular biomedicine Pub Date : 2024-06-07 DOI: 10.1186/s43556-024-00178-y

Yanlin Song, Ming Chen, Yuhao Wei, Xuelei Ma, Huashan Shi

{"title":"Signaling pathways in colorectal cancer implications for the target therapies.","authors":"Yanlin Song, Ming Chen, Yuhao Wei, Xuelei Ma, Huashan Shi","doi":"10.1186/s43556-024-00178-y","DOIUrl":"10.1186/s43556-024-00178-y","url":null,"abstract":"Colorectal carcinoma (CRC) stands as a pressing global health issue, marked by the unbridled proliferation of immature cells influenced by multifaceted internal and external factors. Numerous studies have explored the intricate mechanisms of tumorigenesis in CRC, with a primary emphasis on signaling pathways, particularly those associated with growth factors and chemokines. However, the sheer diversity of molecular targets introduces complexity into the selection of targeted therapies, posing a significant challenge in achieving treatment precision. The quest for an effective CRC treatment is further complicated by the absence of pathological insights into the mutations or alterations occurring in tumor cells. This study reveals the transfer of signaling from the cell membrane to the nucleus, unveiling recent advancements in this crucial cellular process. By shedding light on this novel dimension, the research enhances our understanding of the molecular intricacies underlying CRC, providing a potential avenue for breakthroughs in targeted therapeutic strategies. In addition, the study comprehensively outlines the potential immune responses incited by the aberrant activation of signaling pathways, with a specific focus on immune cells, cytokines, and their collective impact on the dynamic landscape of drug development. This research not only contributes significantly to advancing CRC treatment and molecular medicine but also lays the groundwork for future breakthroughs and clinical trials, fostering optimism for improved outcomes and refined approaches in combating colorectal carcinoma.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"21"},"PeriodicalIF":6.3,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11156834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141285576","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

Signaling pathways in liver cancer: pathogenesis and targeted therapy. 肝癌的信号通路：发病机制和靶向治疗。

IF 6.3

Molecular biomedicine Pub Date : 2024-05-31 DOI: 10.1186/s43556-024-00184-0

Yangtao Xue, Yeling Ruan, Yali Wang, Peng Xiao, Junjie Xu

{"title":"Signaling pathways in liver cancer: pathogenesis and targeted therapy.","authors":"Yangtao Xue, Yeling Ruan, Yali Wang, Peng Xiao, Junjie Xu","doi":"10.1186/s43556-024-00184-0","DOIUrl":"10.1186/s43556-024-00184-0","url":null,"abstract":"Liver cancer remains one of the most prevalent malignancies worldwide with high incidence and mortality rates. Due to its subtle onset, liver cancer is commonly diagnosed at a late stage when surgical interventions are no longer feasible. This situation highlights the critical role of systemic treatments, including targeted therapies, in bettering patient outcomes. Despite numerous studies on the mechanisms underlying liver cancer, tyrosine kinase inhibitors (TKIs) are the only widely used clinical inhibitors, represented by sorafenib, whose clinical application is greatly limited by the phenomenon of drug resistance. Here we show an in-depth discussion of the signaling pathways frequently implicated in liver cancer pathogenesis and the inhibitors targeting these pathways under investigation or already in use in the management of advanced liver cancer. We elucidate the oncogenic roles of these pathways in liver cancer especially hepatocellular carcinoma (HCC), as well as the current state of research on inhibitors respectively. Given that TKIs represent the sole class of targeted therapeutics for liver cancer employed in clinical practice, we have particularly focused on TKIs and the mechanisms of the commonly encountered phenomena of its resistance during HCC treatment. This necessitates the imperative development of innovative targeted strategies and the urgency of overcoming the existing limitations. This review endeavors to shed light on the utilization of targeted therapy in advanced liver cancer, with a vision to improve the unsatisfactory prognostic outlook for those patients.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"20"},"PeriodicalIF":6.3,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141180772","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

Carcinoembryonic antigen potentiates non-small cell lung cancer progression via PKA-PGC-1ɑ axis. 癌胚抗原通过 PKA-PGC-1ɑ 轴促进非小细胞肺癌的进展

IF 6.3

Molecular biomedicine Pub Date : 2024-05-24 DOI: 10.1186/s43556-024-00181-3

Juan Lei, Lei Wu, Nan Zhang, Xudong Liu, Jiangang Zhang, Liwen Kuang, Jiongming Chen, Yijiao Chen, Dairong Li, Yongsheng Li

