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Effects of GATA6-AS/MMP9 on malignant progression of endometrial carcinoma. GATA6-AS/MMP9对子宫内膜癌恶性进展的影响。
Q2 Medicine Pub Date : 2021-09-01
Yimei Zhao, Xiuzhen Zou, Guohua Wang, Yingying Liu, Chenying Zhang, Wei Lu, Qingtao Li

Purpose: Previous studies have shown that long non-coding RNA (lncRNA) GATA6-AS is a tumor suppressor gene. However, the role of GATA6-AS in endometrial cancer (EC) has not been reported. We aimed at investigating the expression characteristics of GATA6-AS in EC tissues and cell lines, and explored whether it inhibits the malignant progression of EC through modulating matrix metalloproteinase-9 (MMP9).

Methods: GATA6-AS expression in 17 pairs of EC tissues and adjacent ones was studied by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Meanwhile, GATA6-AS expression levels in EC cell lines were also evaluated by qRT-PCR assay. In addition, GATA6-AS overexpression model was constructed using lentivirus in EC cell lines KLE and HEC-1B. The impacts of GATA6-AS overexpression model was constructed using lentivirus in EC cell lines KLE and HEC-1B on the proliferation capacity and apoptosis of EC cells were assessed by cell counting kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU), and flow cytometry experiments. Furthermore, we explored the interaction between GATA6-AS and MMP9 in EC cells via performing luciferase assay and cell reverse experiments.

Results: Our data showed that GATA6-AS expression in EC tissue specimens was remarkably lower than that in adjacent ones. In vitro cell experiments revealed that overexpression of GATA6-AS markedly attenuated the proliferation ability of EC cells while elevated their apoptosis. Meanwhile, luciferase assay confirmed the binding relationship between GATA6-AS and MMP9. In addition, cell reverse experiments further demonstrated the mutual regulation between GATA6-AS and MMP9, which was, overexpression of MMP9 reversed the inhibitory influence of upregulation of GATA6-AS on the malignant progression of EC.

Conclusions: lncRNA GATA6-AS, lowly expressed in EC tissue samples. Additionally, lncRNA GATA6-AS may suppress the malignant progression of EC through the modulation of regulating MMP9.

目的:已有研究表明,长链非编码RNA (lncRNA) GATA6-AS是一种肿瘤抑制基因。然而,GATA6-AS在子宫内膜癌(EC)中的作用尚未见报道。我们旨在研究GATA6-AS在EC组织和细胞系中的表达特征,并探讨其是否通过调节基质金属蛋白酶-9 (matrix metalloproteinase-9, MMP9)抑制EC的恶性进展。方法:采用实时荧光定量聚合酶链式反应(qRT-PCR)分析17对EC组织及其邻近组织中GATA6-AS的表达。同时采用qRT-PCR法检测EC细胞株中GATA6-AS的表达水平。此外,利用慢病毒在EC细胞株KLE和HEC-1B中构建了GATA6-AS过表达模型。通过细胞计数试剂盒-8 (CCK-8)、5-乙基-2′-脱氧尿苷(EdU)和流式细胞术实验,研究慢病毒在EC细胞株KLE和HEC-1B中构建GATA6-AS过表达模型对EC细胞增殖能力和凋亡的影响。此外,我们通过荧光素酶测定和细胞反向实验探索了EC细胞中GATA6-AS和MMP9之间的相互作用。结果:我们的数据显示,GATA6-AS在EC组织标本中的表达明显低于邻近组织标本。体外细胞实验表明,过表达GATA6-AS可显著降低EC细胞的增殖能力,同时增加EC细胞的凋亡。同时,荧光素酶测定证实了GATA6-AS与MMP9的结合关系。此外,细胞逆转实验进一步证实了GATA6-AS与MMP9之间的相互调控,即MMP9的过表达逆转了GATA6-AS上调对EC恶性进展的抑制作用。结论:lncRNA GATA6-AS在EC组织中低表达。此外,lncRNA GATA6-AS可能通过调节MMP9抑制EC的恶性进展。
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引用次数: 0
Efficacy of laparoscopic, pelvic and para-aortic lymphadenectomy in the treatment of endometrial carcinoma. 腹腔镜、盆腔及腹主动脉旁淋巴结切除术治疗子宫内膜癌的疗效观察。
Q2 Medicine Pub Date : 2021-09-01
Hongmei Wang, Wenying Li, Naimei Li

Purpose: To investigate the clinical efficacy and safety of laparoscopic pelvic and para-aortic lymphadenectomy in the treatment of endometrial carcinoma.

