European Journal of Histochemistry最新文献_第9页

In memoriam of Prof. Stan Fakan. 纪念Stan Fakan教授。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-02-06 DOI: 10.4081/ejh.2023.3668

Marco Biggiogera, Manuela Malatesta

引用次数: 0

Effects of artificial light with different spectral composition on eye axial growth in juvenile guinea pigs. 不同光谱组成的人造光对幼年豚鼠眼轴生长的影响。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-02-06 DOI: 10.4081/ejh.2023.3634

Xinyu Xu, Jiayu Shi, Chuanwei Zhang, Lixin Shi, Yujie Bai, Wei Shi, Yuliang Wang

{"title":"Effects of artificial light with different spectral composition on eye axial growth in juvenile guinea pigs.","authors":"Xinyu Xu, Jiayu Shi, Chuanwei Zhang, Lixin Shi, Yujie Bai, Wei Shi, Yuliang Wang","doi":"10.4081/ejh.2023.3634","DOIUrl":"https://doi.org/10.4081/ejh.2023.3634","url":null,"abstract":"The purpose of the study was to investigate the effect of artificial light with different spectral composition and distribution on axial growth in guinea pigs. Three-week-old guinea pigs were randomly assigned to groups exposed to natural light, low color temperature light-emitting diode (LED) light, two full spectrum artificial lights (E light and Julia light) and blue light filtered light with the same intensity. Axial lengths of guinea pigs' eyes were measured by A-scan ultrasonography prior to the experiment and every 2 weeks during the experiment. After light exposure for 12 weeks, retinal dopamine (DA), dihydroxy-phenylacetic acid (DOPAC) levels and DOPAC/DA ratio were analyzed by high-pressure liquid chromatography electrochemical detection and retinal histological structure was observed. Retinal melanopsin expression was detected using Western blot and immunohistochemistry. After exposed to different kinds of light with different spectrum for 4 weeks, the axial lengths of guinea pigs' eyes in LED group and Julia light group were significantly longer than those of natural light group. After 6 weeks, the axial lengths in LED light group were significantly longer than those of E light group and blue light filtered group. The difference between axial lengths in E light group and Julia light group showed statistical significance after 8 weeks (p<0.05). After 12 weeks of light exposure, the comparison of retinal DOPAC/DA ratio and melanopsin expression in each group was consistent with that of axial length. In guinea pigs, continuous full spectrum artificial light with no peak or valley can inhibit axial elongation via retinal dopaminergic and melanopsin system.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3a/5f/ejh-67-1-3634.PMC10300426.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10062230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3 signaling pathway. LINC00926通过miR-3194-5p调控JAK1/STAT3信号通路参与缺氧诱导的血管内皮细胞功能障碍。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-16 DOI: 10.4081/ejh.2023.3526

Yong Jiang, Chun-Hui Xu, Ying Zhao, Yun-Han Ji, Xin-Tao Wang, Ying Liu

{"title":"LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3 signaling pathway.","authors":"Yong Jiang, Chun-Hui Xu, Ying Zhao, Yun-Han Ji, Xin-Tao Wang, Ying Liu","doi":"10.4081/ejh.2023.3526","DOIUrl":"https://doi.org/10.4081/ejh.2023.3526","url":null,"abstract":"Vascular endothelial cell (VEC) dysfunction is associated with the development of coronary heart disease (CHD). Long intergenic non-protein coding RNA 926 (LINC00926), a kind of long noncoding RNA (lncRNA), has been found to be abnormally expressed in CHD patients. However, the biological role of LINC00926 has not been reported. In our research, we intended to explore the regulatory mechanism of LINC00926 in hypoxia-exposed HUVEC cells (HUVECs). In our in vitro study, HUVECs were exposed under hypoxic conditions (5% O2) for 24 h. RT-qPCR and Western blotting assay were used to detect the mRNA and protein levels. CCK-8 assay, flow cytometry, transwell assay and in vitro angiogenesis assay were performed to measure cell proliferation, apoptosis, migration and tube formation, respectively. Bioinformatics analysis was applied to predict the target of LINC00926 and miR-3194-5p, which was verified by dual-luciferase reporter assays. The results showed that LINC00926 was highly expressed in CHD patients and hypoxia-exposed HUVECs. LINC00926 overexpression suppressed cell proliferation, migration and tube formation and increased cell apoptosis. MiR-3194-5p was a target of LINC00926 and can target binding to JAK1 3'UTR. LINC00926 could up-regulate JAK1 and p-STAT3 levels via miR-3194-5p. In addition, overexpressed LINC00926 suppressed cell proliferation, migration and tube formation and increased cell apoptosis via miR-3194-5p/JAK1/STAT3 axis. In summary, LINC00926 aggravated endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3 signaling pathway in hypoxia-exposed HUVECs.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/48/ad/ejh-67-1-3526.PMC10300425.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10061644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Phosphorylation mutation impairs the promoting effect of spastin on neurite outgrowth without affecting its microtubule severing ability. 磷酸化突变削弱了痉挛素对神经突生长的促进作用，但不影响其切断微管的能力。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-12 DOI: 10.4081/ejh.2023.3594

