Dendritic cells (DCs) play a pivotal role in initiating robust T cell responses against tumors, yet effective strategies to enhance DC activation remain limited. This study explores the synergistic effects of Lycium barbarum polysaccharide (LBP) and the tumor cell lysate of endothelial progenitor cells (EPC-TCL) to boost DC activation and anti-tumor immunity. Using flow cytometry, the enzyme-linked immunosorbent assay, western blot analysis, and in vivo tumor models, we demonstrate that the combination treatment significantly enhanced expression of co-stimulatory molecules (CD40, CD80, CD86, and MHC-I) in DCs and elevated cytokine levels (IL-6 and IL-12). Co-culture experiments revealed that T cells primed with LBP and EPC-TCL-modified DCs increased proliferation and reduced exhaustion, characterized by upregulated CD69 and downregulated PD-1. Mechanistically, activation of the MAPK and STING signaling pathways was confirmed by phosphorylation of key proteins. Moreover, T cells activated by DCs treated with LBP and EPC-TCL exhibited potent anti-tumor effects, significantly reducing invasiveness of mouse lung carcinoma cells and impairing angiogenesis in vitro. In a mouse axillary tumor model, the combination treatment markedly suppressed tumor growth and induced apoptosis of tumor cells. These findings highlight the potential of LBP and EPC-TCL as novel immunotherapeutic agents targeting DCs to enhance anti-tumor immunity. Future studies will focus on clinical validation and integration into combination therapies for broader cancer applications.

Acute myeloid leukemia (AML) is a blood cancer characterized by uncontrolled growth of myeloid cells. Overcoming AML treatment resistance, particularly to anthracycline-based drugs like doxorubicin (ADR), poses a challenge. This study investigated the role of CELF1, an RNA-binding protein, in ADR resistance and autophagy regulation in AML. CELF1 expression was elevated in multiple tumor types, including AML. AML cell lines exhibit varying levels of CELF1 expression, with drug-resistant cell lines showing higher CELF1 expression compared to parental cells. CELF1 knockdown reduced drug resistance, promoted cell death, and inhibited autophagy. Mechanistic analysis identified ATG5 as a potential CELF1-regulated target gene, with CELF1 knockdown reducing ATG5 expression and mRNA decay. These findings indicate that targeting CELF1 could overcome ADR resistance in AML by modulating autophagy through ATG5 regulation, highlighting its clinical significance as a therapeutic target for enhancing ADR response in AML.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality, necessitating novel therapeutic targets. This study explores the oncogenic role of integrin-linked kinase-associated phosphatase (ILKAP) in HCC and its underlying mechanisms. Database analyses (TCGA, UALCAN) revealed ILKAP overexpression in HCC, correlating with poor prognosis. Functional assays demonstrated that ILKAP knockdown significantly suppressed HCC cell proliferation and migration in vitro, while xenograft models confirmed its role in tumor growth in vivo. RNA sequencing identified 357 differentially expressed genes (DEGs), including 48 protein-coding DEGs, with glycolytic enzyme PGAM1 notably downregulated upon ILKAP silencing. ILKAP and PGAM1 expression were positively correlated in HCC tissues, and elevated PGAM1 levels were linked to worse survival. Notably, restoring PGAM1 in ILKAP-knockdown cells rescued proliferation and invasion, underscoring PGAM1’s critical role in ILKAP-mediated tumor progression. ILKAP depletion also reduced extracellular acidification rates and altered glycolysis-related gene expression, highlighting its role in metabolic reprogramming. These findings suggest that ILKAP drives HCC malignancy by modulating PGAM1 and glycolysis, providing a potential therapeutic target for HCC treatment. Further elucidation of the ILKAP-PGAM1 axis may offer new strategies for liver cancer management.

