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Ethyl Acetate Extract of Oratosquilla Inhibits the Growth of Nasopharyngeal Carcinoma through the Hippo Pathway 桔梗乙酸乙酯提取物通过希波通路抑制鼻咽癌的生长
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-09-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053617
Huaigao Wang, Jizhen Liu, Mengjie Shi, Yuanye Xue, Xinsheng Peng, Bin Gan, Yanfang Zhou, Zhidong Li
The Hippo pathway and its transcription co-activator YAP play a critical role in the regulation of cell proliferation, apoptosis and the control of organ size. In the past several years, YAP has been found to be expressed in various human cancers, however, its expression in Nasopharyngeal Carcinoma ( NPC ) remains unstudied. In this report, we found that YAP was overexpressed in human NPC tissues, and its expression was also significantly higher in five NPC cell lines when compared to the nasopharyngeal epithelial cell line NP69 (p<0.01). CNE1 and CNE1-GL cells treated with EOS had an enhanced expression level of phosphorylated YAP and downregulated expression of survivin, which inhibits the proliferation of CNE1 and CNE1-GL cells. These results highlight an important role of hippo pathway in the growth of nasopharyngeal carcinoma and implicate a potential mechanism of ethyl acetate extract of oratosquilla(EOS) preventing the proliferation of nasopharyngeal carcinoma.
Hippo通路及其转录共激活因子YAP在调节细胞增殖、凋亡和控制器官大小方面发挥着关键作用。过去几年中,YAP在多种人类癌症中被发现表达,但其在鼻咽癌(NPC)中的表达仍未得到研究。在本报告中,我们发现 YAP 在人类鼻咽癌组织中表达过高,而且与鼻咽上皮细胞系 NP69 相比,YAP 在五种鼻咽癌细胞系中的表达也明显更高(p<0.01)。经 EOS 处理的 CNE1 和 CNE1-GL 细胞磷酸化 YAP 表达水平升高,存活素表达下调,而存活素会抑制 CNE1 和 CNE1-GL 细胞的增殖。这些结果凸显了希波通路在鼻咽癌生长过程中的重要作用,并暗示了桔梗乙酸乙酯提取物(EOS)阻止鼻咽癌细胞增殖的潜在机制。的潜在机制。
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引用次数: 0
Identification of Lung Adenocarcinoma Subtypes by Using Growth Hormone-Releasing Hormone-Related Genes and Establishment of Signature to Predict Prognosis and Guide Immunother 利用生长激素释放激素相关基因识别肺腺癌亚型,建立预测预后和指导免疫治疗的特征基因组
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-08-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053370
Kai Zhu, Zhenwu Xu, Xue Peng, Chenhua Xu, Shengjia Chen
Background: Growth hormone-releasing hormone (GH-RH) and its antagonists are believed to influence the progression of varying tumor diseases. However, the specific effects of GH-RH-related genes on lung adenocarcinoma (LUAD) are yet to be deciphered.Methods: GH-RH-related gene set data, LUAD transcriptome data, and clinical data were available for download at GeneCards, TCGA, and GEO databases. R software was implemented to finish differential, regression, cluster, survival, and tumor microenvironment analyses. Drugs associated with model genes were predicted using CellMiner database.Results: 781 LUAD samples (TCGA-LUAD: 600 cases; GSE50081: 181 cases) and data for 1555 GH-RH-related gene sets were obtained from public datasets. Two LUAD subtypes with different GH-RH gene expressions were identified through cluster analysis. Significant differences were unveiled in prognosis between the two subtypes. A prognostic risk scoring model was generated based on genes screened from the PPI network, and afterward, the model was validated. The model comprised 7 genes, specifically CLCA1, CYP17A1, DKK1, IGF2BP1, IGFBP1, RPE65, and VGF. Immune-related analysis revealed significant differences in immune cell infiltration levels between high and low-risk groups (P<0.05), with mast cells and neutrophils showing significantly higher infiltration levels in the low-risk population than the other group.Conclusion: The 7-gene signature in the current study is of paramount importance for predicting overall survival and immune microenvironment of LUAD patients.
