Journal of Biomedical Research最新文献_第6页

Genetic variants in C1GALT1 are associated with gastric cancer risk by influencing immune infiltration. C1GALT1 基因变异与胃癌风险和免疫浸润有关。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230161

Mengfan Guo, Jingyuan Liu, Yujuan Zhang, Jingjing Gu, Junyi Xin, Mulong Du, Haiyan Chu, Meilin Wang, Hanting Liu, Zhengdong Zhang

{"title":"Genetic variants in C1GALT1 are associated with gastric cancer risk by influencing immune infiltration.","authors":"Mengfan Guo, Jingyuan Liu, Yujuan Zhang, Jingjing Gu, Junyi Xin, Mulong Du, Haiyan Chu, Meilin Wang, Hanting Liu, Zhengdong Zhang","doi":"10.7555/JBR.37.20230161","DOIUrl":"10.7555/JBR.37.20230161","url":null,"abstract":"Core 1 synthase glycoprotein-N-acetylgalactosamine 3-β-galactosyltransferase 1 (C1GALT1) is known to play a critical role in the development of gastric cancer, but few studies have elucidated associations between genetic variants in C1GALT1 and gastric cancer risk. By using the genome-wide association study data from the database of Genotype and Phenotype (dbGAP), we evaluated such associations with a multivariable logistic regression model and identified that the rs35999583 G>C in C1GALT1 was associated with gastric cancer risk (odds ratio, 0.83; 95% confidence interval [CI], 0.75-0.92; P = 3.95 × 10 -4). C1GALT1 mRNA expression levels were significantly higher in gastric tumor tissues than in normal tissues, and gastric cancer patients with higher C1GALT1 mRNA levels had worse overall survival rates (hazards ratio, 1.33; 95% CI, 1.05-1.68; P log-rank = 1.90 × 10 -2). Furthermore, we found that C1GALT1 copy number differed in various immune cells and that C1GALT1 mRNA expression levels were positively correlated with the infiltrating levels of CD4 + T cells and macrophages. These results suggest that genetic variants of C1GALT1 may play an important role in gastric cancer risk and provide a new insight for C1GALT1 into a promising predictor of gastric cancer susceptibility and immune status.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"348-357"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Macrophage scavenger receptor A1 promotes skeletal muscle regeneration after hindlimb ischemia. 巨噬细胞清道夫受体-A1促进后肢缺血后的骨骼肌再生

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240117

Siying Wang, Saiya Wang, Wenhan Cai, Jie Wang, Jianan Huang, Qing Yang, Hui Bai, Bin Jiang, Jingjing Ben, Hanwen Zhang, Xudong Zhu, Xiaoyu Li, Qi Chen

{"title":"Macrophage scavenger receptor A1 promotes skeletal muscle regeneration after hindlimb ischemia.","authors":"Siying Wang, Saiya Wang, Wenhan Cai, Jie Wang, Jianan Huang, Qing Yang, Hui Bai, Bin Jiang, Jingjing Ben, Hanwen Zhang, Xudong Zhu, Xiaoyu Li, Qi Chen","doi":"10.7555/JBR.38.20240117","DOIUrl":"10.7555/JBR.38.20240117","url":null,"abstract":"The macrophage-mediated inflammatory response is crucial for the recovery of skeletal muscle following ischemia. Therefore, macrophage-based therapeutic targets need to be explored for ischemic disease. In the current study, we found that the mRNA levels of scavenger receptor A1 ( Sr-a1) were elevated in patients with critical limb ischemia, based on an analysis of the Gene Expression Omnibus data. We then investigated the role and underlying mechanisms of macrophage SR-A1 in a mouse hindlimb ischemia (HLI) model. Compared with the Sr-a1 fl/fl mice, the Lyz Cre/+/ Sr-a1 flox/flox ( Sr-a1 ΔMΦ) mice showed significantly reduced laser Doppler blood flow in the ischemic limb on day seven after HLI. Consistently, histological analysis revealed that the ischemic limb of the Sr-a1 ΔMΦ mice exhibited more severe and prolonged necrotic morphology, inflammation, fibrosis, decreased vessel density, and delayed regeneration than that of the control Sr-a1 fl/fl mice. Furthermore, restoring wild-type myeloid cells to the Sr-a1 knockout mice effectively improved the Doppler perfusion in the ischemic limb and mitigated skeletal muscle damage seven days after HLI. Consistent with these in vivo findings, co-cultivating macrophages with the mouse myoblast cell line C2C12 revealed that the Sr-a1 -/- bone marrow macrophages significantly inhibited myoblast differentiation in vitro. Mechanistically, SR-A1 enhanced the skeletal muscle regeneration in response to HLI by inhibiting oncostatin M production via suppression of the NF-κB signaling activation. These findings indicate that SR-A1 may be a promising candidate protein to improve tissue repair and regeneration in peripheral ischemic arterial disease.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"23-35"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells via regulating β-catenin activation and EMT pathways. 环肽moroidin通过调节β-catenin激活和EMT通路抑制胶质母细胞瘤细胞形成的血管生成模拟。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240015