Vitamin C, also known as ascorbic acid, is an essential vitamin that cannot be synthesized by the human body and must be acquired through our diet. At present, the precursor of vitamin C, 2-keto-l-gulonic acid (2-KGA), is typically produced via a two-step fermentation process utilizing three bacterial strains. The second step of this traditional two-step fermentation method involves mixed-culture fermentation employing 2-KGA-producing bacteria (Ketogulonicigenium vulgare) along with associated bacteria. Because K. vulgare has defects in various metabolic pathways, associated bacteria are needed to provide key substances to promote K. vulgare growth and 2-KGA production. Unlike previous reviews where the main focus was the interaction between associated bacteria and K. vulgare, this Review presents the latest scientific research from the perspective of the metabolic pathways associated with 2-KGA production by K. vulgare and the mechanism underlying the interaction between K. vulgare and the associated bacteria. In addition, the dehydrogenases that are responsible for 2-KGA production, the 2-KGA synthesis pathway, strategies for simplifying 2-KGA production via a one-step fermentation route, and, finally, future prospects and research goals in vitamin C production are also presented.

PURPOSE:Breast cancer (BC) is the most frequent malignant tumor in women worldwide with exceptionally high morbidity. The RNA-binding protein MEX3A plays a crucial role in genesis and progression of multiple cancers. We attempted to explore its clinicopathological and functional significance in BC in which MEX3A is expressed.METHODS:The expression of MEX3A detected by RT-qPCR and correlated the results with clinicopathological variables in 53 BC patients. MEX3A and IGFBP4 profile data of BC patients were downloaded from TCGA and GEO database. Kaplan-Meier (KM) analysis was used to estimate the survival rate of BC patients. Western Blot, CCK-8, EdU, colony formation and flow cytometry were performed to investigate the role of MEX3A and IGFBP4 in BC cell proliferation, invasion and cell cycle in vitro. A subcutaneous tumor mouse model was constructed to analyze in vivo growth of BC cells after MEX3A knockdown. The interactions among MEX3A and IGFBP4 were measured by RNA pull-down and RNA immunoprecipitation.RESULTS:The expression of MEX3A was upregulated in BC tissues compared to adjacent tissues and high expression of MEX3A was associated with poor prognosis. Subsequent in vitro studies demonstrated that MEX3A knockdown inhibited BC cells proliferation and migration, as well as xenograft tumor growth in vivo. The expression of IGFBP4 was significantly negatively correlated with MEX3A in BC tissues. Mechanistic investigation showed that MEX3A binds to IGFBP4 mRNA in BC cells, decreasing IGFBP4 mRNA levels, which further activated the PI3K/AKT and other downstream signaling pathways implicated cell cycle progression and cell migration.CONCLUSION:Our results indicate that MEX3A plays a prominent oncogenic role in BC tumorigenesis and progression by targeting IGFBP4 mRNA and activating PI3K/AKT signaling, which can be used as a novel therapeutic target for BC.

目的 探究白藜芦醇(RES)调控miR-212-3p逆转人肝癌顺铂(DDP)耐药细胞株(Huh-7/DDP)对DDP耐药的可能分子机制.方法 将0、2.5、5、10、20、40 μmol/L的RES处理Huh-7/DDP细胞,采用CCK-8法检测Huh-7/DDP细胞的增殖能力;RES处理Huh-7/DDP细胞后,采用实时荧光定量PCR(RT-qPCR)检测miR-212-3p的表达水平;将Huh-7/DDP细胞分为未处理组,DDP组,RES+DDP组,NC mimic+DDP组,miR-212-3p mimic+DDP组,NC inhibitor+DDP组,NC inhibitor+RES+DDP组,miR-212-3p in-hibitor+DDP组,miR-212-3p inhibitor+RES+DDP组,采用CCK-8法检测Huh-7/DDP细胞的DDP半数抑制浓度(IC50)值;采用流式细胞术检测Huh-7/DDP细胞凋亡比例.采用Western blot法检测p-PI3K、p-Akt、Bcl-2、Bax蛋白的表达水平.结果 单用RES终浓度5μmol/L对Huh-7/DDP细胞生长无明显抑制作用(P＞0.05),为最大无毒剂量.RES+DDP组的DDP IC50明显低于DDP组(P＜0.05).DDP组和RES+DDP组Huh-7/DDP细胞凋亡比例高于未处理组(P＜0.05),且RES+DDP组明显高于DDP组(P＜0.05).RES处理的Huh-7/DDP细胞中miR-212-3p的表达水平明显高于未处理组(P＜0.05).miR-212-3p mimic+DDP组中的DDP IC50值低于NC mimic+DDP组,miR-212-3p mimic+DDP组中的细胞凋亡比例高于NC mimic+DDP组(P＜0.05).miR-212-3p inhibitor+DDP组的DDP IC50明显高于NC inhibitor+DDP组,NC inhibitor+RES+DDP组DDP IC50明显低于NC inhibitor+DDP组,而miR-212-3p inhibitor+RES+DDP组中的DDP IC50值高于NC inhibitor+RES+DDP组.miR-212-3p inhibitor+DDP组的细胞凋亡率明显低于NC inhibitor+DDP组,NC inhibitor+RES+DDP组的细胞凋亡率高于NC inhibitor+DDP组,而miR-212-3p inhibitor+RES+DDP组的细胞凋亡率低于NC inhibitor+RES+DDP组(P＜0.05).DDP组、RES+DDP组中的p-PI3K、p-Akt、Bcl-2蛋白水平低于未处理组(P＜0.05),Bax蛋白水平高于未处理组(P＜0.05),其中RES+DDP组中的p-PI3K、p-Akt、Bcl-2蛋白水平低于DDP组(P＜0.05);RES+DDP组中的Bax蛋白水平高于DDP组(P＜0.05).结论 RES可能通过提高Huh-7/DDP细胞中miR-212-3p的表达水平,抑制PI3 K/Akt通路蛋白的磷酸化,发挥逆转肝癌DDP耐药的作用.