背景:生长激素释放激素(GH-RH)及其拮抗剂被认为会影响各种肿瘤疾病的进展。然而,GH-RH 相关基因对肺腺癌(LUAD)的具体影响尚待破解:方法:在GeneCards、TCGA和GEO数据库中下载GH-RH相关基因组数据、LUAD转录组数据和临床数据。使用R软件完成差异分析、回归分析、聚类分析、生存分析和肿瘤微环境分析。利用CellMiner数据库预测了与模型基因相关的药物:从公共数据集中获得了781个LUAD样本(TCGA-LUAD:600例;GSE50081:181例)和1555个GH-RH相关基因组的数据。通过聚类分析,确定了两种具有不同 GH-RH 基因表达的 LUAD 亚型。两种亚型的预后存在显著差异。根据从 PPI 网络中筛选出的基因生成了一个预后风险评分模型,随后对该模型进行了验证。该模型包括 7 个基因,分别是 CLCA1、CYP17A1、DKK1、IGF2BP1、IGFBP1、RPE65 和 VGF。免疫相关分析显示,免疫细胞浸润水平在高风险组和低风险组之间存在显著差异(P<0.05),其中肥大细胞和中性粒细胞在低风险人群中的浸润水平明显高于其他组别:本研究中的 7 个基因特征对预测 LUAD 患者的总生存率和免疫微环境至关重要。
{"title":"Identification of Lung Adenocarcinoma Subtypes by Using Growth Hormone-Releasing Hormone-Related Genes and Establishment of Signature to Predict Prognosis and Guide Immunother","authors":"Kai Zhu, Zhenwu Xu, Xue Peng, Chenhua Xu, Shengjia Chen","doi":"10.1615/jenvironpatholtoxicoloncol.2024053370","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053370","url":null,"abstract":"Background: Growth hormone-releasing hormone (GH-RH) and its antagonists are believed to influence the progression of varying tumor diseases. However, the specific effects of GH-RH-related genes on lung adenocarcinoma (LUAD) are yet to be deciphered.\u0000Methods: GH-RH-related gene set data, LUAD transcriptome data, and clinical data were available for download at GeneCards, TCGA, and GEO databases. R software was implemented to finish differential, regression, cluster, survival, and tumor microenvironment analyses. Drugs associated with model genes were predicted using CellMiner database.\u0000Results: 781 LUAD samples (TCGA-LUAD: 600 cases; GSE50081: 181 cases) and data for 1555 GH-RH-related gene sets were obtained from public datasets. Two LUAD subtypes with different GH-RH gene expressions were identified through cluster analysis. Significant differences were unveiled in prognosis between the two subtypes. A prognostic risk scoring model was generated based on genes screened from the PPI network, and afterward, the model was validated. The model comprised 7 genes, specifically CLCA1, CYP17A1, DKK1, IGF2BP1, IGFBP1, RPE65, and VGF. Immune-related analysis revealed significant differences in immune cell infiltration levels between high and low-risk groups (P&lt;0.05), with mast cells and neutrophils showing significantly higher infiltration levels in the low-risk population than the other group.\u0000Conclusion: The 7-gene signature in the current study is of paramount importance for predicting overall survival and immune microenvironment of LUAD patients.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"44 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142210272","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
LncRNA linc01105 inhibits gastric cancer growth and metastasis by regulating the miR-650/TCEA3 axis LncRNA linc01105通过调节miR-650/TCEA3轴抑制胃癌的生长和转移
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-08-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024054112
Qiang Zhang, Hui Mi, Huimei Cai, Chenhui Li, Zhou Wu, Jianfang Zhang
Background: Gastric cancer (GC) is a widespread cancerous disease with an unfavorable prognosis, linc01105 appears to have a significant connection with the development of GC, but the precise regulatory mechanism remains obscure.Methods: RT-qPCR was utilized to determine the expression of linc01105, miR-650, and TCEA3. Proliferative capacity of GC cells was measured by CCK8. Cell apoptosis rates were analyzed via flow cytometry assessment. The invasive capability was assessed through the transwell experiment. The targeted regulation of linc01105, miR-650, and TCEA3 was validated through dual luciferase reporter gene assay.Result: Low expression of linc01105, high expression of miR-650, and low expression of TCEA3 were observed in GC tumor tissues and cell lines. High expression of linc01105 was correlated with a positive prognosis in GC patients. Linc01105 affected GC cell function by miR-650/TCEA3 axis.Conclusion: This study suggested that linc01105 may possess inhibitory functions towards GC. In addition, linc01105 may be a prognostic marker for GC.
