Previous studies have suggested that pituitary tumor transforming gene family serves as an oncogene in human cancers. However, the underlying molecular mechanisms of pituitary tumor transforming gene (PTTG) family in gastric cancer are unclear. This study aimed to explore the expression patterns, biological functions, and potential regulatory mechanism of PTTG family in gastric cancer cells. Results showed that the genes of PTTG family were highly expressed in gastric cancer tissues and correlated with low survival outcomes. Further, it was noted that regulation of the PTTG3P expression was associated with miR-129-5p and miR-383-5p. A PTTG3P-miRNA-mRNA regulatory network was established. In addition, results of the functional network analysis revealed that PTTG3P was enriched in transcription and cell signaling pathways. Moreover, results of the LinkedOmics and gene chip technology revealed that PTTG3P was positively correlated with PTTG2, whereas PTTG3P expression was not significantly correlated with PTTG1 expression. In conclusion, these results show that genes of the PTTG family promotes the occurrence and development of gastric cancer with PTTG3P regulating the transcription and cell signaling pathways. PTTG3P has an oncogenic role in gastric cancer by regulating the parental gene PTTG2.

Background: Excision repair cross-complementation group 6 like (ERCC6L), a polo-like kinase 1 (PLK1)-interacting checkpoint helicase, confers a high risk of cancer and enhances the progression of a variety of cancers. The present investigation aimed to elucidate the pan-cancer expression patterns of ERCC6L and to examine the possibility of using this gene for patient diagnosis and prognosis. Methods: The expression patterns of ERCC6L in normal and cancer patients at various clinical stages were explored based on TCGA datasets. Subsequently, Bioinformatics techniques were then used to analyze patient's survival probabilities, Cox multivariate clinical parameters, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) terms related to ERCC6L, the correlation between mRNA expression levels and patient survival, genetic alterations or somatic mutations of ERCC6L, and immune infiltration. Results: Most cancer types had higher ERCC6L mRNA levels than normal tissue. Higher ERCC6L expression levels were correlated with poor prognosis for cancer patients. Thus, ERCC6L may serve as an effective diagnostic and prognostic marker for multiple cancers. Moreover, ERCC6L expression levels were higher in patients with higher clinical tumor grades and were associated with poor prognoses at these stages. GO and KEGG analyses revealed a correlation between ERCC6L expression levels and chromatin and cell cycle events. We also found that the mRNA expression level of the ERCC6L promoter and a favorable prognosis was negatively correlated with the promoter's methylation but not with copy number variation. A quantitative analysis of immune infiltration suggested a positive correlation between ERCC6L levels and the infiltration of Th2 immune cells in main cancer types. Finally, we examined the ERCC6L somatic mutations, especially single-nucleotide variants, and ERCC6L expression-related drug sensitivity. Conclusions: Herein, we reported a comprehensive investigation of the tumor-promoting role of ERCC6L in various cancer types. ERCC6L is a candidate biomarker for diagnosing and unfavorable prognosis of specific cancers.

Background: Mitochondria are at the heart of a number of metabolic pathways providing enormous energy for normal cell growth and regulating tumor cell growth as well as survival. Mitochondrial topoisomerase I (TOP1MT) is a type IB topoisomerase found in the mitochondria of vertebrates. However, no pan-cancer analysis of TOP1MT has been reported. This study aims to explore TOP1MT expression in pan-cancer tissues and identify whether it can be a target for mitochondrial anticancer therapy.Methods and results: The original TOP1MT expression data in 33 different types of cancer patients were downloaded from the TCGA and GTEx databases. TOP1MT was highly expressed in cancer tissues, including BLCA, BRCA, CHOL, COAD, DLBC, ESCA, GBM, HNSC, KIRC, KIRP, LGG, LIHC, LUAD, LUSC, PAAD, PCPG, PRAD, READ, SKCM, STAD, THYM, UCEC, and UCS. According to Kaplan-Meier survival curve analysis, high TOP1MT expression in BLCA, HNSC, KIRP, PAAD, UCEC, and LIHC cancer tissues was linked to poor prognosis of cancer patients, i.e., poor OS, disease-specific survival, and PFI. Linkedomics analysis identified a positive correlation of TOP1MT expression with CNA, but a negative correlation with methylation. TOP1MT expression significantly correlated with immune cells and immune checkpoints in the TIMER database. Functional analysis showed a close relationship between TOP1MT expression and ribosomes.Conclusion: In summary, TOP1MT is a potential biomarker for mitochondrial anticancer therapy and cancer immunotherapy.