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Background: As a special reproductive hormone and ovarian reserve indicator, the role of anti-Mullerian hormone (AMH) in premenopausal women with breast cancer deserves further study. Methods: We conducted an in-depth analysis of the data from the EGOFACT study (NCT02518191), a phase III, randomized, controlled trial involving premenopausal female breast cancer patients in two parallel groups: chemotherapy with or without gonadotropin-releasing hormone analogs (GnRHa). Three hundred thirty premenopausal women aged 25-49 years with operable stage I to III breast cancer were included in this study. The characteristics of ovarian reserve changes marked by AMH in the EGOFACT study and the factors affecting ovarian function in premenopausal women with breast cancer were analyzed. Results: The AMH level of the chemotherapy alone group decreased gradually within one year, while the AMH level of the GnRHa group was significantly higher as early as 6 months after chemotherapy and recovered to close to the baseline level 12 months after chemotherapy (F = 34.991, P < 0.001). Correlation analysis showed that the factors affecting AMH levels mainly included age, menarche age, body mass index (BMI), reproductive history, baseline follicle stimulating hormone (FSH) level, pathological stage and GnRHa application, but they had different effects on the incidence of premature ovarian insufficiency (POI) at different periods. Multivariate logistic regression analysis showed that menarche age younger than 14 years (OR 0.470 [0.259, 0.852], P = 0.013), baseline AMH level higher than 0.5 ng/mL (OR 9.590 [3.366, 27.320], P < 0.001), pathological stage I (OR 0.315 [0.124, 0.798], P = 0.015) and GnRHa application (OR 0.090 [0.045, 0.183], P < 0.001) were independent factors conducive to protection of ovarian reserve, as well as to recovery of ovarian reserve. Conclusions: Age, menarche age, baseline AMH level, and GnRHa application are the most important influencing factors for ovarian reserve in premenopausal women with breast cancer.

Esophageal squamous cell carcinoma (ESCC) is one of the most common types of cancer and the leading cause of cancer-related mortality worldwide, especially in Asia. In this study, the gene CKAP2L was selected by GEO, TCGA, and GTEx database analysis. The high expression of CKAP2L is related to the occurrence and development of ESCC. In addition, CKAP2L knockdown can inhibit the growth and migration of ESCC cells, while CKAP2L overexpression has the opposite effect. Furthermore, in vivo experiments indicated that down-regulation of CKAP2L can inhibit the tumorigenesis of ESCC cells. KEGG pathway analysis and the STRING database explored the relationship between cell cycle and CKAP2L and verified that depletion of CKAP2L markedly arrested cell cycle in the G2/M phase. Meanwhile, CKAP2L knockdown increased the sensitivity of ESCC cells to flavopiridol, the first CDK inhibitor to be tested in clinical trials, leading to an observable reduction in cell proliferation and an increase in cellular apoptosis. In brief, we identified CKAP2L as a tumor promoter, potential prognostic indicator, and therapeutic target of ESCC, which may play a role in regulating cell cycle progression.