背景:胃癌(GC)是一种广泛存在且预后不良的癌症,linc01105似乎与GC的发生发展有重要关系,但其确切的调控机制仍不清楚:方法:利用 RT-qPCR 检测 linc01105、miR-650 和 TCEA3 的表达。用 CCK8 测定 GC 细胞的增殖能力。细胞凋亡率通过流式细胞术评估进行分析。侵袭能力通过透孔实验进行评估。通过双荧光素酶报告基因实验验证了 linc01105、miR-650 和 TCEA3 的靶向调控作用:结果:在 GC 肿瘤组织和细胞系中观察到 linc01105 低表达、miR-650 高表达和 TCEA3 低表达。Linc01105 的高表达与 GC 患者的预后呈正相关。Linc01105通过miR-650/TCEA3轴影响GC细胞功能:这项研究表明,linc01105可能对GC具有抑制作用。结论:这项研究表明,linc01105可能对GC具有抑制作用,此外,linc01105可能是GC的预后标志物。
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引用次数: 0
Molecular mechanism of lncRNAs in ovarian cancer: lncRNA CASC19 regulates the malignant progression of ovarian cancer through miR-761/CBX2 axis lncRNA在卵巢癌中的分子机制:lncRNA CASC19通过miR-761/CBX2轴调控卵巢癌的恶性进展
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-08-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053797
KharChuen Wong, Peng Dai, Yuan Li, Li Liu, Shuanghua Liang
Background: Long non-coding RNAs (lncRNAs) are involved in the numerous types of tumors. The aim of this study is to comprehend the pathological mechanism of lncRNA CASC19 in ovarian cancer.Methods: CASC19, miR-761 and CBX2 expression in the samples was quantitatively detected by real-time quantitative polymerase chain reaction (RT-qPCR) reaction. The proliferation and apoptosis levels of ovarian cancer cells were evaluated via cell counting kit-8 (CCK-8) and Flow cytometry assays. The targeting relationship and correlation of CASC19, miR-761 and CBX2 were investigated through luciferase reporter assay and Pearson assay.Results: CASC19 and CBX2 were enriched in ovarian cancer, while miR-761 expression was decreased. Silencing CASC19 suppressed the cell growth and promoted cell apoptosis. CASC19 targeted the inhibition of miR-761 expression and regulated the level of CBX2. In addition, the miR-761 inhibitor reversed the inhibitory effect of si-CASC19 on the biological activity of ovarian cancer cells, while si-CBX2 restored the regulation of miR-761 inhibitor on the development of ovarian cancer.Conclusion: LncRNA CASC19 mediated the malignant progression of ovarian cancer through miR-761/CBX2 axis, which provided a potential therapeutic target for the cure of patients.