Methods: The clinical data of 110 patients with endometrial carcinoma were retrospectively reviewed. All patients were categorized into two groups. The pelvic lymphadenectomy (PLD) group was subjected to pelvic lymph node dissection alone, while the para-aortic lymphadenectomy (PALD)+PLD group underwent pelvic and para-aortic lymphadenectomy. The operation time, intraoperative bleeding, volume of postoperative drainage, number of resected lymph nodes, number of positive lymph nodes, and incidence of postoperative complications were compared between the two groups of patients. In addition, the tumor recurrence and survival were followed up and compared.

Results: The operation time was significantly longer in the PALD+PLD group than that in the PLD group (p<0.001). The average number of resected lymph nodes and the number of positive lymph nodes in the PALD+PLD group were significantly greater than those in the PLD group. The total recurrence rate was 9.1% (5/55) vs. 20.0% (11/55) between the PLD group and PALD+PLD group, indicating a statistically significant difference (p=0.045). Moreover, the recurrence rate of stage III patients was 50.0% (3/6) and 25.0% (5/55) in the PLD group and PALD+PLD group, respectively, showing a statistically significant difference (p=0.034). During the follow-up period, the 3-year overall survival (OS) was 90.9% (50/55) and 96.4% (53/55) in the PLD group and PALD+PLD group, respectively, indicating no statistically significant difference (p=0.249, log-rank test).

Conclusion: Laparoscopic pelvic and para-aortic lymphadenectomy for endometrial carcinoma can increase the number of resected lymph nodes and reduce the recurrence rate. Moreover, it does not increase the incidence rate of surgical complications.

目的:探讨腹腔镜盆腔及腹主动脉旁淋巴结切除术治疗子宫内膜癌的临床疗效和安全性。方法:回顾性分析110例子宫内膜癌患者的临床资料。所有患者分为两组。盆腔淋巴结切除术(PLD)组单独行盆腔淋巴结清扫,腹主动脉旁淋巴结切除术(PALD)+PLD组同时行盆腔和腹主动脉旁淋巴结清扫。比较两组患者的手术时间、术中出血量、术后引流量、切除淋巴结数、阳性淋巴结数、术后并发症发生率。并对肿瘤复发率和生存率进行随访比较。结果:PALD+PLD组手术时间明显长于PLD组(p结论:腹腔镜子宫内膜癌盆腔及腹主动脉旁淋巴结切除术可增加切除淋巴结数量,降低复发率。此外,它不会增加手术并发症的发生率。
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引用次数: 0
Joint prediction of solitary pulmonary module malignant probability based on logistic regression and malignant tendency comprehensive score. 基于logistic回归和恶性倾向综合评分的孤立肺模块恶性概率联合预测。
Q2 Medicine Pub Date : 2021-09-01
Shutong Zhou, Qun Wang, Tianyu Tang, Meizhu Cao, Yan Tan, Kaixian Bai, Wenjun Liu

Purpose: We analyzed the relationship between clinical data, tumor markers, chest high-resolution CT(HRCT) and pathology in patients with solitary pulmonary nodules (SPN) and explored the joint discrimination scheme to improve the accuracy of noninvasive diagnosis.

Methods: 242 SPNs with the largest diameter D<2cmwere divided into training set (161 cases) and test set (81 cases). We screened the risk factors by single factor analysis. Then, we established the prediction equation model (PE model) based on logistic regression and malignant tendency comprehensive score model (MTCS model) based on the evaluation criteria of SPN. The weight of the two sub models was used to determine the joint evaluation model (JE model).

Results: Age, CEA content, maximum diameter, pleural adhesions, spicule sign, and ground glass component were independent factors of malignant prediction (p<0.05) recorded as x1~x6, and PE model was established as P1=ex/(1+ex),x=0.052x1+0.0327x2+0.212x3+1.849x4+ 1.066x5+1.769x6-7.582.According to the different performance of different manifestations of the corresponding score, we could get each score S of SPN. The MTCS model was S/8.5. The JE model was P=0.76P1+0.24S/8.5. The results of test set showed the AUC values of JE, PE, MTCS, Mayo, VA and Li Yun model for D≤2cm SPN were 0.930(95% CI:0.877-0.983), 0.922(95% CI:0.870-0.974), 0.900(95% CI:0.879-0.921), 0.782(95% CI:0.749-0.815), 0.744(95% CI:0.731-0.756) and 0.801(95% CI:0.739-0.863). The sensitivity of JE, PE, MTCS model were 87.2%, 79.2%, 73.3%, the specificity was 90.1%, 89.2%, 82.2%, and the accuracy was 89.9%, 85.5%, 81.2%.