Gastric cancer (GC) remains one of the leading causes of cancer-related deaths worldwide due to the lack of specific biomarkers for the early diagnosis and universal accepted therapy for advanced GC. Lower levels of miR-5701 were found in the GC tissue from the online sequencing data and confirmed in the GC tissues and GC cell lines. Overexpression of miR-5701 inhibited the proliferation and migration of GC cells and promoted the apoptosis of these cells. Bioinformatics analyses and luciferase assay showed that miR-5701 targeted FGFR2, which acted as an oncogene in GC. Nude mice with GC cells overexpressing miR-5701 exhibited smaller tumor sizes and less lung metastases. The miR-5701 expression was directly, transcriptionally inhibited by MBD1 together with HDAC3 by binding together to form a complex. Knocked down MBD1 or HDAC3 increased the miR-5701 expression. These results indicated the potential use of exogenously administered miR-5701 or agents that elevated endogenous miR-5701 to inhibit GC, improving the prognosis of patients with GC.

目的:探讨lncRNA SNHG11对非小细胞肺癌(NSCLC)A549细胞增殖、侵袭和迁移的影响及其可能机制.方法:qPCR检测人胚肺细胞HEL-1和NSCLC细胞A549、H1299、HCC827中lncRNA SNHG11和miR-193a-5p的表达水平,向A549细胞中转染SNHG11小干扰RNA(si-SNHG11)、miR-193a模拟物(miR-193a mimic)或miR-193a抑制剂(miR-193a inhibitor)后,CCK-8法检测其对细胞增殖的影响,Transwell小室和细胞划痕实验检测对细胞侵袭和迁移的影响,WB法检测对细胞增殖抗原Ki67、细胞周期蛋白D1(cyclin D1)表达的影响,双荧光素酶报告实验验证lncRNA SNHG11与miR-193a-5p的靶向关系.结果:与人胚肺细胞HEL-1相比,NSCLC细胞A549、H1299、HCC827中lncRNA SNHG11均呈高表达、miR-193a-5p呈低表达(均P<0.05);沉默lncRNA SNHG11可抑制A549细胞的增殖、侵袭和迁移,降低细胞中Ki67和Cyclin D1蛋白的表达水平(均P<0.05);过表达miR-193a-5p可抑制A549细胞增殖和侵袭迁移(均P<0.05).lncRNA SNHG11可靶向吸附miR-193a-5p,抑制miR-139a-5p可部分逆转沉默lncRNA SNHG11对A549细胞增殖、侵袭和迁移的作用(均P<0.05).结论:lncRNA SNHG11通过吸附miR-193a-5p促进NSCLC A549细胞的增殖、侵袭和迁移.