背景:长非编码RNA(lncRNA)与多种肿瘤有关。本研究旨在了解lncRNA CASC19在卵巢癌中的病理机制:方法:采用实时定量聚合酶链式反应(RT-qPCR)定量检测样本中CASC19、miR-761和CBX2的表达。通过细胞计数试剂盒-8(CCK-8)和流式细胞术检测卵巢癌细胞的增殖和凋亡水平。通过荧光素酶报告实验和皮尔逊实验研究了CASC19、miR-761和CBX2的靶向关系和相关性:结果:CASC19和CBX2在卵巢癌中富集,而miR-761表达下降。沉默CASC19可抑制细胞生长,促进细胞凋亡。CASC19靶向抑制了miR-761的表达,并调节了CBX2的水平。此外,miR-761抑制剂逆转了si-CASC19对卵巢癌细胞生物活性的抑制作用,而si-CBX2则恢复了miR-761抑制剂对卵巢癌发展的调控作用:结论:LncRNA CASC19通过miR-761/CBX2轴介导卵巢癌的恶性进展,为治愈患者提供了潜在的治疗靶点。
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引用次数: 0
Analysis of the clinical value of hsa_circ_0001955 in papillary thyroid cancer treated with 131 iodine 用 131 碘治疗甲状腺乳头状癌中 hsa_circ_0001955 的临床价值分析
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-07-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053337
Chong Cheng, Ling Zhang, Quanyong Wang, Mingyou Yang, Wenlin Liu
Background: The prevalent histological variant within differentiated thyroid carcinoma is papillary thyroid carcinoma, also known as PTC. The study investigated the clinical performance of serum hsa_circ¬_0001955 in predicting the prognosis of PTC treated with radical thyroidectomy and iodine 131 nail clearance.Method: The relative expression of serum circ_0001955 of PTC patients was detected before and after accepting radical thyroidectomy combined with 131I thyroid remnant ablation by RT-qPCR. Serum thyroglobulin (Tg) and thyroglobulin antibody (TgAb) levels were quantified by an automatic chemiluminescence immunoassay analyzer. Multivariate logistic regression analysis was employed to investigate the risk factors associated with the prognosis of PTC patients with postoperative 131I therapy.Results: The serum circ_0001955 levels in 127 PTC patients were higher than that in 96 multinodular goiter patients and 110 healthy controls before treatment and had diagnostic values for PTC patients. After 131I treatment, serum circ_0001955 levels and Tg value have a correlation with potential recurrence (WBS positive). Serum circ_0001955, Tg, and TgAb value, and their combination may have diagnostic value in predicting recurrence.Conclusion: Serum circ_0001955 levels in patients with PTC after radical thyroidectomy and iodine 131 thyroidectomy may help predict recurrence.
背景:分化型甲状腺癌中最常见的组织学变异是甲状腺乳头状癌,又称PTC。本研究探讨了血清hsa_circ¬_0001955在预测接受根治性甲状腺切除术和碘131钉清除术治疗的PTC预后方面的临床表现:方法:采用RT-qPCR技术检测PTC患者接受甲状腺根治性切除术联合131碘甲状腺残甲消融术前后血清circ_0001955的相对表达量。血清甲状腺球蛋白(Tg)和甲状腺球蛋白抗体(TgAb)水平通过自动化学发光免疫分析仪进行量化。采用多变量逻辑回归分析研究与术后接受 131I 治疗的 PTC 患者预后相关的危险因素:结果:127 例 PTC 患者的血清 circ_0001955 水平高于治疗前的 96 例多结节性甲状腺肿患者和 110 例健康对照组,具有 PTC 患者的诊断价值。131I 治疗后,血清 circ_0001955 水平和 Tg 值与潜在复发(WBS 阳性)有相关性。血清circ_0001955、Tg和TgAb值及其组合在预测复发方面可能具有诊断价值:甲状腺根治术和碘 131 甲状腺切除术后的 PTC 患者血清 circ_0001955 水平可能有助于预测复发。
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引用次数: 0
HIF-1α activates hypoxia-induced MXRA5 expression in the progression of ovarian cancer HIF-1α 在卵巢癌进展过程中激活缺氧诱导的 MXRA5 表达
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-07-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053641
Fen Fu, Liju Nie, Linfeng Huang, Qizhou Zhu, Qinglan Yao, Yiguo Wu, Lu Zhao, Lamei Yu