Yunlong Zhang, Xin He, Jianyu Zou, Jie Yang, Ao Ma, Minghui Tan

{"title":"Phosphorylation mutation impairs the promoting effect of spastin on neurite outgrowth without affecting its microtubule severing ability.","authors":"Yunlong Zhang, Xin He, Jianyu Zou, Jie Yang, Ao Ma, Minghui Tan","doi":"10.4081/ejh.2023.3594","DOIUrl":"https://doi.org/10.4081/ejh.2023.3594","url":null,"abstract":"Spastin, a microtubule-severing enzyme, is known to be important for neurite outgrowth. However, the role of spastin post-translational modification, particularly its phosphorylation regulation in neuronal outgrowth, remains unclear. This study aimed to investigate the effects of eliminating spastin phosphorylation on the neurite outgrowth of rat hippocampal neurons. To accomplish this, we constructed a spastin mutant with eleven potential phosphorylation sites mutated to alanine. The phosphorylation levels of the wildtype spastin (WT) and the mutant (11A) were then detected using Phos-tag SDS-PAGE. The spastin constructs were transfected into COS7 cells for the observation of microtubule severing, and into rat hippocampal neurons for the detection of neuronal outgrowth. The results showed that compared to the spastin WT, the phosphorylation levels were significantly reduced in the spastin 11A mutant. The spastin mutant 11A impaired its ability to promote neurite length, branching, and complexity in hippocampal neurons, but did not affect its ability to sever microtubules in COS7 cells. In conclusion, the data suggest that mutations at multiple phosphorylation sites of spastin do not impair its microtubule cleavage ability in COS7 cells, but reduce its ability to promote neurite outgrowth in rat hippocampal neurons.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/98/6d/ejh-67-1-3594.PMC10300427.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9707749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neurokinin-1 receptor is highly expressed in cervical cancer and its antagonist induces cervical cancer cell apoptosis. 神经激肽-1受体在宫颈癌中高表达，其拮抗剂可诱导宫颈癌细胞凋亡。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-11 DOI: 10.4081/ejh.2023.3570

Liyun Guan, Shifa Yuan, Jing Ma, Hong Liu, Lizhen Huang, Fengzhen Zhang

{"title":"Neurokinin-1 receptor is highly expressed in cervical cancer and its antagonist induces cervical cancer cell apoptosis.","authors":"Liyun Guan, Shifa Yuan, Jing Ma, Hong Liu, Lizhen Huang, Fengzhen Zhang","doi":"10.4081/ejh.2023.3570","DOIUrl":"https://doi.org/10.4081/ejh.2023.3570","url":null,"abstract":"Neurokinin-1 receptor (NK1R) belongs to tachykinin receptor family. Recent studies have suggested that NK1R was upregulated in cancer tissues including breast cancer, glioma and melanoma. Furthermore, NK1R antagonists have been employed to exert anti-tumor effect and promote cancer cell apoptosis. However, the role of NK1R in cervical cancer remains largely unknown. In this study, we aimed to detect the expression of NK1R in cervical cancer and evaluate the anti-tumor effects of NK1R antagonist on cervical cancer cells. We found that NK1R was highly expressed in cervical cancer tissues than in adjacent normal cervical tissues. Furthermore, by using NK1R antagonist we demonstrated that NK1R antagonist inhibited the viability and induced the apoptosis of cervical cancer cells in a dose-dependent manner, and the mechanism may be related to the inhibition of ERK activation and the regulation of apoptosis proteins Bcl-2 and BAX. In conclusion, these findings suggest that NK1R plays an oncogenic role in cervical cancer and is a promising target for cervical cancer therapy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/50/70/ejh-67-1-3570.PMC10300428.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9704884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Differential antigen expression between human apocrine sweat glands and eccrine sweat glands. 人大汗腺与小汗腺抗原的差异表达。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-02 DOI: 10.4081/ejh.2023.3559

