Pub Date : 2024-06-01DOI: 10.1615/critreveukaryotgeneexpr.2024054055
Abdul Rauf Shakoori, Quratulain Amjad, Gary S. Stein, Andre van Wijnen, Abdul Rauf Shakoori
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.
{"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":null,"pages":null},"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}
Pub Date : 2024-05-01DOI: 10.1615/critreveukaryotgeneexpr.2024053243
Xiang Zhou, Liang Zhou, Jiayi Sun, Juan Zhang, Lei Sun
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.
{"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":null,"pages":null},"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}
Pub Date : 2024-05-01DOI: 10.1615/critreveukaryotgeneexpr.2024053577
Weipeng Ji, Yang Jin, Wen Jiang
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.
{"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":null,"pages":null},"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}
Pub Date : 2024-05-01DOI: 10.1615/critreveukaryotgeneexpr.2024053542
Nanzi Xie, Sisi Yang, Changlan Dai, Wei Chen
This study aimed to investigate the roles of PALMD in ovarian cancer. mRNA expression was detected using RT-qPCR. The aldehyde dehydrogenase (ALDH) activity and biomarkers of ovarian cancer stem cells were determined using flow cytometry. The stemness of ovarian cancer cells was determined using sphere formation assay. Cell viability was determined using CCK-8 assay. The number of colonies was determined using colony formation assay. Cell migration was detected using wound healing assay. Cell invasion was determined using transwell assay. The results showed that PALMD was downregulated in ovarian cancer. Overexpressed PALMD inhibited the proliferative, migrative and invasive ability of ovarian cancer cells. Moreover, PALMD inhibited the stem-like properties of ovarian cancer cells. Additionally, PALMD downregulated ring finger protein 145 (RNF145) expression, overexpression of which contributed to the aggressiveness of ovarian cancer cells. Taken together, PALMD suppressed ovarian cancer cell stem specification via inhibiting RNF145 expression.
{"title":"Palmdelphin inhibits ovarian cancer cell stem specification via downregulating ring finger protein 145","authors":"Nanzi Xie, Sisi Yang, Changlan Dai, Wei Chen","doi":"10.1615/critreveukaryotgeneexpr.2024053542","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053542","url":null,"abstract":"This study aimed to investigate the roles of PALMD in ovarian cancer. mRNA expression was detected using RT-qPCR. The aldehyde dehydrogenase (ALDH) activity and biomarkers of ovarian cancer stem cells were determined using flow cytometry. The stemness of ovarian cancer cells was determined using sphere formation assay. Cell viability was determined using CCK-8 assay. The number of colonies was determined using colony formation assay. Cell migration was detected using wound healing assay. Cell invasion was determined using transwell assay. The results showed that PALMD was downregulated in ovarian cancer. Overexpressed PALMD inhibited the proliferative, migrative and invasive ability of ovarian cancer cells. Moreover, PALMD inhibited the stem-like properties of ovarian cancer cells. Additionally, PALMD downregulated ring finger protein 145 (RNF145) expression, overexpression of which contributed to the aggressiveness of ovarian cancer cells. Taken together, PALMD suppressed ovarian cancer cell stem specification via inhibiting RNF145 expression.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141150859","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}
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.
{"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":null,"pages":null},"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}
Pub Date : 2024-05-01DOI: 10.1615/critreveukaryotgeneexpr.2024053711
Domenico RIBATTI
Pathological conditions can be considered as alterations in the relationships between the cells of different tissues and organs and the microenvironment that surrounds them, primarily the different constituents of the extracellular matrix. The epithelial-mesenchymal transition is an example of how alterations in the relationships between epithelial cells can induce an alteration of their phenotypic characteristics and induce their migratory and invasive capacity.
{"title":"The alteration of the relationship between cells and their context is the basis of a pathological condition","authors":"Domenico RIBATTI","doi":"10.1615/critreveukaryotgeneexpr.2024053711","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053711","url":null,"abstract":"Pathological conditions can be considered as alterations in the relationships between the cells of different tissues and organs and the microenvironment that surrounds them, primarily the different constituents of the extracellular matrix. The epithelial-mesenchymal transition is an example of how alterations in the relationships between epithelial cells can induce an alteration of their phenotypic characteristics and induce their migratory and invasive capacity.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141064190","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}
Pub Date : 2024-04-01DOI: 10.1615/critreveukaryotgeneexpr.2024053036
Yasaman Daneshian, Eric Lewallen, Amr Badreldin, Allan Dietz, Gary Stein, Simon Cool, Hyun-Mo Ryoo, Young Dan Cho, Andre van Wijnen
Regenerative dental medicine continuously expands to improve treatments for prevalent clinical problems in dental and oral medicine. Stem cell based translational opportunities include regenerative therapies for tooth restoration, root canal therapy and inflammatory processes (e.g., periodontitis). The potential of regenerative approaches relies on the biological properties of dental stem cells. These and other multipotent somatic mesenchymal stem cell (MSC) types can in principle be applied as either autologous or allogeneic sources in dental procedures. Dental stem cells have distinct developmental origins and biological markers that determine their translational utility. Dental regenerative medicine is supported by mechanistic knowledge of the molecular pathways that regulate dental stem cell growth and differentiation. Cell fate determination and lineage progression of dental stem cells is regulated by multiple cell signaling pathways (e.g., WNTs, BMPs) and epigenetic mechanisms, including DNA modifications, histone modifications, and non-coding RNAs (e.g., miRNAs and lncRNAs). This review also considers a broad range of novel approaches in which stem cells are applied in combination with biopolymers, ceramics and composite materials, as well as small molecules (agonistic or anti-agonistic ligands) and natural compounds. Promising concepts in bone and dental tissue engineering continue to drive innovation in dental and non-dental restorative procedures.