目的 探讨血清胃蛋白酶原(PG)和促胃液素-17对胃癌癌前病变的筛查价值.方法 选取2017年12月至2019年7月在嘉兴市第一医院消化科行胃镜检查的472例消化道疾病患者为研究对象,根据胃镜和病理学检查结果,分析比较不同病理分型(浅表性胃炎组、萎缩性胃炎组、异型增生组)、萎缩性胃炎患者不同萎缩部位(胃体萎缩组、胃窦萎缩组、胃窦+胃体萎缩组)血清PG-Ⅰ、PG-Ⅱ、PG-Ⅰ/PG-Ⅱ比值(PGR)、促胃液素-17水平差异.采用受试者工作特征曲线(ROC曲线)计算血清PG和促胃液素-17诊断萎缩性胃炎的最佳临界值.结果 萎缩性胃炎组和异型增生组患者血清PG-Ⅰ、PGR水平明显低于浅表性胃炎组[61.8(56.0,95.6)μg/L、57.8(32.6,85.6)μg/L比93.2(84.5,149.4)μg/L,7.9(4.9,11.5)、6.4(4.2,8.2)比13.0(9.5,18.5)](P<0.05);三组间PG-Ⅱ水平比较差异无统计学意义(P>0.05).胃窦萎缩组患者血清PG-Ⅰ、PGR高于胃体萎缩组[139.7(79.1,193.1)μg/L比59.8(42.6,77.1)μg/L、16.7(8.8,20.8)比5.6(2.4,7.9)](P<0.05).胃窦萎缩组和胃窦+胃体萎缩组患者血清促胃液素-17水平均明显低于胃体萎缩组[5.5(5.2,8.5)pmol/L、6.7(5.2,9.2)pmol/L比10.8(7.7,17.5)pmol/L](P<0.05).根据ROC曲线,以PGR≤10.95为萎缩性胃炎的临界值,其灵敏度和特异度分别为98.6％、68.7％,以促胃液素-17≥9.95 pmol/L为临界值,其灵敏度和特异度分别为86.1％、64.1％.胃癌癌前病变组PGR与促胃液素-17联合检测的检出率高于浅表性胃炎组(P<0.05).结论 PGR对提示胃黏膜病变具有较高稳定性,促胃液素-17对提示胃窦萎缩具有独特优势,PGR和促胃液素-17可作为胃癌癌前病变的筛查指标.

胃癌是常见的消化道恶性肿瘤.胃镜检查是检出胃癌的主要手段,尤其是窄带成像放大内镜对判断胃黏膜病变的准确性具有显著优势.而胃蛋白酶和胃泌素-17作为临床上筛查早期胃癌无创、简单、易普及的血清学标志物,广泛应用于临床.本文综述胃蛋白酶原、胃泌素-17、窄带成像技术及放大内镜在早期胃癌筛查中的临床应用. 1 胃蛋白酶原与早期胃癌 胃蛋白酶原(PG)是胃粘膜分泌的具有特异功能性酶-天冬氨酸蛋白酶的前体,在酸性条件下易被激活,主要由2个亚型组成,即胃蛋白酶原-I(PG-I)和胃蛋白酶原-Ⅱ(PG-II).PG-I主要由胃底腺体的胃主细胞和颈粘液细胞分泌.

目的 探讨血清PG、G-17结合窄带成像放大内镜对早期胃癌的诊断价值.方法 选择2017年1月至2020年4月因上腹不适等上消化道症状就诊的患者573例,同期进行普通白光胃镜检查及胃黏膜组织活检,根据病检结果分为A组(非萎缩性胃炎组)、B组(胃癌癌前病变组)和C组(早期胃癌组).比较各组血清PGⅠ、PGⅡ和G-17水平,利用ROC曲线分析PGⅠ、G-17单独或联合检测对早期胃癌的诊断价值.结果 573例患者均进行了白光内镜检查,218例行NBI+ME精查,其中92例行靶向活检,126例行ESD术,其中A组387例、B组123例、C组63例.与A组比较,B组和C组PGⅠ、PGR水平较低,G-17水平较高,差异有统计学意义(P<0.05);与B组比较,C组PGⅠ、PGR水平较低,G-17水平较高,差异有统计学意义(P<0.05).以血清PGⅠ<70.1?μg/L且血清G-17>14.1?pmol/L为标准,诊断早期胃癌的敏感度和特异度分别为85.7％和96.5％,联合诊断敏感度和特异度均高于单独诊断(P<0.05);三组血清学指标异常检出率分别为1.3％、7.3％和88.9％,B组、C组血清学指标异常检出率均高于A组(P<0.05),C组血清学指标异常检出率高于B组(P<0.05).结论 PGⅠ降低、G-17升高提示胃癌癌前病变、早期胃癌的高风险,PGⅠ与G-17联合检测结合白光内镜、NBI+ME精查、靶向活检及诊断性ESD可进一步提高诊断准确性.