{"title":"Carcinoembryonic antigen potentiates non-small cell lung cancer progression via PKA-PGC-1ɑ axis.","authors":"Juan Lei, Lei Wu, Nan Zhang, Xudong Liu, Jiangang Zhang, Liwen Kuang, Jiongming Chen, Yijiao Chen, Dairong Li, Yongsheng Li","doi":"10.1186/s43556-024-00181-3","DOIUrl":"10.1186/s43556-024-00181-3","url":null,"abstract":"Carcinoembryonic antigen (CEA) is a tumor-associated antigen primarily produced by tumor cells. It has been implicated in various biological processes such as cell adhesion, proliferation, differentiation, and metastasis. Despite this, the precise molecular mechanisms through which CEA enhances tumor cell proliferation remain largely unclear. Our study demonstrates that CEA enhances the proliferation and migration of non-small cell lung cancer (NSCLC) while also inhibiting cisplatin-induced apoptosis in NSCLC cells. Treatment with CEA led to an increase in mitochondrial numbers and accumulation of lipid droplets in A549 and H1299 cells. Additionally, our findings indicate that CEA plays a role in regulating the fatty acid metabolism of NSCLC cells. Inhibiting fatty acid metabolism significantly reduced the CEA-mediated proliferation and migration of NSCLC cells. CEA influences fatty acid metabolism and the proliferation of NSCLC cells by activating the PGC-1α signaling pathway. This regulatory mechanism involves CEA increasing intracellular cAMP levels, which in turn activates PKA and upregulates PGC-1α. In NSCLC, inhibiting the PKA-PGC-1α signaling pathway reduces both fatty acid metabolism and the proliferation and migration induced by CEA, both in vitro and in vivo. These results suggest that CEA contributes to the promotion of proliferation and migration by modulating fatty acid metabolism. Targeting CEA or the PKA-PGC-1ɑ signaling pathway may offer a promising therapeutic approach for treating NSCLC.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"19"},"PeriodicalIF":6.3,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11116303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086317","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 different treatments for type 2 diabetes mellitus on mortality of coronavirus disease from 2019 to 2021 in China: a multi-institutional retrospective study. 2019年至2021年中国2型糖尿病不同治疗方法对冠状病毒病死亡率的影响：一项多机构回顾性研究。

IF 4

Molecular biomedicine Pub Date : 2024-05-17 DOI: 10.1186/s43556-024-00183-1

Ke Xu, Wu He, Bo Yu, Kaineng Zhong, Da Zhou, Dao Wen Wang

{"title":"Effects of different treatments for type 2 diabetes mellitus on mortality of coronavirus disease from 2019 to 2021 in China: a multi-institutional retrospective study.","authors":"Ke Xu, Wu He, Bo Yu, Kaineng Zhong, Da Zhou, Dao Wen Wang","doi":"10.1186/s43556-024-00183-1","DOIUrl":"10.1186/s43556-024-00183-1","url":null,"abstract":"The coronavirus disease (COVID-19) pandemic has continued for 5 years. Sporadic cases continue to occur in different locations. Type 2 diabetes mellitus (T2DM) is associated with a high risk of a poor prognosis in patients with COVID-19. Successful control of blood glucose levels can effectively decrease the risks of severe infections and mortality. However, the effects of different treatments were reported differently and even adversely. This retrospective study included 4,922 patients who have been diagnosed as COVID-19 and T2DM from 138 Hubei hospitals. The clinical characteristics and outcomes were compared and calculated their risk for death using multivariate Cox regression and Kaplan-Meier curves. After adjustment of age, sex, comorbidities, and in-hospital medications, metformin and alpha-glucosidase inhibitor (AGI) use performed lower all-cause mortality (adjusted hazard ratio [HR], 0.41; 95% confidence interval [CI]: 0.24-0.71; p = 0.001 for metformin; 0.53, 0.35-0.80, p = 0.002 for AGIs), while insulin use was associated with increased all-cause mortality (adjusted HR, 2.07, 95% CI, 1.61-2.67, p < 0.001). After propensity score-matched (PSM) analysis, adjusted HRs for insulin, metformin, and AGIs associated with all-cause mortality were 1.32 (95% CI, 1.03-1.81; p = 0.012), 0.48 (95% CI, 0.23-0.83, p = 0.014), and 0.59 (95% CI, 0.35-0.98, p = 0.05). Therefore, metformin and AGIs might be more suitable for patients with COVID-19 and T2DM while insulin might be used with caution.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"18"},"PeriodicalIF":4.0,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961078","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

Heterogeneity and molecular landscape of melanoma: implications for targeted therapy. 黑色素瘤的异质性和分子结构：对靶向治疗的影响。

IF 6.3

Molecular biomedicine Pub Date : 2024-05-10 DOI: 10.1186/s43556-024-00182-2

Yasaman Zohrab Beigi, Hossein Lanjanian, Reyhane Fayazi, Mahdieh Salimi, Behnaz Haji Molla Hoseyni, Mohammad Hafez Noroozizadeh, Ali Masoudi-Nejad