{"title":"Fundamentals and translational applications of stem cells and biomaterials in dental, oral and craniofacial regenerative medicine","authors":"Yasaman Daneshian, Eric Lewallen, Amr Badreldin, Allan Dietz, Gary Stein, Simon Cool, Hyun-Mo Ryoo, Young Dan Cho, Andre van Wijnen","doi":"10.1615/critreveukaryotgeneexpr.2024053036","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053036","url":null,"abstract":"Regenerative dental medicine continuously expands to improve treatments for prevalent clinical problems in dental and oral medicine. Stem cell based translational opportunities include regenerative therapies for tooth restoration, root canal therapy and inflammatory processes (e.g., periodontitis). The potential of regenerative approaches relies on the biological properties of dental stem cells. These and other multipotent somatic mesenchymal stem cell (MSC) types can in principle be applied as either autologous or allogeneic sources in dental procedures. Dental stem cells have distinct developmental origins and biological markers that determine their translational utility. Dental regenerative medicine is supported by mechanistic knowledge of the molecular pathways that regulate dental stem cell growth and differentiation. Cell fate determination and lineage progression of dental stem cells is regulated by multiple cell signaling pathways (e.g., WNTs, BMPs) and epigenetic mechanisms, including DNA modifications, histone modifications, and non-coding RNAs (e.g., miRNAs and lncRNAs). This review also considers a broad range of novel approaches in which stem cells are applied in combination with biopolymers, ceramics and composite materials, as well as small molecules (agonistic or anti-agonistic ligands) and natural compounds. Promising concepts in bone and dental tissue engineering continue to drive innovation in dental and non-dental restorative procedures.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140563331","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}
Pub Date : 2024-04-01DOI: 10.1615/critreveukaryotgeneexpr.2024052889
William Cates, Janet Denbeigh, Ralph Salvagno, Sanjeev Kakar, Andre van Wijnen, Charles Eaton
Dupuytren Disease is a common fibroproliferative disease that can result in debilitating hand deformities. Partial correction and return of deformity are common with surgical or clinical treatments at present. While current treatments are limited to local procedures for relatively late effects of the disease, the pathophysiology of this connective tissue disorder is associated with both local and systemic processes (e.g., fibrosis, inflammation). Hence, a better understanding of the systemic circulation of Dupuytren related cytokines and growth factors may provide important insights into disease progression. In addition, systemic biomarker analysis could yield new concepts for treatments of Dupuytren that attenuate circulatory factors (e.g., anti-inflammatory agents, neutralizing antibodies). Progress in the development of any disease modifying biologic treatment for Dupuytren has been hampered by the lack of clinically useful biomarkers. The characterization of nonsurgical Dupuytren biomarkers will permit disease staging from diagnostic and prognostic perspectives, as well as allows evaluation of biologic responses to treatment. Identification of such markers may transcend their use in Dupuytren treatment, because fibrotic biological processes fundamental to Dupuytren are relevant to fibrosis in many other connective tissues and organs with collagen-based tissue compartments. There is a wide range of potential Dupuytren biomarker categories that could be informative, including disease determinants linked to genetics, collagen metabolism, as well as immunity and inflammation (e.g., cytokines, chemokines). This narrative review provides a broad overview of previous studies
{"title":"Inflammatory Markers Involved in the Pathogenesis of Dupuytren Contracture","authors":"William Cates, Janet Denbeigh, Ralph Salvagno, Sanjeev Kakar, Andre van Wijnen, Charles Eaton","doi":"10.1615/critreveukaryotgeneexpr.2024052889","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024052889","url":null,"abstract":"Dupuytren Disease is a common fibroproliferative disease that can result in debilitating hand deformities. Partial correction and return of deformity are common with surgical or clinical treatments at present. While current treatments are limited to local procedures for relatively late effects of the disease, the pathophysiology of this connective tissue disorder is associated with both local and systemic processes (e.g., fibrosis, inflammation). Hence, a better understanding of the systemic circulation of Dupuytren related cytokines and growth factors may provide important insights into disease progression. In addition, systemic biomarker analysis could yield new concepts for treatments of Dupuytren that attenuate circulatory factors (e.g., anti-inflammatory agents, neutralizing antibodies). Progress in the development of any disease modifying biologic treatment for Dupuytren has been hampered by the lack of clinically useful biomarkers. The characterization of nonsurgical Dupuytren biomarkers will permit disease staging from diagnostic and prognostic perspectives, as well as allows evaluation of biologic responses to treatment. Identification of such markers may transcend their use in Dupuytren treatment, because fibrotic biological processes fundamental to Dupuytren are relevant to fibrosis in many other connective tissues and organs with collagen-based tissue compartments. There is a wide range of potential Dupuytren biomarker categories that could be informative, including disease determinants linked to genetics, collagen metabolism, as well as immunity and inflammation (e.g., cytokines, chemokines). This narrative review provides a broad overview of previous studies","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140563409","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}
Pub Date : 2024-04-01DOI: 10.1615/critreveukaryotgeneexpr.2024053672
Scott Perrapato, Nicholas Farina, Adrian Berg, James Wallace, Steven Ades, Thomas Ahern, Janet Stein, Gary Stein, Jane Lian
Objective criteria are required for prostate cancer risk assessment, treatment decisions, evaluation of therapy, and initial indications of recurrence. Circulating microRNAs were utilized as biomarkers to distinguish prostate cancer patients from cancer-free subjects or those encountering benign prostate hyperplasia. A panel of sixty microRNAs was developed with established roles in prostate cancer initiation, progression, metastasis, and recurrence. Utilizing the FirePlex® platform for microRNA analysis, we demonstrated the efficacy and reproducibility of a rapid, high-throughput, serum-based assay for prostate cancer biomarkers that circumvents the requirement for extraction and fractionation of patient specimens supporting feasibility for expanded clinical research and diagnostic applications.