IMPORTANCE:Studies of the use of gonadotropin-releasing hormone analogs (GnRHa) to protect ovarian function have shown mixed results.OBJECTIVE:To determine whether administering GnRHa during chemotherapy in premenopausal women with breast cancer can reduce ovarian impairment.DESIGN, SETTING, AND PARTICIPANTS:This randomized clinical trial, conducted at the Shanghai Jiao Tong University Affiliated Shanghai Sixth People's Hospital and Zhejiang Cancer Hospital in China, was an open-label trial involving premenopausal women aged 18 to 49 years with operable stage I to III breast cancer for which treatment with adjuvant or neoadjuvant cyclophosphamide-containing chemotherapy was planned in 2 parallel groups: treatment with chemotherapy with or without GnRHa. Enrollment occurred from September 2015 to August 2017, and follow-up ended December 2020. The data were analyzed in March 2021. A total of 405 patients were enrolled in the study, among whom 27 patients (6.7%) quit participation voluntarily, 33 (8.1%) did not meet the inclusion criteria and were excluded, and 15 (3.7%) were lost to follow-up. Ultimately 330 patients were included in the primary analysis, including 29 patients with baseline anti-Müllerian hormone levels less than 0.5ng/ mL.INTERVENTIONS:Eligible patients were randomly assigned (1:1) to receive chemotherapy with (n = 165) or without (n = 165) GnRHa. In patients randomized to receive GnRHa, 3.6 mg of goserelin or 3.75 mg of leuprorelin was injected subcutaneously once every 28 days from 1 to 2 weeks before the first cycle of chemotherapy to 4 weeks after the last cycle of chemotherapy.MAIN OUTCOMES AND MEASURES:The primary end point was the rate of premature ovarian insufficiency (POI) at 12 months after chemotherapy. Premature ovarian insufficiency was defined as anti-Müllerian hormone levels of less than 0.5 ng/mL in this study. The secondary end point was overall survival (OS) and tumor-free survival (TFS).RESULTS:A total of 330 eligible patients could be evaluated with complete data, among whom 301 patients (91.2%; GnRHA group: mean [SD] age, 40.6 [6.7] years; control group: mean [SD] age, 40.2 [5.9] years) were eligible for primary end point analysis. At 12 months after the completion of chemotherapy, the POI rate was 10.3% (15 of 146) in the GnRHa group and 44.5% (69 of 155) in the control group (odds ratio, 0.23; 95% CI, 0.14-0.39; P < .001). Anti-Müllerian hormone resumption in the GnRHa group was significantly better than that in the control group (15 of 25 vs 6 of 44; odds ratio, 4.40; 95% CI, 1.96-9.89; P < .001). After a median follow-up of 49 months (range, 25-60 months), the differences in 4-year OS and TFS between the 2 groups were not significant. A post hoc analysis showed that in patients younger than 35 years, the TFS was higher in the GnRHa group than in the control group (93% vs 62%; P = .004; hazard ratio, 0.15; 95% CI, 0.03-0.82; P = .03).CONCLUSIONS AND RELEVANCE:This randomized clinical trial found that administering GnRHa in treatment with chemotherapy for premenopausal patients with breast cancer reduces the risk of POI, which promotes the recovery of ovarian function.TRIAL REGISTRATION:ClinicalTrials.gov Identifier: NCT02518191.

Small nucleolar RNA host gene 17 (SNHG17), a novel functional long noncoding RNA, has been demonstrated to play an essential role in the oncogenesis of several tumors. However, for esophageal squamous cell carcinoma (ESCC) the expression pattern and detailed function of SNHG17 are largely unknown. Hence, we conducted this study to explore potential roles and underlying oncogenic mechanisms for SNHG17 in ESCC progression. Results demonstrated SNHG17 to be markedly upregulated in ESCC. Knockdown of SNHG17 significantly suppressed ESCC cell proliferation, invasion, and epithelial–mesenchymal transition in vitro and tumor growth in vivo. Online database software analysis found miR-338-3p to interact with SNHG17 with the level of miR-338-3p negatively correlated with SNHG17 levels in ESCC samples. Further, miR-338-3p was found to directly target SRY-box transcription factor 4 (SOX4) in ESCC cells. Mechanistic analysis suggested that SNHG17 acts as an endogenous “sponge” competing with miR-338-3p to regulate SOX4, thereby promoting tumor progression. These results suggest that these molecular interactions may be potential therapeutic targets for ESCC.

Background Cyclin-dependent kinase 6 (CDK6) is an important regulatory protein of the cell cycle and plays an important role in tumor progression. The aim of this study was to investigate the expression of CDK6 in T1 stage non-small cell lung cancer (NSCLC) and to explore the association of CDK6 with the clinicopathological features of the disease. Methods CDK6 expression was analyzed by real-time PCR (RT-PCR) and immunohistochemistry (IHC) in tumor tissue samples and the distal normal tissue samples from 56 T1 stage NSCLC patients. The correlation between CDK6 expression and clinicopathological features was analyzed using the independent samples t-test and nonparametric tests. Results We found CDK6 had a tendency to increase in tumor tissues compared to normal tissues at the transcriptional level (P=0.073). Moreover, the expression of CDK6 protein in NSCLC tissues was also significantly higher than in normal lung tissues (P=0.003). With an increase of smoking quantity, the expression of CDK6 mRNA was increased (P=0.009). Remarkably, CDK6 expression was increased in squamous cell carcinoma (SCC) tissues but decreased in adenocarcinoma (AD) tissues at both the transcription and protein levels (P<0.001). After stratification based on pathological type, CDK6 gene expression was not associated with any clinicopathological features in SCC, while it was negatively associated with tumor diameter in AD (P=0.049). Conclusions Taken together, these results indicated that abnormal expression of the CDK6 gene in NSCLC might be associated with pathological type, which may serve as a diagnostic biomarker for NSCLC.