Pengxiang Min, Yingying Li, Cuirong Wang, Junting Fan, Shangming Liu, Xiang Chen, Yamin Tang, Feng Han, Aixia Zhang, Lili Feng

{"title":"Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells via regulating β-catenin activation and EMT pathways.","authors":"Pengxiang Min, Yingying Li, Cuirong Wang, Junting Fan, Shangming Liu, Xiang Chen, Yamin Tang, Feng Han, Aixia Zhang, Lili Feng","doi":"10.7555/JBR.38.20240015","DOIUrl":"10.7555/JBR.38.20240015","url":null,"abstract":"Glioblastoma (GBM) is a highly vascularized malignant brain tumor with poor clinical outcomes. Vasculogenic mimicry (VM) formed by aggressive GBM cells is an alternative approach for tumor blood supply and contributes to the failure of anti-angiogenic therapy. To date, there is still a lack of effective drugs that target VM formation in GBM. In the present study, we evaluated the effects of the plant cyclopeptide moroidin on VM formed by GBM cells and investigated its underlying molecular mechanisms. Moroidin significantly suppressed cell migration, tube formation, and the expression levels of α-smooth muscle actin and matrix metalloproteinase-9 in human GBM cell lines at sublethal concentrations. The RNA sequencing data suggested the involvement of the epithelial-mesenchymal transition (EMT) pathway in the mechanism of moroidin. Exposure to moroidin led to a concentration-dependent decrease in the expression levels of the EMT markers N-cadherin and vimentin in GBM cells. Moreover, moroidin significantly reduced the level of phosphorylated extracellular signal-regulated protein kinase (p-ERK) and inhibited the activation of β-catenin. Finally, we demonstrated that the plant cyclopeptide moroidin inhibited VM formation by GBM cells through inhibiting the ERK/β-catenin-mediated EMT. Therefore, our study indicates a potential application of moroidin as an anti-VM agent in the treatment of GBM.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"322-333"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic variation of circHIBADH enhances prostate cancer risk through regulating HNRNPA1-related RNA splicing. circHIBADH的基因变异通过调节HNRNPA1相关的RNA剪接提高了患前列腺癌的风险。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240030

Yifei Cheng, Rongjie Shi, Shuai Ben, Silu Chen, Shuwei Li, Junyi Xin, Meilin Wang, Gong Cheng