Conclusions: The joint evaluation model has better diagnostic efficiency and can provide reference for the diagnosis of SPN with D≤2cm.

目的:分析孤立性肺结节(SPN)患者的临床资料、肿瘤标志物、胸部高分辨率CT(HRCT)与病理的关系,探讨联合鉴别方案,提高无创诊断的准确性。结果:年龄、CEA含量、最大直径、胸膜粘连、针状征像、磨玻璃成分是预测恶性的独立因素(p)结论:联合评价模型具有较好的诊断效率,可为D≤2cm的SPN的诊断提供参考。
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引用次数: 0
Association between breast cancer risk factors and tumor subtypes. 乳腺癌危险因素与肿瘤亚型之间的关系
Q2 Medicine Pub Date : 2021-09-01
Kadri Altundag
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引用次数: 0
Meta-analysis on the safety and efficacy of early oral feeding after total laryngectomy. 全喉切除术后早期口服喂养安全性和有效性的meta分析。
Q2 Medicine Pub Date : 2021-09-01
Xuelian Yi, Chunhong Hu, Yi Peng, Zili Wen, Xue Li, Linlin Ye, Qingsong Huang

Purpose: To evaluate the safety and efficacy of early oral feeding (≤ 3 days) and delayed oral feeding (≥ 7 days) following total laryngectomy.

Methods: Relevant literatures on early and delayed oral feeding following total laryngectomy published before January, 2019 were searched in PubMed, EMBASE, Web of Science, Cochrane Library, CNKI and Wanfang Database. Two reviewers were responsible for selecting literatures, extracting data and cross-check. The incidence of pharyngocutaneous fistula (PCF) was evaluated by calculating OR and 95%CI. Difference in length of stay (LOS) of patients undergoing early oral feeding or delayed oral feeding was compared using standardized mean difference (SMD) and 95%CI. Sensitivity analysis and publication bias examination were conducted.

Results: 14 eligible literatures were enrolled, including 1824 patients who underwent total laryngectomy, with 1250 cases of early oral feeding and 574 cases of delayed oral feeding. The incidence of PCF was similar in patients receiving early oral feeding or delayed oral feeding following total laryngectomy (OR=1.12, 95%CI=0.81-1.54). LOS was shorter in cases of early oral feeding than those of delayed oral feeding (SMD=-0.77, 95%CI=-1.18-0.36). Reliable conclusions were obtained without obvious publication bias.

Conclusions: Early oral feeding following total laryngectomy shortens LOS relative to delayed oral feeding. No significant difference in the incidence of PCF is observed between early oral feeding and delayed oral feeding, suggesting that early oral feeding following total laryngectomy is safe and efficacious.

目的:评价全喉切除术后早期口服喂养(≤3天)和延迟口服喂养(≥7天)的安全性和有效性。方法:检索PubMed、EMBASE、Web of Science、Cochrane Library、中国知网(CNKI)和万方数据库2019年1月前发表的全喉切除术后早期和延迟口服喂养的相关文献。两名审稿人负责选择文献、提取资料和交叉检查。通过计算OR和95%CI评估咽皮瘘(PCF)的发生率。采用标准化平均差(SMD)和95%CI比较早期口服喂养和延迟口服喂养患者的住院时间(LOS)差异。进行敏感性分析和发表偏倚检验。结果:纳入14篇符合条件的文献,其中行全喉切除术患者1824例,早期口服喂养1250例,延迟口服喂养574例。全喉切除术后早期口服喂养和延迟口服喂养患者的PCF发生率相似(or =1.12, 95%CI=0.81-1.54)。早期口服喂养组的LOS较延迟口服喂养组短(SMD=-0.77, 95%CI=-1.18-0.36)。结论可靠,无明显发表偏倚。结论:全喉切除术后早期口服喂养相对于延迟口服喂养缩短了LOS。早期口服喂养与延迟口服喂养的PCF发生率无显著差异,提示全喉切除术后早期口服喂养是安全有效的。
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引用次数: 0
Expression of miR-410 in peripheral blood of patients with clear cell renal cell carcinoma and its effect on proliferation and invasion of Caki-2 cells. miR-410在透明细胞肾细胞癌患者外周血中的表达及其对Caki-2细胞增殖和侵袭的影响
Q2 Medicine Pub Date : 2021-09-01
Zhi Liu, Jun Zhang, Xuechun Hu, Qingyu Ge, Jun Xiao, Chrismis Novalinda Ginting

Purpose: To explore the significance of miR-410 expression in clear cell renal cell carcinoma (CCRCC) and its biological function in CCRCC.