Background: The hypoxic microenvironment of tumor cells is closely related to the progression of ovarian cancer. This study aims to explore the role of matrix-remodeling associated 5 (MXRA5) in regulating cellular hypoxia in ovarian cancer.Methods: The MXRA5 expression and its clinical significance in ovarian cancer were evaluated using GEPIA2, Kaplan-Meier plotter databases, and immunohistochemistry assay. Ovarian cancer cells were treated with normoxia and hypoxia conditions. The siRNAs were used to knock down the MXRA5 expression in hypoxic cells. The cellular capacities were detected by CCK-8 assay, EdU assay, Transwell invasion assay, and TUNEL assay, respectively.Results: The MXRA5 level was increased in ovarian cancer and associated with the PFS and survival of ovarian cancer patients. The proliferation and invasion abilities of ovarian cancer cells were promoted, while apoptosis capacities were inhibited in hypoxic cells. After the knockdown of MXRA5 in hypoxic cells, the proliferation and invasion abilities of the cells were reduced, and the apoptosis capacities were enhanced. Moreover, mechanistically, HIF-1α is a key transcription factor in response to hypoxia that binds to the MXRA5 promoter.Conclusion: MXRA5 expression was induced by hypoxia and had prognostic performance in ovarian cancer. MXRA5 is one of the potential targets of tumor hypoxia regulation. Knockdown of MXRA5 can inhibit proliferation and invasion in ovarian cancer cells caused by HIF-1α, revealing that MXRA5 is one potential targets for tumor hypoxia regulation in ovarian cancer.
背景:肿瘤细胞的缺氧微环境与卵巢癌的进展密切相关。本研究旨在探讨基质重塑相关 5(MXRA5)在调节卵巢癌细胞缺氧中的作用:方法:采用 GEPIA2、Kaplan-Meier plotter 数据库和免疫组化方法评估 MXRA5 在卵巢癌中的表达及其临床意义。卵巢癌细胞分别在常氧和低氧条件下处理。用 siRNA 敲除缺氧细胞中 MXRA5 的表达。分别用 CCK-8 检测法、EdU 检测法、Transwell 侵袭检测法和 TUNEL 检测法检测细胞能力:结果:MXRA5水平在卵巢癌中升高,并与卵巢癌患者的PFS和生存期相关。缺氧会促进卵巢癌细胞的增殖和侵袭能力,同时抑制细胞的凋亡能力。在缺氧细胞中敲除 MXRA5 后,细胞的增殖和侵袭能力降低,凋亡能力增强。此外,从机理上讲,HIF-1α是缺氧反应的关键转录因子,它与MXRA5启动子结合:结论:缺氧会诱导 MXRA5 的表达,并对卵巢癌的预后产生影响。MXRA5是肿瘤缺氧调控的潜在靶点之一。敲除MXRA5可抑制HIF-1α导致的卵巢癌细胞增殖和侵袭,揭示了MXRA5是卵巢癌肿瘤缺氧调控的潜在靶点之一。
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引用次数: 0
Histone-lysine N-methyltransferase 2D (KMT2D) impending therapeutic target for the management of cancer: The giant rats tail 组蛋白-赖氨酸 N-甲基转移酶 2D (KMT2D)即将成为治疗癌症的靶点:巨鼠尾巴
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-07-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053872
Meshak Dhanashekaran Cecileya Jasmin, N Radhakrishnan, Venugopal Vinod Prabhu, Kunnathur Murugesan Sakthivel, Rasmi Rajan Radha
The Histone-lysine N-methyltransferase 2D (KMT2D), tumor suppressor gene which is the major component of histone H3K4 mono-methyltransferase in mammals and has significant role in regulation of a gene which are frequently mutated that lead to many different types of cancers that includenon-Hodgkin lymphoma, medulloblastoma, prostate carcinoma, renal carcinoma, bladder carcinoma and lung carcinoma. KMT2D gene epigenetic alterations in histone methylation play a significant role for the initiation and progression of cancers from pre-cancerous lesions, yet its complete function in oncogenesis remains unsolved. KMT2D deficiency - loss are thought of initial mediators of cancer development and cell migration such as B‐cell lymphoma, medulloblastoma, melanoma, pancreas and lung cancer. The KMT2D loss has know to activate glycolytic genes that promote aggressive tumor progression. Therefore, the present review serves to underline the update on recent research pertaining toKMT2D gene, that could be a potential therapeutic target in down regulating glycolytic genes such as Pgk1,Ldha, Pgam1 and Gapdh; 2, tyrosine kinases EGFR - ERBB2, RTK-RAS signaling, Ras activator genes Rgl1, Rasgrp1, Rasgrf1, Rasgrf2 and Rapgef5 in suppressing the tumor progression that may represent novel targeted therapy for the management of cancer. This review will facilitate to understand the gene expression that inhibits cancer progression and which could serve as a potential molecular target in understanding cancer pathogenesis.