Manxiu Cao, Lei Zhang, Jiaqi Chen, Cangyu Wang, Junhong Zhao, Xiang Liu, Yongjing Yan, Yue Tang, Zixiu Chen, Haihong Li

{"title":"Differential antigen expression between human apocrine sweat glands and eccrine sweat glands.","authors":"Manxiu Cao, Lei Zhang, Jiaqi Chen, Cangyu Wang, Junhong Zhao, Xiang Liu, Yongjing Yan, Yue Tang, Zixiu Chen, Haihong Li","doi":"10.4081/ejh.2023.3559","DOIUrl":"https://doi.org/10.4081/ejh.2023.3559","url":null,"abstract":"Bromhidrosis has a great negative impact on personal occupation and social psychology. It is not yet clear whether bromhidrosis is caused by apocrine sweat glands or the co-action of apocrine sweat glands and eccrine sweat glands. To distinguish between apocrine sweat glands and eccrine sweat glands, specific antigen markers for apocrine sweat glands and eccrine sweat glands must be found first. In the study, we detected the expression of K7, K18, K19, Na+-K+-2Cl- cotransporter 1 (NKCC1), carbonic anhydrase II (CAII), Forkhead transcription factor a1 (Foxa1), homeobox transcription factor engrailed homeobox1 (En1), gross cystic disease fluid protein-15 (GCDFP-15), mucin-1 (MUC-1), cluster of differentiation 15 (CD15) and apolipoprotein (APOD) in eccrine sweat glands and apocrine sweat glands by immunofluorescence staining. The results showed that K7, K18, K19, Foxa1, GCDFP-15 and MUC-1 were expressed in both apocrine and eccrine sweat glands, CD15 and APOD were only expressed in apocrine sweat glands, and CAII, NKCC1 and En1 were only expressed in eccrine sweat glands. We conclude that CD15 and APOD can serve as specific markers for apocrine sweat glands, while CAII, NKCC1 and En1 can serve as specific markers for eccrine sweat glands to differentiate the two sweat glands.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ab/7a/ejh-67-1-3559.PMC9827426.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10573747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decreased VEGFA alleviates the symptoms of LPS-induced sepsis in a mouse model by inhibiting glycolysis and thereby regulating the polarization of macrophages. 在小鼠模型中，VEGFA的减少通过抑制糖酵解从而调节巨噬细胞的极化来缓解lps诱导的脓毒症的症状。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-02 DOI: 10.4081/ejh.2023.3528