Methods: A total of 113 patients with CCRCC admitted to our hospital and 113 healthy individuals over the same period were enrolled. MiR-410 in the tissues and serum of patients with CCRCC was quantified, and the diagnostic value of miR-410 in CCRCC and the relationship between miR-410 and prognosis of patients with CCRCC were analyzed. In addition, miR-410 mimic and miR-410 inhibitor were adopted to regulate miR-410 in CCRCC cells (Caki-2), and then the changes in the proliferation, migration, invasion, and cell cycle of Caki-2 cells were determined. Moreover, tumorigenicity in nude mice was carried out to determine the effect of miR-410 on the tumor growth of CCRCC.

Results: MiR-410 was expressed at a high level in CCRCC patients, and had a high diagnostic accuracy [area under the curve (AUC) = 0.916]. In addition, miR-410 was an independent risk factor for the survival prognosis of patients with CCRCC, and its high expression indicated poor prognosis of the patients. Inhibiting miR-410 suppressed cell proliferation, cycle progression, migration, invasion and tumor growth in vivo and promoted cell apoptosis.

Conclusion: MiR-410 is a possible biological indicator for the diagnosis and prognosis of CCRCC, and is also an independent risk factor for the survival prognosis of CCRCC patients. In addition, miR-410 plays a role as an oncogene in CCRCC and promotes the malignant progression of CCRCC.

目的:探讨miR-410在透明细胞肾细胞癌(CCRCC)中的表达及其生物学功能。方法:选取我院同期收治的113例CCRCC患者和113例健康人作为研究对象。量化CCRCC患者组织及血清中MiR-410的水平,分析MiR-410在CCRCC中的诊断价值及与CCRCC患者预后的关系。此外,采用miR-410 mimic和miR-410 inhibitor调控CCRCC细胞(Caki-2)中miR-410的表达,测定Caki-2细胞增殖、迁移、侵袭和细胞周期的变化。此外,我们还在裸鼠中进行了致瘤性实验,以确定miR-410对CCRCC肿瘤生长的影响。结果:MiR-410在CCRCC患者中表达水平较高,诊断准确率较高[曲线下面积(AUC) = 0.916]。此外,miR-410是影响CCRCC患者生存预后的独立危险因素,其高表达表明患者预后较差。抑制miR-410在体内抑制细胞增殖、周期进展、迁移、侵袭和肿瘤生长,促进细胞凋亡。结论:MiR-410可能是CCRCC诊断和预后的生物学指标,也是影响CCRCC患者生存预后的独立危险因素。此外,miR-410在CCRCC中作为癌基因发挥作用,促进CCRCC的恶性进展。
{"title":"Expression of miR-410 in peripheral blood of patients with clear cell renal cell carcinoma and its effect on proliferation and invasion of Caki-2 cells.","authors":"Zhi Liu,&nbsp;Jun Zhang,&nbsp;Xuechun Hu,&nbsp;Qingyu Ge,&nbsp;Jun Xiao,&nbsp;Chrismis Novalinda Ginting","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Purpose: </strong>To explore the significance of miR-410 expression in clear cell renal cell carcinoma (CCRCC) and its biological function in CCRCC.</p><p><strong>Methods: </strong>A total of 113 patients with CCRCC admitted to our hospital and 113 healthy individuals over the same period were enrolled. MiR-410 in the tissues and serum of patients with CCRCC was quantified, and the diagnostic value of miR-410 in CCRCC and the relationship between miR-410 and prognosis of patients with CCRCC were analyzed. In addition, miR-410 mimic and miR-410 inhibitor were adopted to regulate miR-410 in CCRCC cells (Caki-2), and then the changes in the proliferation, migration, invasion, and cell cycle of Caki-2 cells were determined. Moreover, tumorigenicity in nude mice was carried out to determine the effect of miR-410 on the tumor growth of CCRCC.</p><p><strong>Results: </strong>MiR-410 was expressed at a high level in CCRCC patients, and had a high diagnostic accuracy [area under the curve (AUC) = 0.916]. In addition, miR-410 was an independent risk factor for the survival prognosis of patients with CCRCC, and its high expression indicated poor prognosis of the patients. Inhibiting miR-410 suppressed cell proliferation, cycle progression, migration, invasion and tumor growth in vivo and promoted cell apoptosis.</p><p><strong>Conclusion: </strong>MiR-410 is a possible biological indicator for the diagnosis and prognosis of CCRCC, and is also an independent risk factor for the survival prognosis of CCRCC patients. In addition, miR-410 plays a role as an oncogene in CCRCC and promotes the malignant progression of CCRCC.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":" ","pages":"2059-2066"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39610449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
DDX46 accelerates the proliferation of glioblastoma by activating the MAPK-p38 signaling. DDX46通过激活MAPK-p38信号通路加速胶质母细胞瘤的增殖。
Q2 Medicine Pub Date : 2021-09-01
Ji Ma, Zhenying Gao, Xueni Liu