{"title":"Heterogeneity and molecular landscape of melanoma: implications for targeted therapy.","authors":"Yasaman Zohrab Beigi, Hossein Lanjanian, Reyhane Fayazi, Mahdieh Salimi, Behnaz Haji Molla Hoseyni, Mohammad Hafez Noroozizadeh, Ali Masoudi-Nejad","doi":"10.1186/s43556-024-00182-2","DOIUrl":"10.1186/s43556-024-00182-2","url":null,"abstract":"Uveal cancer (UM) offers a complex molecular landscape characterized by substantial heterogeneity, both on the genetic and epigenetic levels. This heterogeneity plays a critical position in shaping the behavior and response to therapy for this uncommon ocular malignancy. Targeted treatments with gene-specific therapeutic molecules may prove useful in overcoming radiation resistance, however, the diverse molecular makeups of UM call for a patient-specific approach in therapy procedures. We need to understand the intricate molecular landscape of UM to develop targeted treatments customized to each patient's specific genetic mutations. One of the promising approaches is using liquid biopsies, such as circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA), for detecting and monitoring the disease at the early stages. These non-invasive methods can help us identify the most effective treatment strategies for each patient. Single-cellular is a brand-new analysis platform that gives treasured insights into diagnosis, prognosis, and remedy. The incorporation of this data with known clinical and genomics information will give a better understanding of the complicated molecular mechanisms that UM diseases exploit. In this review, we focused on the heterogeneity and molecular panorama of UM, and to achieve this goal, the authors conducted an exhaustive literature evaluation spanning 1998 to 2023, using keywords like \"uveal melanoma, \"heterogeneity\". \"Targeted therapies\",\" \"CTCs,\" and \"single-cellular analysis\".","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"17"},"PeriodicalIF":6.3,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11082128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140900525","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

Construction of novel multi-epitope-based diagnostic biomarker HP16118P and its application in the differential diagnosis of Mycobacterium tuberculosis latent infection. 基于多表位的新型诊断生物标记 HP16118P 的构建及其在结核分枝杆菌潜伏感染鉴别诊断中的应用。

IF 6.3

Molecular biomedicine Pub Date : 2024-04-29 DOI: 10.1186/s43556-024-00177-z

Jie Wang, Fan Jiang, Peng Cheng, Zhaoyang Ye, Linsheng Li, Ling Yang, Li Zhuang, Wenping Gong

{"title":"Construction of novel multi-epitope-based diagnostic biomarker HP16118P and its application in the differential diagnosis of Mycobacterium tuberculosis latent infection.","authors":"Jie Wang, Fan Jiang, Peng Cheng, Zhaoyang Ye, Linsheng Li, Ling Yang, Li Zhuang, Wenping Gong","doi":"10.1186/s43556-024-00177-z","DOIUrl":"10.1186/s43556-024-00177-z","url":null,"abstract":"Tuberculosis (TB) is an infectious disease that significantly threatens human health. However, the differential diagnosis of latent tuberculosis infection (LTBI) and active tuberculosis (ATB) remains a challenge for clinicians in early detection and preventive intervention. In this study, we developed a novel biomarker named HP16118P, utilizing 16 helper T lymphocyte (HTL) epitopes, 11 cytotoxic T lymphocyte (CTL) epitopes, and 8 B cell epitopes identified from 15 antigens associated with LTBI-RD using the IEDB database. We analyzed the physicochemical properties, spatial structure, and immunological characteristics of HP16118P using various tools, which indicated that it is a hydrophilic and relatively stable alkaline protein. Furthermore, HP16118P exhibited good antigenicity and immunogenicity, while being non-toxic and non-allergenic, with the potential to induce immune responses. We observed that HP16118P can stimulate the production of high levels of IFN-γ+ T lymphocytes in individuals with ATB, LTBI, and health controls. IL-5 induced by HP16118P demonstrated potential in distinguishing LTBI individuals and ATB patients (p=0.0372, AUC=0.8214, 95% CI [0.5843 to 1.000]) with a sensitivity of 100% and specificity of 71.43%. Furthermore, we incorporated the GM-CSF, IL-23, IL-5, and MCP-3 induced by HP16118P into 15 machine learning algorithms to construct a model. It was found that the Quadratic discriminant analysis model exhibited the best diagnostic performance for discriminating between LTBI and ATB, with a sensitivity of 1.00, specificity of 0.86, and accuracy of 0.93. In summary, HP16118P has demonstrated strong antigenicity and immunogenicity, with the induction of GM-CSF, IL-23, IL-5, and MCP-3, suggesting their potential for the differential diagnosis of LTBI and ATB.","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"15"},"PeriodicalIF":6.3,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11056354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140873867","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: annexin A5-DM1 protein-drug conjugate for the treatment of triple-negative breast cancer. 更正：用于治疗三阴性乳腺癌的附件蛋白 A5-DM1 蛋白-药物共轭物。

IF 4

Molecular biomedicine Pub Date : 2024-04-02 DOI: 10.1186/s43556-024-00180-4

Alexis Woodward, Benjamin Southard, Sampurna Chakraborty, Aaron O Bailey, Gabriela N F Faria, Patrick McKernan, Wajeeha Razaq, Roger G Harrison

引用次数: 0