{"title":"Genetic variation of circHIBADH enhances prostate cancer risk through regulating HNRNPA1-related RNA splicing.","authors":"Yifei Cheng, Rongjie Shi, Shuai Ben, Silu Chen, Shuwei Li, Junyi Xin, Meilin Wang, Gong Cheng","doi":"10.7555/JBR.38.20240030","DOIUrl":"10.7555/JBR.38.20240030","url":null,"abstract":"The current study aimed to investigate associations of circRNAs and related genetic variants with the risk of prostate cancer (PCa) as well as to elucidate biological mechanisms underlying the associations. We first compared expression levels of circRNAs between 25 paired PCa and adjacent normal tissues to identify risk-associated circRNAs by using the MiOncoCirc database. We then used logistic regression models to evaluate associations between genetic variants in candidate circRNAs and PCa risk among 4662 prostate cancer patients and 3114 healthy controls, and identified circHIBADH rs11973492 T>C as a significant risk-associated variant (odds ratio = 1.20, 95% confidence interval: 1.08-1.34, P = 7.06 × 10 -4) in a dominant genetic model, which altered the secondary structure of the corresponding RNA chain. In the in silico analysis, we found that circHIBADH sponged and silenced 21 RNA-binding proteins (RBPs) enriched in the RNA splicing pathway, among which HNRNPA1 was identified and validated as a hub RBP using an external RNA-sequencing data as well as the in-house (four tissue samples) and publicly available single-cell transcriptomes. Additionally, we demonstrated that HNRNPA1 influenced hallmarks including MYC target, DNA repair, and E2F target signaling pathways, thereby promoting carcinogenesis. In conclusion, genetic variants in circHIBADH may act as sponges and inhibitors of RNA splicing-associated RBPs including HNRNPA1, playing an oncogenic role in PCa.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"358-368"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel anti-inflammatory peptide alleviates liver ischemia-reperfusion injury. 新型抗炎肽可减轻肝脏缺血再灌注损伤

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240020

Xuejun Xu, Kaineng Sun, Hao Chang, Chunxiang Shen, Xiangdong Li, Yangyue Ni, Yuxiao Zhu, Huiquan Wang, Ruiyan Xiong, Jon Rob Padde, Zhipeng Xu, Lin Chen, Lu Chen, Min Hou, Liyong Pu, Minjun Ji

{"title":"Novel anti-inflammatory peptide alleviates liver ischemia-reperfusion injury.","authors":"Xuejun Xu, Kaineng Sun, Hao Chang, Chunxiang Shen, Xiangdong Li, Yangyue Ni, Yuxiao Zhu, Huiquan Wang, Ruiyan Xiong, Jon Rob Padde, Zhipeng Xu, Lin Chen, Lu Chen, Min Hou, Liyong Pu, Minjun Ji","doi":"10.7555/JBR.38.20240020","DOIUrl":"10.7555/JBR.38.20240020","url":null,"abstract":"Ischemia-reperfusion injury (IRI) remains an unavoidable challenge in liver surgery, with macrophages playing a critical role in its pathogenesis. However, the mechanisms by which macrophages regulate the pathogenesis of IRI are not well understood. Through a target-guided screening approach, we identified a small 3 kDa peptide (SjDX5-271) from various schistosome egg-derived peptides that induced M2 macrophage polarization. SjDX5-271 treatment protected mice against liver IRI by promoting M2 macrophage polarization, and this protective effect was abrogated when the macrophages were depleted. Transcriptomic sequencing showed that the TLR signaling pathway was significantly inhibited in macrophages from the SjDX5-271 treatment group. We further identified that SjDX5-271 promoted M2 macrophage polarization by inhibiting the TLR4/MyD88/NF-κB signaling pathway and alleviated hepatic inflammation in liver IRI. Collectively, SjDX5-271 exhibited some promising therapeutic effects in IRI and represented a novel therapeutic approach, potentially applicable to other immune-related diseases. The current study demonstrates the potential of new biologics from the parasite, enhances our understanding of host-parasite interplay, and provides a blueprint for future therapies for immune-related diseases.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"61-75"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mycobacterium smegmatis enhances shikonin-induced immunogenic cell death-an efficient in situ tumor vaccine strategy. 烟肉分枝杆菌可增强志贺宁诱导的免疫原性细胞死亡--一种高效的原位肿瘤疫苗策略。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240049