Purpose: To analyze the influence of DDX46 on the proliferative and migratory potentials of glioblastoma (GBM).

Methods: Differential levels of DDX46 in GBM cases and controls were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. By intervening DDX46 in U87 and U251 cells, proliferative and migratory changes were determined by colony formation assay, 5-Ethynyl-2'- deoxyuridine (EdU) assay and Transwell assay, respectively. Protein levels of p-p38, p38, cyclin D1 and MMP7 in GBM cells intervened by DDX46 or the inhibitor of p38 MAPK were detected.

Results: DDX46 was upregulated in GBM cases. Knockdown of DDX46 attenuated the proliferative capacity of GBM cells, and its overexpression enhanced the proliferative rate. The migratory capacity of GBM was not affected by DDX46. Overexpression of DDX46 upregulated p-p38 and cyclin D1 in GBM cells. The regulatory effect of DDX46 on GBM proliferation could be partially reversed by the treatment of doramapimod.

Conclusions: DDX46 is upregulated in GBM, which strengthens the proliferative capacity of GBM by activating the MAPK-p38 signaling.

目的:分析DDX46对胶质母细胞瘤(GBM)增殖和迁移潜能的影响。方法:采用实时荧光定量聚合酶链反应(quantitative real-time polymerase chain reaction, qRT-PCR)和Western blot检测GBM患者与对照组DDX46的差异水平。通过DDX46干预U87和U251细胞,分别用菌落形成法、5-乙基-2′-脱氧尿苷(EdU)法和Transwell法检测其增殖和迁移的变化。检测DDX46或p38 MAPK抑制剂干预的GBM细胞中p-p38、p38、cyclin D1和MMP7的蛋白水平。结果:DDX46在GBM中表达上调。低表达DDX46可降低GBM细胞的增殖能力,而过表达DDX46可提高细胞的增殖率。DDX46对GBM的迁移能力没有影响。过表达DDX46可上调GBM细胞中的p-p38和cyclin D1。DDX46对GBM增殖的调节作用可被多马莫德部分逆转。结论:DDX46在GBM中表达上调,通过激活MAPK-p38信号通路增强GBM的增殖能力。
{"title":"DDX46 accelerates the proliferation of glioblastoma by activating the MAPK-p38 signaling.","authors":"Ji Ma,&nbsp;Zhenying Gao,&nbsp;Xueni Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Purpose: </strong>To analyze the influence of DDX46 on the proliferative and migratory potentials of glioblastoma (GBM).</p><p><strong>Methods: </strong>Differential levels of DDX46 in GBM cases and controls were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. By intervening DDX46 in U87 and U251 cells, proliferative and migratory changes were determined by colony formation assay, 5-Ethynyl-2'- deoxyuridine (EdU) assay and Transwell assay, respectively. Protein levels of p-p38, p38, cyclin D1 and MMP7 in GBM cells intervened by DDX46 or the inhibitor of p38 MAPK were detected.</p><p><strong>Results: </strong>DDX46 was upregulated in GBM cases. Knockdown of DDX46 attenuated the proliferative capacity of GBM cells, and its overexpression enhanced the proliferative rate. The migratory capacity of GBM was not affected by DDX46. Overexpression of DDX46 upregulated p-p38 and cyclin D1 in GBM cells. The regulatory effect of DDX46 on GBM proliferation could be partially reversed by the treatment of doramapimod.</p><p><strong>Conclusions: </strong>DDX46 is upregulated in GBM, which strengthens the proliferative capacity of GBM by activating the MAPK-p38 signaling.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":" ","pages":"2084-2089"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39610451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Serpin peptidase inhibitor, clade E nexin group 1 promotes cellular proliferative capacities and malignant behaviors in glioblastoma through upregulating hairy and enhancer of split-1. 丝氨酸肽酶抑制剂,clade E连接蛋白组1通过上调分裂-1的毛状和增强子促进胶质母细胞瘤细胞的增殖能力和恶性行为。
Q2 Medicine Pub Date : 2021-09-01
Tao Ma, Kai Qian, Tuoye Xu, Xi Wang, Tengda Qian, Jing Shi, Lixin Li

Purpose: Glioblastoma (GBM) remains one of the most fatal malignancy with limited available treatment. Serpin peptidase inhibitor, clade E nexin group 1 (SERPINE1) was found up-regulated in multiple cancers and play crucial roles in facilitating tumor progression and metastasis respectively. However, the role of SERPINE1 in glioblastoma was poorly understood.