{"title":"A MicroRNA Approach to Evaluate Elevated Prostate Cancer Risk in Cancer-Free Men","authors":"Scott Perrapato, Nicholas Farina, Adrian Berg, James Wallace, Steven Ades, Thomas Ahern, Janet Stein, Gary Stein, Jane Lian","doi":"10.1615/critreveukaryotgeneexpr.2024053672","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024053672","url":null,"abstract":"Objective criteria are required for prostate cancer risk assessment, treatment decisions, evaluation of therapy, and initial indications of recurrence. Circulating microRNAs were utilized as biomarkers to distinguish prostate cancer patients from cancer-free subjects or those encountering benign prostate hyperplasia. A panel of sixty microRNAs was developed with established roles in prostate cancer initiation, progression, metastasis, and recurrence. Utilizing the FirePlex® platform for microRNA analysis, we demonstrated the efficacy and reproducibility of a rapid, high-throughput, serum-based assay for prostate cancer biomarkers that circumvents the requirement for extraction and fractionation of patient specimens supporting feasibility for expanded clinical research and diagnostic applications.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140811694","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}
Pub Date : 2024-03-01DOI: 10.1615/critreveukaryotgeneexpr.2024052788
Jipeng Guo, Chongwen Gong, Hao Wang
Lung cancer is the most common malignancy worldwide. Long non-coding RNA (lncRNA) PURPL is abnormally in various cancers. However, the reports on its roles in lung cancer are limited. The purpose of present study is to investigate the potentials of lncRNA PURPL in lung cancer. PURPL and mRNA expression was determined using RT-qPCR. The location of PURPL was detected using RNA FISH assay. Protein expression was detected using western blot. Cellular functions were determined using flow cytometry. The interaction between PURPL and RBM4 was confirmed using RIP assay. PURPL was overexpressed in lung cancer cells and patients. Overexpressed PURPL promoted M2 macrophage polarization and suppressed ferroptosis. Additionally, PURPL maintained the mRNA stability of xCT via regulating RBM4. xCT knockdown antagonized the effects of overexpressed PURPL and inhibited M2 macrophage polarization via inducing macrophage ferroptosis. PURPL/RBM4/xCT axis promoted M2 macrophage polarization in lung cancer. Therefore, PURPL may be a potential target of lung cancer.
{"title":"PURPL promotes M2 macrophage polarization in lung cancer via regulating RBM4/xCT signaling","authors":"Jipeng Guo, Chongwen Gong, Hao Wang","doi":"10.1615/critreveukaryotgeneexpr.2024052788","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024052788","url":null,"abstract":"Lung cancer is the most common malignancy worldwide. Long non-coding RNA (lncRNA) PURPL is abnormally in various cancers. However, the reports on its roles in lung cancer are limited. The purpose of present study is to investigate the potentials of lncRNA PURPL in lung cancer. PURPL and mRNA expression was determined using RT-qPCR. The location of PURPL was detected using RNA FISH assay. Protein expression was detected using western blot. Cellular functions were determined using flow cytometry. The interaction between PURPL and RBM4 was confirmed using RIP assay. PURPL was overexpressed in lung cancer cells and patients. Overexpressed PURPL promoted M2 macrophage polarization and suppressed ferroptosis. Additionally, PURPL maintained the mRNA stability of xCT via regulating RBM4. xCT knockdown antagonized the effects of overexpressed PURPL and inhibited M2 macrophage polarization via inducing macrophage ferroptosis. PURPL/RBM4/xCT axis promoted M2 macrophage polarization in lung cancer. Therefore, PURPL may be a potential target of lung cancer.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140198193","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}
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