Jun Lin, Liping Jiang, Kun Guo, Ning Feng

{"title":"Decreased VEGFA alleviates the symptoms of LPS-induced sepsis in a mouse model by inhibiting glycolysis and thereby regulating the polarization of macrophages.","authors":"Jun Lin, Liping Jiang, Kun Guo, Ning Feng","doi":"10.4081/ejh.2023.3528","DOIUrl":"https://doi.org/10.4081/ejh.2023.3528","url":null,"abstract":"The immune imbalance caused by excessive inflammatory reactions is the primary cause of sepsis. Macrophages with M1 and M2 polarization states are important immune cells that regulate the balance of the inflammatory response in sepsis. Encouraging the conversion of macrophages from the M1 to the M2 type is an important strategy for relieving sepsis. Here, we demonstrated the upregulation of vascular endothelial growth factor A (VEGFA) in a mouse model of sepsis. Then, siRNA technology was applied to inhibit the expression of VEGFA in macrophages. Flow cytometry and RT‒qPCR results showed that low expression of VEGFA inhibited LPS-induced M1 polarization of macrophages. Decreased VEGFA was also proven to lower TNF-α, IL-1β, and IL-6 secretion by LPS-induced macrophages. In addition, the effects of knocking down VEGFA on the energy metabolism pattern of macrophages were investigated by glycolysis pressure tests and mitochondrial pressure tests, and VEGFA knockdown reversed the induction of glycolysis in macrophages by LPS. The mitochondrial content and ATP content results also confirmed this finding. After the tail vein of septic mice was injected with macrophages transfected with si-VEGFA, the liver and kidney damage and the pathological conditions of the lung were alleviated. The secretion of TNF-α and IL-6 was decreased, while IL-10 was increased in their serum. Immunohistochemical staining revealed decreased expression of CD86 and increased expression of CD206 in the si-VEGFA group. This study demonstrates that decreased VEGFA inhibits glycolysis and thus inhibits LPS-induced M1 polarization of macrophages, ultimately relieving sepsis.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f8/06/ejh-67-1-3528.PMC9827425.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10573750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

An ex vivo experimental system to track fluorescent nanoparticles inside skeletal muscle. 追踪骨骼肌内荧光纳米颗粒的离体实验系统。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-02 DOI: 10.4081/ejh.2023.3596

Laura Calderan, Flavia Carton, Ilaria Andreana, Valeria Bincoletto, Silvia Arpicco, Barbara Stella, Manuela Malatesta

{"title":"An ex vivo experimental system to track fluorescent nanoparticles inside skeletal muscle.","authors":"Laura Calderan, Flavia Carton, Ilaria Andreana, Valeria Bincoletto, Silvia Arpicco, Barbara Stella, Manuela Malatesta","doi":"10.4081/ejh.2023.3596","DOIUrl":"https://doi.org/10.4081/ejh.2023.3596","url":null,"abstract":"The development of novel nanoconstructs for biomedical applications requires the assessment of their biodistribution, metabolism and clearance in single cells, organs and entire organisms in a living environment. To reduce the number of in vivo experiments performed and to refine the methods used, in accordance with the 3Rs principle, this work proposes an ex vivo experimental system to monitor, using fluorescence microscopy, the distribution of nanoparticles in explanted murine skeletal muscle maintained in a bioreactor that can preserve the structural and functional features of the organ for long periods of time. Fluorescently-labelled liposomes and poly(lactide-co-glycolide) (PLGA)-based nanoparticles were injected into the intact soleus muscle (in the distal region close to the tendon) immediately after explants, and their distribution was analysed at increasing incubation times in cross cryosections from the proximal region of the belly. Both nanocarriers were clearly recognized in the muscle and were found to enter and migrate inside the myofibres, whereas their migration in the connective tissue seemed to be limited. In addition, some fluorescent signals were observed inside the macrophages, demonstrating the physiological clearance of the nanocarriers that did not enter the myofibres. Our ex vivo system therefore provides more information than previous in vitro experiments on cultured muscle cells, highlighting the need for the appropriate functionalization of nanocarriers if myofibre targeting is to be improved.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/20/a6/ejh-67-1-3596.PMC9827424.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10573745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Growth hormone inhibits the JAK/STAT3 pathway by regulating SOCS1 in endometrial cells in vitro: a clue to enhance endometrial receptivity in recurrent implantation failure. 生长激素通过体外调控子宫内膜细胞SOCS1抑制JAK/STAT3通路:复发性着床失败中子宫内膜接受性增强的线索

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-02 DOI: 10.4081/ejh.2023.3580

Haixia Li, Ning Sun, Yaqiao Zhu, Wei Wang, Meihong Cai, Xiaohuan Luo, Wei Xia, Song Quan