Methods: We tested the hypothesis that SERPINE1 mediated malignant behaviors in GBM via regulating hairy and enhancer of split-1 (HES1).

Results: First, SERPINE1 is confirmed to be up-regulated in GBM, while further functional analysis demonstrated that SERPINE1 promoted cell proliferation, migration and invasion in GBM by performing the CCK-8 assay, colony formation assay, wound healing assay and transwell assay. Finally, it was proved that SERPINE1 achieved its pro-tumor functions in GBM via regulating the expression of HES1.

Conclusions: Collectively, our results highlight the critical contribution of SERPINE1 in a series of malignant characteristics of GBM via regulating the expression of HES1, which shed new light on a new direction to develop a more effective therapeutic management of malignant tumors like GBM.

目的:胶质母细胞瘤(GBM)仍然是最致命的恶性肿瘤之一,治疗方法有限。丝氨酸肽酶抑制剂clade E连接蛋白组1 (SERPINE1)在多种癌症中被发现上调,并分别在促进肿瘤进展和转移中发挥重要作用。然而,SERPINE1在胶质母细胞瘤中的作用尚不清楚。方法:我们验证了SERPINE1通过调节分裂-1的毛状和增强子(HES1)介导GBM恶性行为的假设。结果:首先,通过CCK-8实验、菌落形成实验、伤口愈合实验和transwell实验,证实SERPINE1在GBM中表达上调,进一步的功能分析表明SERPINE1在GBM中促进细胞增殖、迁移和侵袭。最后证明SERPINE1在GBM中通过调节HES1的表达实现其促瘤功能。综上所述,我们的研究结果突出了SERPINE1通过调节HES1的表达在GBM的一系列恶性特征中的重要作用,这为开发更有效的GBM等恶性肿瘤的治疗管理提供了新的方向。
{"title":"Serpin peptidase inhibitor, clade E nexin group 1 promotes cellular proliferative capacities and malignant behaviors in glioblastoma through upregulating hairy and enhancer of split-1.","authors":"Tao Ma,&nbsp;Kai Qian,&nbsp;Tuoye Xu,&nbsp;Xi Wang,&nbsp;Tengda Qian,&nbsp;Jing Shi,&nbsp;Lixin Li","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Purpose: </strong>Glioblastoma (GBM) remains one of the most fatal malignancy with limited available treatment. Serpin peptidase inhibitor, clade E nexin group 1 (SERPINE1) was found up-regulated in multiple cancers and play crucial roles in facilitating tumor progression and metastasis respectively. However, the role of SERPINE1 in glioblastoma was poorly understood.</p><p><strong>Methods: </strong>We tested the hypothesis that SERPINE1 mediated malignant behaviors in GBM via regulating hairy and enhancer of split-1 (HES1).</p><p><strong>Results: </strong>First, SERPINE1 is confirmed to be up-regulated in GBM, while further functional analysis demonstrated that SERPINE1 promoted cell proliferation, migration and invasion in GBM by performing the CCK-8 assay, colony formation assay, wound healing assay and transwell assay. Finally, it was proved that SERPINE1 achieved its pro-tumor functions in GBM via regulating the expression of HES1.</p><p><strong>Conclusions: </strong>Collectively, our results highlight the critical contribution of SERPINE1 in a series of malignant characteristics of GBM via regulating the expression of HES1, which shed new light on a new direction to develop a more effective therapeutic management of malignant tumors like GBM.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":" ","pages":"2074-2083"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39610452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
miR-99a inhibits proliferation and migration of cervical cancer cells by targeting IGF1R. miR-99a通过靶向IGF1R抑制宫颈癌细胞的增殖和迁移。
Q2 Medicine Pub Date : 2021-09-01
Li Han

Purpose: To explore the effects of miR-99a on the proliferation and migration of cervical cancer cells (CCCs) by targeting IGF1R.