组蛋白-赖氨酸 N-甲基转移酶 2D(KMT2D)是哺乳动物中组蛋白 H3K4 单甲基转移酶的主要成分,是肿瘤抑制基因,在调控基因突变方面发挥着重要作用,而基因突变会导致多种不同类型的癌症,包括非霍奇金淋巴瘤、髓母细胞瘤、前列腺癌、肾癌、膀胱癌和肺癌。KMT2D 基因在组蛋白甲基化方面的表观遗传学改变对癌症从癌前病变到癌症的发生和发展起着重要作用,但它在致癌过程中的全部功能仍未得到解决。KMT2D 缺失被认为是癌症发展和细胞迁移的初始介质,如 B 细胞淋巴瘤、髓母细胞瘤、黑色素瘤、胰腺癌和肺癌。KMT2D缺失可激活糖酵解基因,促进侵袭性肿瘤进展。因此,本综述旨在强调与 KMT2D 基因有关的最新研究进展,KMT2D 基因可能是下调 Pgk1、Ldha、Pgam1 和 Gapdh 等糖酵解基因的潜在治疗靶点;2、酪氨酸激酶表皮生长因子受体(EGFR)- ERBB2、RTK-RAS 信号转导、Ras 激活基因 Rgl1、Rasgrp1、Rasgrf1、Rasgrf2 和 Rapgef5 在抑制肿瘤进展方面的作用,这可能是治疗癌症的新型靶向疗法。本综述将有助于了解抑制癌症进展的基因表达,这些基因可作为了解癌症发病机制的潜在分子靶点。
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引用次数: 0
PRMT4 reduced erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Nrf2/GPX4 pathway PRMT4 通过 Nrf2/GPX4 通路降低了依拉斯汀诱导的顺铂耐药鼻咽癌细胞的铁蛋白沉积率
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-07-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053754
Xiaoping Pu, Hong Wu, Xiaoyan Liu, Fang Yang
Nasopharyngeal carcinoma (NPC) is one of the common malignant tumors in clinic. In the current study, we aim to investigate the effects of PRMT4 on erastin-induced ferroptosis in NPC by cisplatin resistant.PRMT4 expression in patients with Nasopharyngeal carcinoma by cisplatin was up-regulated. PRMT4 up-regulation promoted cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. PRMT4 down-regulation reduced cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. PRMT4 promoted Tumor volume in mice model of erastin-induced Nasopharyngeal carcinoma by cisplatin. PRMT4 up-regulation reduced erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Mitochondrial damage. PRMT4 up-regulation induced Nrf2 protein expression in model of erastin-induced Nasopharyngeal carcinoma by cisplatin. Nrf2 reduced the effects of si-PRMT4 on cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. Nrf2 inhibitor reduced the effects of PRMT4 on cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. Nrf2 reduced the effects of si-PRMT4 on erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Mitochondrial damage. PRMT4 protein interlinked with Nrf2 protein to decrease Nrf2 Ubiquitination. Methylation increased PRMT4 DNA stability.Collectively, our data reveal that PRMT4 reduced erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Nrf2/GPX4 pathway, suggesting that targeting PRMT4 may present as a potential strategy against the develo