{"title":"Growth hormone inhibits the JAK/STAT3 pathway by regulating SOCS1 in endometrial cells in vitro: a clue to enhance endometrial receptivity in recurrent implantation failure.","authors":"Haixia Li, Ning Sun, Yaqiao Zhu, Wei Wang, Meihong Cai, Xiaohuan Luo, Wei Xia, Song Quan","doi":"10.4081/ejh.2023.3580","DOIUrl":"https://doi.org/10.4081/ejh.2023.3580","url":null,"abstract":"Recurrent implantation failure (RIF) is defined as failure to achieve clinical pregnancy after at least 3 transfers of good-quality embryos by natural or artificial means. RIF is often a complex problem with a wide variety of etiologies and mechanisms as well as treatment options. In this study, using immunohistochemistry and Western blot, we demonstrated that the expression of leukemia inhibitory factor (LIF), Janus kinase 1 (JAK1), and signal transducer and activator of transcription 3 (STAT3) was increased, while that of suppressor of cytokine signaling 1 (SOCS1) was decreased in RIF patients. Growth hormone (GH) administration proved to have positive effects on embryo implantation in RIF patients, but the action mechanism of GH has not been elucidated yet. To this aim, we studied the effects of GH on the proliferation in vitro of endometrial adenocarcinoma Ishikawa cells. GH stimulated the expression of LIF and SOCS1, and through SOCS1 inhibits the expression of phosphorylated STAT3, and finally inhibits the occurrence of RIF. Excessive phosphorylation of STAT can lead to decreased endometrial receptivity and abnormal embryo implantation. We also examined the effects of LIF overexpression and an LIF inhibitor (EC330) on the JAK/STAT pathway. LIF promoted cell proliferation, and the up-regulation of LIF increased the expression of SOCS1 and JAK1/STAT3 pathway-related genes in Ishikawa cells. As GH can inhibit the JAK1/STAT3 pathway through LIF, we hypothesize that upregulating SOCS1 may be a potential approach to treat RIF at the molecular level. GH can inhibit the JAK1/STAT3 pathway through LIF, up-regulating SOCS1 to treat RIF at the molecular level.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5d/7b/ejh-67-1-3580.PMC9827423.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10573751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DPY30 promotes the growth and survival of osteosarcoma cell by regulating the PI3K/AKT signal pathway. DPY30通过调控PI3K/AKT信号通路促进骨肉瘤细胞生长和存活。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-01-02 DOI: 10.4081/ejh.2023.3413

Gong Cheng, Fengmin An, Zhilin Cao, Mingdi Zheng, Zhongyuan Zhao, Hao Wu

{"title":"DPY30 promotes the growth and survival of osteosarcoma cell by regulating the PI3K/AKT signal pathway.","authors":"Gong Cheng, Fengmin An, Zhilin Cao, Mingdi Zheng, Zhongyuan Zhao, Hao Wu","doi":"10.4081/ejh.2023.3413","DOIUrl":"https://doi.org/10.4081/ejh.2023.3413","url":null,"abstract":"Osteosarcoma (OS) is characterized by aggressive features including invasiveness and high incidence of metastasis. OS patients with metastases are difficult to treat and suffer from a poor prognosis. DPY30 (protein dpy-30 homolog) is a key component of SET1/MLL family of H3K4 methyltransferases, which is implicated in the progression of multiple cancers. However, the potential functional engagement of DPY30 in OS remains to be unveiled. The objective of this study is to investigate the potential roles of DPY30 in the regulation of malignant phenotypes of OS cells. We examined DPY30 expression from a published dataset (GSE28424) as well as in OS tissues and adjacent normal tissues from OS patients. The association of DPY30 expression level and clinicopathologic parameters was assessed by Chi-square test. The role of DPY30 in regulating the malignant phenotype of OS cells and tumorigenesis was examined by in vitro functional assays and xenograft mouse model. We reported an upregulation of DPY30 in OS tumor tissues in both published dataset and clinical samples. A high level of DPY30 expression was associated with larger tumor size and more metastasis in OS patients, as well as poor overall survival. DPY30 knockdown in OS cells significantly impairs proliferation, migration and invasion, but induced cellular apoptosis. We further demonstrated that the agonist of PI3K/AKT pathway can rescue the inhibitory effects of DPY30 knockdown in OS cells. Together, our data indicate that DPY30 functions as an oncogene to promote the malignancy of OS cells possibly through PI3K/AKT pathway. The dependency of OS cells on DPY30 overexpression is a targetable vulnerability in OS cells.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/07/91/ejh-67-1-3413.PMC9827427.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10573746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0