目的 构建一种用于检测细胞角蛋白19片段(CYFRA21-1)的高灵敏电化学生物传感器.方法 合成三维石墨烯@金纳米粒子(3D-G@Au)复合材料,用其修饰玻碳电极,通过壳聚糖、戊二醛与抗CYFRA21-1抗体交联,构建用于检测CYFRA21-1的3D-G@Au的电化学生物传感器.对构建成功的3D-G@Au的电化学生物传感器的电化学性能及检测性能进行初步评价.结果 循环伏安图显示裸玻碳电极、3D-G修饰玻碳电极和3D-G@Au修饰玻碳电极的氧化还原峰逐渐升高,提示3D-G@Au电化学生物传感器构建成功.传感器抗原-抗体相互作用的最佳温育时间为60 min,最佳孵育温度为35℃.采用3D-G@Au电化学生物传感器检测CYFRA21-1,线性范围为0.1～300.0 ng/mL,检测限为0.1 ng/mL(信噪比=3),10 mmol/L维生素C、10 mmol/L多巴胺和10 mmol/L尿酸对检测无干扰,重现性较好[相对标准偏差(RSD)分别为1.08％、3.11％],与化学发光法比较,RSD为1.96％～4.78％.制备好的3D-G@Au电化学生物传感器可在4℃条件下稳定30 d.结论 构建的3D-G@Au电化学生物传感器可用于血清CYFRA21-1的检测.

Under the outbreak of COVID-19, it was urgent to analyze the cases from clinical features and epidemiological factors, as well as understand the effectiveness of measures taken on disease prevent and control. A retrospective study was applied for descriptive analysis of clinical features and epidemiological factors of confirmed cases in four cities of Zhejiang. The Onset-admission interval was calculated and plotted as well. The provincial measures regarding the response of COVID-19 were summed up and sorted out. The distribution and sex and age were under normality distribution, and the age of 20 to 80 were all in risk of developing the disease. Clinical features of fever and cough were found mostly happen on patients. More than half of the patients had image changed on chest from reported data. The factor of closely contacted with confirmed cases was the most cause to the disease. The median onset-admission interval was 6 days in Zhejiang province. As of the efficient health system, COVID-19 had been successfully prevented and controlled in Zhejiang. Males and females were all vulnerable to COVID-19. Preventing contact with confirmed cases could largely avoid the disease to happen. The government should take emergent and effective measures to prevent and treatment of the pandemic disease.

Objective:To analyze the value of combined detection of C reactive protein (CRP), serum amyloid A (SAA), carcinoembryonic antigen (CEA), carbohydrate antigen (CA)242, CA50 in the diagnosis of colon cancer.Methods:177 inpatients with first-diagnosed colon cancer in Cancer Hospital of University of Chinese Academy of Sciences from January 2019 to June 2019, 74 patients with non-cancerous colonic polyps, 58 healthy subjects were respectively collected as colon cancer group, colonic polyps group and healthy control group. The levels of CRP, SAA, CEA, CA242 and CA50 in each group were compared and the diagnostic efficiency was calculated. The significance in different stages of colon cancer was evaluated.Results:The levels of CRP, SAA, CEA, CA242 and CA50 in colon cancer group were significantly higher than those in colonic polyps group and healthy control group ( P<0.05); the levels of CRP, SAA and CEA in colonic polyps group were significantly higher than those in healthy control group ( P<0.05). The area under the curve (AUC) of CRP, SAA, CEA, CA242 and CA50 in the diagnosis of colon cancer was 0.818, and the sensitivity and specificity were higher than those of single detection ( P<0.05). The levels of CRP, SAA, CEA, CA242 and CA50 in stage Ⅳ colon cancer were significantly higher than those in stage 0-Ⅲ ( P<0.05). Conclusions:The combined detection of CRP, SAA, CEA, CA242, CA50 can improve diagnostic efficiency of colon cancer. Besides, the detected levels of CRP, SAA, CEA, CA242 and CA50 are helpful to the diagnosis of colon cancer, especially in stage Ⅳ colon cancer with distant metastasis.

