Critical Reviews in Eukaryotic Gene Expression最新文献_第3页

MS4A3 promotes the chemosensitivity of lung cancer via THAP1/EGFR pathways MS4A3 通过 THAP1/EGFR 通路促进肺癌的化疗敏感性

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-06-01 DOI: 10.1615/critreveukaryotgeneexpr.2024053662

Zhihui Duan

{"title":"MS4A3 promotes the chemosensitivity of lung cancer via THAP1/EGFR pathways","authors":"Zhihui Duan","doi":"10.1615/critreveukaryotgeneexpr.2024053662","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053662","url":null,"abstract":"MS4A3 functions as a tumor suppressor in multi-type cancer. However, the role of MS4A3 in lung cancer is still unknown. Therefore, this study aims to investigate the potential of MS4A3 in lung cancer. RT-qPCR is carried out to detect mRNA expression. CCK-8 and colony formation assay are conducted to determine cell proliferation. Tube formation assay is performed to determine angiogenesis. Flow cytometry is used to calculate apoptosis rates. JASPAR is used to determine the binding motif of THAP1. Luciferase and ChIP assay are conducted to verify that MS4A3 can interact with THAP1 to transcriptionally inactivate EGFR. MS4A3 is downregulated in non-small cell lung cancer (NSCLC) patients, which predicts poor clinical outcomes of NSCLC patients. Overexpressed MS4A3 enhances the chemosensitivity of NSCLC cells to Osimertinib. Moreover, MS4A3 suppresses the proliferation and angiogenesis and promotes the apoptosis of NSCLC cells. Moreover, MS4A3 upregulates apoptosis-related THAP1 to inactivate EGFR. However, THAP1 knockdown attenuates the effects of MS4A3 and promotes the malignant behavior of NSCLC cells. MS4A3 functions as an anti-tumor gene in NSCLC. MS4A3/THAP1/EGFR signaling enhances the chemosensitivity of lung cancer to EGFR tyrosine kinase inhibitor (TKI).","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"32 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141253651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FTO-mediated m6A modification of FTH1 inhibits ferroptosis of neurons in neonatal cerebral hypoxic ischaemia FTO 介导的 FTH1 m6A 修饰可抑制新生儿脑缺氧缺血时神经元的铁蜕变

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-06-01 DOI: 10.1615/critreveukaryotgeneexpr.2024054011

Yanhong Chen, Jia Huang

{"title":"FTO-mediated m6A modification of FTH1 inhibits ferroptosis of neurons in neonatal cerebral hypoxic ischaemia","authors":"Yanhong Chen, Jia Huang","doi":"10.1615/critreveukaryotgeneexpr.2024054011","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024054011","url":null,"abstract":"FTO is aberrantly expressed in brain disorders. However, the roles of FTO in neonatal hypoxic-ischemic brain injury (HIE) are still unclear. This study aims to investigate the potential of FTO in neonatal HIE. Oxygen-glucose deprivation (OGD) was used to establish HIE in vitro. mRNA levels were detected by RT-qPCR. Protein expression was detected by western blot. The levels of MDA, SOD, Fe2+ and GSH was detected by specific kit. m6A sites were analyzed using SRAMP and further verify by MeRIP assay. Cell proliferation was determined by CCK-8. Cell death was determined by PI staining. FTO was downregulated in patients with neonatal HIE and OGD-treated neurons. Moreover, FTO mRNA expression was decreased in ferroptosis inducer, especially FAC. However, overexpression of FTO inhibited the ferroptosis of neurons. Moreover, FTO-mediated m6A modification of FTH1 suppressed its mRNA expression and stability, inhibiting its protein expression. However, overexpression of FTH1 abrogated the effects of FTO and promoted the ferroptosis of neurons. In summary, FTO functions as a protective role in neonatal HIE via inhibiting FTH1 signaling. Thence, targeting may be a promising strategy for FTO neonatal HIE.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"24 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141501318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

KDM6A promotes angiogenesis, migration, and invasion of pancreatic cancer via activating LAMP3 KDM6A 通过激活 LAMP3 促进胰腺癌的血管生成、迁移和侵袭

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-06-01 DOI: 10.1615/critreveukaryotgeneexpr.2024054038

Liang Xu, Sunfu Fan, Dafei Xie, Yongqi Yu

引用次数: 0

Runx2 as a Prognostic Factor in Human Cancers 作为人类癌症预后因素的 Runx2

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-06-01 DOI: 10.1615/critreveukaryotgeneexpr.2024054162

Jennifer Toner, Jonathan Gordon, Haley Greenyer, Peter Kaufman, Janet Stein, Gary Stein, Jane Lian