Methods: miR-99a and IGF1R expression in C-33 A and C-4 II cells was interfered. Their effects on the proliferation, apoptosis, and migration of CCCs were analyzed by MTT assay, flow cytometry, and Transwell assay. The mechanism of action of miR-99a was analyzed by a rescue experiment and a dual luciferase reporter gene assay (DLRGA). Differences in miR-99a and IGF1R expression were detected in cervical cancer and adjacent tissues (n=30 each), and the correlation of the expression with clinicopathological characteristics of patients with cervical cancer was analyzed.

Results: miR-99a expression was lower but IGF1R expression was higher in C-33 A and C-4 II cells than that in normal cervical epithelial cells. The results showed that both the promotion and the inhibition significantly decreased the proliferation and migration of the two CCCs, but increased their apoptosis. To further verify the correlation of miR-99a with IGF1R in cervical cancer, we co-transfected miR-99a and IGF1R overexpression vectors into the cells and found that compared with CCCs transfected with miR-99a overexpression vectors alone, the expression of IGF1R in the co-transfection group increased, while the expression of miR-99a did not change significantly. Additionally, the proliferation and migration of the cells in the co-transfection group increased, while their apoptotic rate decreased. DLRGA showed the targeted inhibition of miR-99a on IGF1R expression.

Conclusions: miR-99a can specifically inhibit IGF1R expression and thus inhibit the proliferation and migration of CCCs.

目的:探讨miR-99a靶向IGF1R对宫颈癌细胞(CCCs)增殖和迁移的影响。方法:干扰C-33 A和C-4 II细胞中miR-99a和IGF1R的表达。采用MTT法、流式细胞术和Transwell法分析其对CCCs增殖、凋亡和迁移的影响。通过救援实验和双荧光素酶报告基因测定(DLRGA)分析miR-99a的作用机制。检测miR-99a和IGF1R在宫颈癌及癌旁组织中的表达差异(各30例),并分析其表达与宫颈癌患者临床病理特征的相关性。结果:C-33 A和C-4 II细胞中miR-99a表达低于正常宫颈上皮细胞,而IGF1R表达高于正常宫颈上皮细胞。结果表明,促进和抑制均能显著降低两种CCCs的增殖和迁移,但增加其凋亡。为了进一步验证miR-99a与IGF1R在宫颈癌中的相关性,我们将miR-99a和IGF1R过表达载体共转染到细胞中,发现与单独转染miR-99a过表达载体的CCCs相比,共转染组IGF1R的表达增加,而miR-99a的表达没有明显变化。此外,共转染组细胞的增殖和迁移能力增强,细胞凋亡率降低。DLRGA显示miR-99a对IGF1R表达的靶向抑制。结论:miR-99a可以特异性抑制IGF1R的表达,从而抑制CCCs的增殖和迁移。
{"title":"miR-99a inhibits proliferation and migration of cervical cancer cells by targeting IGF1R.","authors":"Li Han","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Purpose: </strong>To explore the effects of miR-99a on the proliferation and migration of cervical cancer cells (CCCs) by targeting IGF1R.</p><p><strong>Methods: </strong>miR-99a and IGF1R expression in C-33 A and C-4 II cells was interfered. Their effects on the proliferation, apoptosis, and migration of CCCs were analyzed by MTT assay, flow cytometry, and Transwell assay. The mechanism of action of miR-99a was analyzed by a rescue experiment and a dual luciferase reporter gene assay (DLRGA). Differences in miR-99a and IGF1R expression were detected in cervical cancer and adjacent tissues (n=30 each), and the correlation of the expression with clinicopathological characteristics of patients with cervical cancer was analyzed.</p><p><strong>Results: </strong>miR-99a expression was lower but IGF1R expression was higher in C-33 A and C-4 II cells than that in normal cervical epithelial cells. The results showed that both the promotion and the inhibition significantly decreased the proliferation and migration of the two CCCs, but increased their apoptosis. To further verify the correlation of miR-99a with IGF1R in cervical cancer, we co-transfected miR-99a and IGF1R overexpression vectors into the cells and found that compared with CCCs transfected with miR-99a overexpression vectors alone, the expression of IGF1R in the co-transfection group increased, while the expression of miR-99a did not change significantly. Additionally, the proliferation and migration of the cells in the co-transfection group increased, while their apoptotic rate decreased. DLRGA showed the targeted inhibition of miR-99a on IGF1R expression.</p><p><strong>Conclusions: </strong>miR-99a can specifically inhibit IGF1R expression and thus inhibit the proliferation and migration of CCCs.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":" ","pages":"1782-1788"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39610702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Development and validation of a nomogram for specific survival in osteosarcoma patients less than 60 years old: a population-based study. 60岁以下骨肉瘤患者特异性生存率nomogram发展和验证:一项基于人群的研究
Q2 Medicine Pub Date : 2021-09-01
Jun Zhao, Jianfei Jiao, Yu Su, Long Mu

Purpose: The present study aimed to develop a nomogram to predict the overall survival of patients with osteosarcoma, especially those less than 60 years old.