Zhaoye Qian, Zhe Zhang, Lanqi Cen, Yaohua Ke, Jie Shao, Manman Tian, Baorui Liu

{"title":"Mycobacterium smegmatis enhances shikonin-induced immunogenic cell death-an efficient in situ tumor vaccine strategy.","authors":"Zhaoye Qian, Zhe Zhang, Lanqi Cen, Yaohua Ke, Jie Shao, Manman Tian, Baorui Liu","doi":"10.7555/JBR.38.20240049","DOIUrl":"10.7555/JBR.38.20240049","url":null,"abstract":"Tumor vaccines are a promising avenue in cancer immunotherapy. Despite the progress in targeting specific immune epitopes, tumor cells lacking these epitopes can evade the treatment. Here, we aimed to construct an efficient in situ tumor vaccine called Vac-SM, utilizing shikonin (SKN) to induce immunogenic cell death (ICD) and Mycobacterium smegmatis as an immune adjuvant to enhance in situ tumor vaccine efficacy. SKN showed a dose-dependent and time-dependent cytotoxic effect on the tumor cell line and induced ICD in tumor cells as evidenced by the CCK-8 assay and the detection of the expression of relevant indicators, respectively. Compared with the control group, the in situ Vac-SM injection in mouse subcutaneous metastatic tumors significantly inhibited tumor growth and distant tumor metastasis, while also improving survival rates. Mycobacterium smegmatis effectively induced maturation and activation of bone marrow-derived dendritic cells (DCs), and in vivo tumor-draining lymph nodes showed an increased maturation of DCs and a higher proportion of effector memory T-cell subsets with the Vac-SM treatment, based on flow cytometry analysis results. Collectively, the Vac-SM vaccine effectively induces ICD, improves antigen presentation by DCs, activates a specific systemic antitumor T-cell immune response, exhibits a favorable safety profile, and holds the promise for clinical translation for local tumor immunotherapy.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"369-381"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential clinical application of microRNAs in bladder cancer. 微RNA在膀胱癌中的潜在临床应用。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230245

Pei Wang, Xiaowei Wei, Xiaojun Qu, Yefei Zhu

{"title":"Potential clinical application of microRNAs in bladder cancer.","authors":"Pei Wang, Xiaowei Wei, Xiaojun Qu, Yefei Zhu","doi":"10.7555/JBR.37.20230245","DOIUrl":"10.7555/JBR.37.20230245","url":null,"abstract":"Bladder cancer (BC) is the tenth most prevalent malignancy globally, presenting significant clinical and societal challenges because of its high incidence, rapid progression, and frequent recurrence. Presently, cystoscopy and urine cytology serve as the established diagnostic methods for BC. However, their efficacy is limited by their invasive nature and low sensitivity. Therefore, the development of highly specific biomarkers and effective non-invasive detection strategies is imperative for achieving a precise and timely diagnosis of BC, as well as for facilitating an optimal tumor treatment and an improved prognosis. microRNAs (miRNAs), short noncoding RNA molecules spanning around 20-25 nucleotides, are implicated in the regulation of diverse carcinogenic pathways. Substantially altered miRNAs form robust functional regulatory networks that exert a notable influence on the tumorigenesis and progression of BC. Investigations into aberrant miRNAs derived from blood, urine, or extracellular vesicles indicate their potential roles as diagnostic biomarkers and prognostic indicators in BC, enabling miRNAs to monitor the progression and predict the recurrence of the disease. Simultaneously, the investigation centered on miRNA as a potential therapeutic agent presents a novel approach for the treatment of BC. This review comprehensively analyzes biological roles of miRNAs in tumorigenesis and progression, and systematically summarizes their potential as diagnostic and prognostic biomarkers, as well as therapeutic targets for BC. Additionally, we evaluate the progress made in laboratory techniques within this field and discuss the prospects.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"289-306"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

WITHDRAWN: Coronary atherosclerotic plaque regression strategies. 冠状动脉粥样硬化斑块消退策略。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230223

Anastasia V Poznyak, Alexey A Yakovlev, Mikhail А Popov, Alexander D Zhuravlev, Vasily N Sukhorukov, Alexander N Orekhov

引用次数: 0

Medical ozone alleviates acute lung injury by enhancing phagocytosis targeting NETs via AMPK/SR-A1 axis. 医用臭氧通过 AMPK/SR-A1 轴增强针对 NET 的吞噬作用，从而缓解急性肺损伤。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-25 DOI: 10.7555/JBR.38.20240038

Chenxiao Yan, Yong Zhang, Lai Jin, Xiaojie Liu, Xuexian Zhu, Qifeng Li, Yu Wang, Liang Hu, Xueming He, Hongguang Bao, Xia Zhu, Qian Wang, Wen-Tao Liu