{"title":"Runx2 as a Prognostic Factor in Human Cancers","authors":"Jennifer Toner, Jonathan Gordon, Haley Greenyer, Peter Kaufman, Janet Stein, Gary Stein, Jane Lian","doi":"10.1615/critreveukaryotgeneexpr.2024054162","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024054162","url":null,"abstract":"The RUNX2 transcription factor was discovered as an essential transcriptional regulator for commitment to osteoblast lineage cells and bone formation. Expression of Runx2 in other tissues, such as breast, prostate and lung, has been linked to oncogenesis, cancer progression and metastasis. In this study, we sought to determine the extent of Runx2 involvement in other tumors using a pan–cancer analysis strategy. We correlated RUNX2 expression and clinical-pathological parameters in human cancers by interrogating using publicly available multiparameter clinical data. Our analysis demonstrated that altered RUNX2 expression or function is associated with several cancer types from different tissues. We identified that 3 tumor types were associated with increased RUNX2 expression and decreased expression of RUNX2 is associated with 4 other cancer types. Our pan-cancer analysis for RUNX2 revealed numerous other discoveries for RUNX2 regulation of different cancers identified in each of the pan-cancer databases we used. Both up and down regulation of RUNX2 was observed during progression of specific types of cancers in promoting the distinct types of cancers.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"59 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141192647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer cell type dependent modifications of metastatic parameters by SLIT2-ROBO1 and RHOA cAMP signaling in response to TGFB1 and FGF2 癌细胞类型依赖于 SLIT2-ROBO1 和 RHOA cAMP 信号对 TGFB1 和 FGF2 转移参数的改变

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-06-01 DOI: 10.1615/critreveukaryotgeneexpr.2024054055

Abdul Rauf Shakoori, Quratulain Amjad, Gary S. Stein, Andre van Wijnen, Abdul Rauf Shakoori

{"title":"Cancer cell type dependent modifications of metastatic parameters by SLIT2-ROBO1 and RHOA cAMP signaling in response to TGFB1 and FGF2","authors":"Abdul Rauf Shakoori, Quratulain Amjad, Gary S. Stein, Andre van Wijnen, Abdul Rauf Shakoori","doi":"10.1615/critreveukaryotgeneexpr.2024054055","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024054055","url":null,"abstract":"The epithelial to mesenchymal transition (EMT) is a multistep process involving structural and functional alterations that are required for cancer metastasis, as well as loss of epithelial markers (e.g., E-cadherin/CDH1) and gain of mesenchymal markers (e.g., N-cadherin/CDH2, vimentin/VIM). Pathological events modify cell-cell interactions, cell-matrix adhesion and extra cellular matrix integrity leading to cell migration, evasion from the primary tumor and augmented invasiveness in the metastatic niche. This transformation is modulated by multiple paracrine factors (e.g., chemokines, growth factor), as well as SLIT2-ROBO1 signaling that collectively regulate expression of RHO GTPases (e.g., RHOA) and EMT marker genes. Yet, the roles of SLIT proteins in cancer remain enigmatic. In some cancer types, SLIT2 is anti-tumorigenic, while in other cancers it contributes towards the metastatic phenotype. Here we investigated the ambivalent metastatic activity of SLIT2 by analyzing how cAMP/RHOA signal transduction modulates SLIT-ROBO controlled metastatic parameters in response to the phosphodiesterase inhibitor IBMX (3-isobutyl-1-methylxanthine) and paracrine factors (TGF-β/TGFB1 and FGF2). Upon SLIT2 administration cell migration and proliferation increases in colon cancer cells and decreases in cervical cancer cells, while altering cell morphology and proliferation in both cancer types. These effects are reinforced by TGF-β/TGBF1 and FGF2, but attenuated by elevation of cAMP with IBMX, depending on the cancer cell type. Our data indicate that SLIT2 represents a potential biomarker for cancer diagnosis, prognosis, and therapy.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"15 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141551616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Electroacupuncture alleviates Parkinson’s disease via promoting METTL9-catalyzed histidine methylation of NF-κB 电针通过促进 METTL9 催化的 NF-κB 组氨酸甲基化缓解帕金森病

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-05-01 DOI: 10.1615/critreveukaryotgeneexpr.2024053243

Xiang Zhou, Liang Zhou, Jiayi Sun, Juan Zhang, Lei Sun

{"title":"Electroacupuncture alleviates Parkinson’s disease via promoting METTL9-catalyzed histidine methylation of NF-κB","authors":"Xiang Zhou, Liang Zhou, Jiayi Sun, Juan Zhang, Lei Sun","doi":"10.1615/critreveukaryotgeneexpr.2024053243","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053243","url":null,"abstract":"This study aimed to investigate the effects of electroacupuncture (EA) treatment on PD. MPTP administration was used establish PD mice model. The number of neurons was determined using TH staining. mRNA expression was detected using RT-qPCR. Protein expression was detected using western blot. Gene expression was determined using immunofluorescence and immunohistochemistry. The functions of neurons were determined using TUNEL and flow cytometry assay. The binding sites on NF-κB RELA in the promoter of NLRP3 was predicted by JASPAR and verified by luciferase and ChIP assays. EA treatment improved motor dysfunction in patients with PD. In vivo assays showed that MPTP administration induced the loss of neurons in mice, which was restored by EA treatment. Moreover, EA treatment attenuates motor deficits in MPTP-induced PD mice. EA treatment also inhibited the enrichment of pro-inflammatory cytokines and LDH, and suppressed neuronal pyroptosis. EA treatment increased the expression of METTL9. However, METTL9 deficiency dampened the effects of EA treatment and induced neuronal pyroptosis. Additionally, METTL9 promoted histidine methylation of NF-κB RELA, resulting the inhibition of epigenetic transcription of NLRP3. EA treatment restored neuronal function and improved motor dysfunction via promoting METTL9 histidine methylation of NF-κB/NLRP3 signaling.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"78 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141059103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Foxm1-mediated transcriptional inactivation of NLRP3 inflammasome promotes immunosuppression in cervical cancer Foxm1 介导的 NLRP3 炎症小体转录失活可促进宫颈癌的免疫抑制