目的:探讨TIAM1下调表达对食管癌(ESCA)细胞恶性增殖和迁移的影响.方法:采用免疫组织化学方法和RT-qPCR检测TIAM1在食管鳞癌临床组织中的表达情况;使用慢病毒介导的小干扰RNA构建TIAM1低表达的Eca109细胞株;CCK-8试验和集落形成测定评估TIAM1的表达对细胞增殖的影响.细胞划痕实验检测TIAM1对细胞迁移活性的影响;结果:相比于癌旁正常组织,ESCA组织中检测到的TIAM1表达水平更高(P<0.05).下调TIAM1表达抑制了细胞增殖和集落形成(P<0.05),降低了细胞的迁移能力.结论:TIAM1在ESCA细胞的增殖和迁移中起着至关重要的作用,提示TIAM1可作为ESCA诊断及治疗中的潜在生物标志物.

The serum lipid profile and clinical outcomes of cancer patients are commonly correlated in a wide range of carcinomas. However, few studies have investigated the serum lipid profile of patients with thyroid cancer (TC). The present study therefore aimed to analyze the lipid profiles of patients with TC. The serum proteomes of 31 participants with stage I-IV TC were screened using Orbitrap Q Exactive Plus. Analytical data collected between November 1, 2013 and November 11, 2018 from the laboratory information system included the total cholesterol (CHO), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1 (ApoA1), lipoprotein (a) and apolipoprotein B (ApoB) levels that were used to validate the screening results. A total of 3875 outpatients were enrolled in this study. A number of 17 differentially expressed proteins were identified. An Ingenuity pathway analysis identified activation of the liver X receptor/retinoid X receptor (LXR/RXR) activation, which is a crucial pathway involved in lipid metabolism. The results demonstrated that the total CHO levels were significantly different between patients with TC and control groups, both in men and women. In women, the levels of TG, HDL-C, Apo A1 and LDL-C/HDL-C were significantly different between patients with TC and control groups (all P<0.05). Higher concentrations of TG and LDL-C/HDL-C were observed in the cancer group compared with the control group. However, lower levels of Apo A1 and HDL-C were observed in women from the cancer group compared with the control group. The results from the present study revealed the presence of a disordered lipid profile in patients with TC. The molecular mechanism underlying the association between lipid metabolism and cancer requires further investigation and may be used to develop novel diagnostic biomarkers and therapeutic targets in human cancers.

Activated platelets play a multifaceted role in tumorigenesis and progression. Platelet distribution width (PDW) is generally applied platelet parameters from routine blood test. Preoperative PDW has been considered a prognostic factor in many cancers. Nevertheless, the prognostic value of PDW in esophageal squamous cell carcinoma (ESCC) remains unknown. The study aimed to investigate whether preoperative PDW could serve as a prognostic factor in patients with ESCC. A total of 495 patients with ESCC undergoing curative surgery were enrolled. The relationship between PDW and clinical features in ESCC was analyzed using chi-square tests. Receiver operating characteristic (ROC) curve was used to determine the optimal cut-off value. Overall survival (OS) and disease-free survival (DFS) stratified by PDW were evaluated by Kaplan–Meier method and log-rank test. Univariate and multivariate Cox regression were used to evaluate the prognostic effect of PDW. Of the 495 patients, elevated PDW was observed in 241(48.7%) of the patients, respectively. An elevated PDW was correlated with depth of tumor (T stage, P = 0.031), nerve infiltration (P = 0.016), hospital time after operation (P = 0.020), platelet (P < 0.001), red cell distribution width (P < 0.001), and aspartate transaminase (P = 0.001). Moreover, elevated PDW (PDW ≥ 13.4 fL) predicted a worse OS and DFS in patients with ESCC (both P < 0.001). Multivariate analyses revealed that PDW was independently associated with OS (hazard ratios 1.194; 95% confidence interval 1.120–1.273; P < 0.001) and DFS (hazard ratios 2.562; 95% confidence interval 1.733–3.786; P < 0.001). Our findings indicated that elevated PDW could serve as an independent worse survival in ESCC.