{"title":"Medical ozone alleviates acute lung injury by enhancing phagocytosis targeting NETs via AMPK/SR-A1 axis.","authors":"Chenxiao Yan, Yong Zhang, Lai Jin, Xiaojie Liu, Xuexian Zhu, Qifeng Li, Yu Wang, Liang Hu, Xueming He, Hongguang Bao, Xia Zhu, Qian Wang, Wen-Tao Liu","doi":"10.7555/JBR.38.20240038","DOIUrl":"10.7555/JBR.38.20240038","url":null,"abstract":"Acute lung injury (ALI) linked to sepsis has a high mortality rate, with limited treatment options available. In recent studies, medical ozone has shown promising results in alleviating inflammation and infection. Here, we aimed to evaluate the therapeutic potential of medical ozone in sepsis-induced ALI using a mouse model, measuring behavioral assessments, lung function, and blood flow. Western blot was used to quantify the levels of protein. In vitro, experiments on BMDM cells examine the impact of AMPK inhibitors and agonists on phagocytic activity. Results indicate that medical ozone can enhance the survival rate, ameliorate lung injury, and improve lung function and limb microcirculation in mice with ALI. Notably, it inhibits NETs formation, a crucial player in ALI development. Medical ozone also counteracts elevated TF, MMP-9, and IL-1β levels. In ALI mice, the effects of ozone are nullified and BMDMs exhibit impaired engulfment of NETs following Sr-a1 knockout. Under normal physiological conditions, the use of an AMPK antagonist produces similar effects to Sr-a1 knockout, significantly inhibiting the phagocytosis of NETs by BMDMs. On the contrary, AMPK agonists enhance this phagocytic process. In conclusion, medical ozone can alleviate sepsis-induced lung injury via the AMPK/SR-A1 pathway, thereby enhancing phagocytosis of NETs by macrophages.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-16"},"PeriodicalIF":2.2,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PAK2 promotes proliferation, migration, and invasion of lung squamous cell carcinoma through LIMK1/cofilin signaling pathway. PAK2 通过 LIMK1/cofilin 信号通路促进肺鳞癌的增殖、迁移和侵袭。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-25 DOI: 10.7555/JBR.37.20230317

Congcong Wang, Junyan Wang, Ruifeng Xu, Xia Huang, Qiushuang Li, Chenxi Zhang, Baiyin Yuan

{"title":"PAK2 promotes proliferation, migration, and invasion of lung squamous cell carcinoma through LIMK1/cofilin signaling pathway.","authors":"Congcong Wang, Junyan Wang, Ruifeng Xu, Xia Huang, Qiushuang Li, Chenxi Zhang, Baiyin Yuan","doi":"10.7555/JBR.37.20230317","DOIUrl":"10.7555/JBR.37.20230317","url":null,"abstract":"Although the p21-activated kinase 2 (PAK2) is an essential serine/threonine protein kinase, its role in lung squamous cell carcinoma (LUSC) progression has yet to be fully understood. We analyzed PAK2 mRNA levels and DNA copy numbers as well as protein levels by quantitative real-time PCR and immunohistochemical staining, respectively, in human LUSC tissues and adjacent normal tissues. Then, we used colony formation assays, cell counting kit-8 assays, matrigel invasion assays, wound healing assays and xenograft models in nude mice to investigate the functions of PAK2 in LUSC progression. We demonstrated that the mRNA levels, DNA copy numbers, and protein levels of PAK2 were up-regulated in human LUSC tissues than in adjacent normal tissues. In addition, a higher PAK2 expression was correlated with a poorer prognosis in LUSC patients. In the in vitro study, we found that PAK2 promoted cell growth, migration, invasion, EMT process, and cell morphology regulation in LUSC cells. Furthermore, PAK2 enhanced tumor cell proliferation, migration, and invasion by regulating actin dynamics through the LIMK1/cofilin signaling. Our findings implicated that the PAK2/LIMK1/cofilin signaling pathway is likely a potential clinical marker and therapeutic target for LUSC.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-14"},"PeriodicalIF":2.2,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0