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-05-01 DOI: 10.1615/critreveukaryotgeneexpr.2024053577

Weipeng Ji, Yang Jin, Wen Jiang

{"title":"Foxm1-mediated transcriptional inactivation of NLRP3 inflammasome promotes immunosuppression in cervical cancer","authors":"Weipeng Ji, Yang Jin, Wen Jiang","doi":"10.1615/critreveukaryotgeneexpr.2024053577","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053577","url":null,"abstract":"Foxm1 function as an oncogene in multiple human malignancies, including cervical cancer. However, the potential of Foxm1 in the tumor microenvironment (TME) is still unknown. The purpose of the present study is to investigate the role of Foxm1 in CD8+ T cell anti-tumor immunity. RT-qPCR is conducted to calculate mRNA levels. JASPAR is used to predict the binding sites between Foxm1 and NLRP3. ChIP assay is performed to verify the occupancy of Foxm1 on the promoter of NLRP3. Modulatory relationship between Foxm1 and NLRP3 is verified by luciferase assay. In vivo assays are conducted to further verify the role of Foxm1/NLRP3 axis in cervical cancer. HE staining assay is applied for histological analysis. Fow cytometry is conducted to determine the functions of immune cells. We found that Foxm1 knockdown decreases tumor burden and suppresses tumor growth of cervical cancer. Foxm1 knockdown promotes the infiltration of CD8+ T cells. Foxm1 deficiency inhibits the exhaustion of CD8+ T cells and facilitates the maintenance of CD8+ effector and stem-like T cells. Moreover, Foxm1 transcriptionally inactivates NLRP3 and suppressed the expression of innate cytokines IL-1β and IL-18. However, inhibition of NLRP3 inflammasome or neutralizing IL-1β and IL-18 inhibits anti-tumor immunity and promoted tumor growth in Foxm1 deficiency in CD8+ T cells. In summary, targeting Foxm1 mediates the activation of NLRP3 inflammasome and stimulates CD8+ T cell anti-tumor immunity in cervical cancer.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"62 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141166756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Palmdelphin inhibits ovarian cancer cell stem specification via downregulating ring finger protein 145 掌叶素通过下调环指蛋白145抑制卵巢癌细胞干的分化

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-05-01 DOI: 10.1615/critreveukaryotgeneexpr.2024053542

Nanzi Xie, Sisi Yang, Changlan Dai, Wei Chen

引用次数: 0

Expression and clinicopathological significance of extracellular matrix remodeling markers in esophageal squamous carcinoma 细胞外基质重塑标记物在食管鳞癌中的表达及其临床病理学意义

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-05-01 DOI: 10.1615/critreveukaryotgeneexpr.2024053646

Zhiqin Fan, Fei Chen, Yingmin Liu, Xiaotong Huang, Siyue Tian, Yuqing Ma

{"title":"Expression and clinicopathological significance of extracellular matrix remodeling markers in esophageal squamous carcinoma","authors":"Zhiqin Fan, Fei Chen, Yingmin Liu, Xiaotong Huang, Siyue Tian, Yuqing Ma","doi":"10.1615/critreveukaryotgeneexpr.2024053646","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053646","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is a common malignancy of the gastrointestinal tract with a single therapeutic option and a lack of effective clinical therapeutic biomarkers.Extracellular matrix (ECM) remodelling plays a pro-carcinogenic role in a variety of malignancies, but its role in esophageal squamous carcinoma remains to be elucidated.In this study, we examined the expression levels of ECM remodelling markers in 71 pairs of esophageal squamous carcinoma tissues and normal tissues adjacent to the carcinoma using immunohistochemical staining, and analysed their relationship with clinicopathological features and prognosis.The results suggested that extracellular matrix remodelling markers (Integrin αV, Fibronectin, MMP9) were abnormally highly expressed in esophageal squamous carcinoma tissues.There was a statistically significant difference between the positive expression of ECM remodelling and the TNM stage of esophageal squamous carcinoma, and there was no statistically significant correlation with age, gender and carcinoembryonic antigen expression, differentiation degree, T stage and lymph node metastasis.Overall survival rate and overall survival time were significantly lower in patients with positive ECM remodelling expression, which was an independent risk factor for poor prognosis of esophageal squamous carcinoma.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"41 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140884522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The alteration of the relationship between cells and their context is the basis of a pathological condition 细胞与其环境之间关系的改变是病理状态的基础

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-05-01 DOI: 10.1615/critreveukaryotgeneexpr.2024053711

Domenico RIBATTI

引用次数: 0