鼻咽癌(NPC)是临床上常见的恶性肿瘤之一。本研究旨在探讨 PRMT4 对顺铂耐药的鼻咽癌患者中厄拉斯汀诱导的铁蛋白沉积的影响。PRMT4的上调促进了顺铂耐药鼻咽癌细胞中依拉斯汀诱导的铁蛋白沉积的细胞生长。PRMT4下调会降低依拉斯汀诱导的顺铂耐药鼻咽癌铁中毒细胞的生长。PRMT4 促进了顺铂诱导的依拉斯汀鼻咽癌小鼠模型的肿瘤体积。PRMT4上调可减少依拉斯特诱导的顺铂耐药鼻咽癌细胞线粒体损伤的铁变态反应。上调 PRMT4 可诱导 Nrf2 蛋白在顺铂诱导的厄拉斯汀鼻咽癌模型中的表达。Nrf2能降低si-PRMT4对顺铂耐药鼻咽癌细胞中依拉斯汀诱导的铁突变细胞生长的影响。Nrf2 抑制剂降低了 PRMT4 对顺铂耐药鼻咽癌细胞中麦拉宁诱导的铁蛋白沉积对细胞生长的影响。Nrf2通过线粒体损伤降低了si-PRMT4对依拉斯汀诱导的顺铂耐药鼻咽癌铁中毒的影响。PRMT4 蛋白与 Nrf2 蛋白相互连接,减少了 Nrf2 的泛素化。总之,我们的数据揭示了PRMT4通过Nrf2/GPX4途径减少了厄拉斯汀诱导的顺铂耐药鼻咽癌细胞的铁卟啉沉着,这表明靶向PRMT4可能是一种潜在的抗癌策略。
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引用次数: 0
Ethnopharmacology, genetic diversity, phytochemistry and pharmacological effects of Panax vietnamensis Ha et Grushv.: A review Panax vietnamensis Ha et Grushv.的民族药理学、遗传多样性、植物化学和药理作用:综述
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-06-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024052414
Hoang Ngau Tran, Chau Phan Kim Dieu, Chau Phan Kim Hue, Duyen Thi Ngoc Huynh, Bich Hang Do, Luong Do Huynh
Ginseng is considered as a beneficial herbal remedy and over recent years its efficacy and safety have been verified in clinical therapy. There are two typical species of ginseng concluding Asian and American ginseng. The varieties of both species have been applied for commercialized materials in different stages of processing from raw to processed products. Panax vietnamensis Ha et Grushv. (P. vietnamensis) belongs to Asian ginseng and has been utilized as effective herbal remedy. P. vietnamensis is believed to improve immune response, longevity and consequent health. There are more than 300 bioactive compounds have been isolated from P. vietnamensis and classified in various groups, such as ginsenosides, flavonoids, phenolics .... These biological activities consist of anti-tumor, anti-inflammatory, neuroprotective and anti-stress, which are validated by in vitro and in vivo studies. In this review, we systematize the literatures about ethnopharmacology, major bioactive constituents, and toxicology of P. vietnamensis, which were certified by various studies. Furthermore, we also summarize the current method to micro-propagate and lists of extracting sources of bioactive compounds (root, leave, stem…) and the solvents deployed during extraction process. Therefore, this review would provide the firm-evidences and premise for the therapeutic potentials of P. vietnamensis in the future.