Methods: 903 osteosarcoma patients less than 60 years old were collected from the Surveillance, Epidemiology, and End Results (SEER) database.Univariate and multivariate analyses identified the independent prognostic factors of osteosarcoma. Nomogram was used to predict 3- and 5-year overall survival (OS) of osteosarcoma.The accuracy of the model was determined using the concordance index (C‑index), calibration curves, the area under the receiver operating characteristic curves (ROC),as well as decision curve analysis (DCA).

Results: Osteosarcoma patients less than 60 years old were randomly assigned into a training cohort (n=635) or validation cohort (n=268). Age, tumor site, tumor grade, tumor size, and tumor stage were identified as independent prognostic factors via univariate and multivariate Cox analyses (all p<0.05) and then included in the prognostic nomogram. The concordance indices(C-index) for OS prediction in the training cohort was 0.788 (95% CI 0.751-0.852) and in the external validation cohort was 0.779 (95% CI 0.712-0.846). Calibration plots and the area under the ROC revealed excellent consistency between actual survival and nomogram prediction. Finally, DCA demonstrated that the prognostic nomogram was clinically meaningful.

Conclusion: A nomogram could accurately predict the OS of osteosarcoma patients less than 60 years old and contribute to making better clinical treatment decisions for the treating doctors.

目的:本研究旨在建立一种预测骨肉瘤患者,特别是小于60岁患者总生存期的nomogram生存图。方法:从监测、流行病学和最终结果(SEER)数据库中收集903例年龄小于60岁的骨肉瘤患者。单因素和多因素分析确定了骨肉瘤的独立预后因素。采用Nomogram预测骨肉瘤的3年和5年总生存期(OS)。采用一致性指数(C - index)、校准曲线、受试者工作特征曲线下面积(ROC)和决策曲线分析(DCA)来确定模型的准确性。结果:年龄小于60岁的骨肉瘤患者被随机分为训练组(n=635)和验证组(n=268)。通过单因素和多因素Cox分析,确定年龄、肿瘤部位、肿瘤分级、肿瘤大小和肿瘤分期为独立预后因素(均为p)。结论:nomogram可以准确预测60岁以下骨肉瘤患者的OS,有助于临床医生更好地制定临床治疗决策。
{"title":"Development and validation of a nomogram for specific survival in osteosarcoma patients less than 60 years old: a population-based study.","authors":"Jun Zhao,&nbsp;Jianfei Jiao,&nbsp;Yu Su,&nbsp;Long Mu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Purpose: </strong>The present study aimed to develop a nomogram to predict the overall survival of patients with osteosarcoma, especially those less than 60 years old.</p><p><strong>Methods: </strong>903 osteosarcoma patients less than 60 years old were collected from the Surveillance, Epidemiology, and End Results (SEER) database.Univariate and multivariate analyses identified the independent prognostic factors of osteosarcoma. Nomogram was used to predict 3- and 5-year overall survival (OS) of osteosarcoma.The accuracy of the model was determined using the concordance index (C‑index), calibration curves, the area under the receiver operating characteristic curves (ROC),as well as decision curve analysis (DCA).</p><p><strong>Results: </strong>Osteosarcoma patients less than 60 years old were randomly assigned into a training cohort (n=635) or validation cohort (n=268). Age, tumor site, tumor grade, tumor size, and tumor stage were identified as independent prognostic factors via univariate and multivariate Cox analyses (all p<0.05) and then included in the prognostic nomogram. The concordance indices(C-index) for OS prediction in the training cohort was 0.788 (95% CI 0.751-0.852) and in the external validation cohort was 0.779 (95% CI 0.712-0.846). Calibration plots and the area under the ROC revealed excellent consistency between actual survival and nomogram prediction. Finally, DCA demonstrated that the prognostic nomogram was clinically meaningful.</p><p><strong>Conclusion: </strong>A nomogram could accurately predict the OS of osteosarcoma patients less than 60 years old and contribute to making better clinical treatment decisions for the treating doctors.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":" ","pages":"2097-2105"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39610865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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