人参被认为是一种有益的草药,近年来,其疗效和安全性已在临床治疗中得到验证。人参有两个典型品种,即亚洲人参和西洋参。这两个品种的人参在从原料到加工产品的不同加工阶段都被用作商业化材料。越南人参(Panax vietnamensis Ha et Grushv.(P. vietnamensis) 属于亚洲人参,一直被用作有效的草药。人们认为越南三七能提高免疫反应,延年益寿,从而促进健康。目前已从越南刺五加中分离出 300 多种生物活性化合物,分为人参皂苷、黄酮类、酚类 .... 等不同类别。这些生物活性包括抗肿瘤、抗炎、神经保护和抗应激,并通过体外和体内研究得到了验证。在这篇综述中,我们系统梳理了有关越南罂粟的民族药理学、主要生物活性成分和毒理学的文献,这些文献已得到各种研究的证实。此外,我们还总结了当前的微繁殖方法、生物活性化合物的提取来源(根、叶、茎......)清单以及提取过程中使用的溶剂。因此,这篇综述将为越南鹅掌楸未来的治疗潜力提供可靠的证据和前提。
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引用次数: 0
Expression and significance of circ_0001438 in development of gastric cancer circ_0001438 在胃癌发病过程中的表达及其意义
IF 2.4 4区 医学 Q3 TOXICOLOGY Pub Date : 2024-06-01 DOI: 10.1615/jenvironpatholtoxicoloncol.2024053645
Bo Ren, Chunyue Zhang, Yanmin Zhang, Yan Wang, Liyan Liu
Background: Gastric cancer has become a great challenge to human health in the world. We studied the expression and role of circ_0001438 with the aim of finding a biomarker to assess the prognosis of gastric cancer.Methods: Through a polymerase chain reaction, circ_0001438 expression in gastric cancer was detected. Chi-square test, multi-factor Cox regression, and Kaplan-Meier analyses were used to determine the association between circ_0001438 and the patients' clinical condition and prognosis. Using the luciferase reporter gene system, the interaction between circ_0001438 and miR-1290 was analyzed, and the regulatory impact of circ_0001438/miR-1290 on the activity of gastric cancer cells was examined flowing the Transwell assay and CCK8 assay.Results: In gastric cancer tissues and cells, circ_0001438 expression was downregulated, and miR-1290 expression was upregulated and the two were negatively correlated. miR-1290 inhibitors were transfected and significantly increased the activity of circ_0001438 luciferase, while miR-1290 mimics decreased the activity. Overexpression of circ_0001438 decreased miR-1290 expression and inhibited the proliferation and metastasis of gastric cancer cells, which was reversed when miR-1290 mimics were transfected. Additionally, there was a correlation between circ_0001438 expression and lymph node metastases, tumor size, and TNM stage of gastric cancer. Low circ_0001438 expression predicts poor prognosis of gastric cancer patients.Conclusions: Circ_0001438 is a biomarker for tumor development and clinical prognosis in gastric cancer. It works by downregulating miR-1290 to control the activity of gastric cancer cells.
背景:胃癌已成为全球人类健康的一大挑战。我们研究了 circ_0001438 的表达和作用,旨在找到一种评估胃癌预后的生物标志物:方法:通过聚合酶链反应检测胃癌中 circ_0001438 的表达。方法:通过聚合酶链反应检测circ_0001438在胃癌中的表达,采用卡方检验、多因素Cox回归和Kaplan-Meier分析确定circ_0001438与患者临床状况和预后的关系。利用荧光素酶报告基因系统分析了circ_0001438和miR-1290之间的相互作用,并通过Transwell试验和CCK8试验检测了circ_0001438/miR-1290对胃癌细胞活性的调控作用:结果:在胃癌组织和细胞中,circ_0001438表达下调,miR-1290表达上调,二者呈负相关。过表达circ_0001438会降低miR-1290的表达,抑制胃癌细胞的增殖和转移,而转染miR-1290模拟物则会逆转这种情况。此外,circ_0001438的表达与胃癌的淋巴结转移、肿瘤大小和TNM分期存在相关性。circ_0001438的低表达预示着胃癌患者的不良预后:Circ_0001438是胃癌肿瘤发生和临床预后的生物标志物。它通过下调 miR-1290 来控制胃癌细胞的活性。
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Journal of Environmental Pathology Toxicology and Oncology
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