Cuprotosis is recognized as a novel form of programmed cell death pathway. Dihydrolipoamide dehydrogenase (DLD) functions as a critical gene regulating cuprotosis. Here, we designed to analyze the utility of consideration of the prognostic and immunological significance of cuproptosis-related gene DLD across human cancers. Utilizing the TCGA, GTEx, and HPA databases, this study systematically evaluated DLD expression at both the mRNA and protein levels. Our analysis leveraged TCGA data to explore how DLD relates to survival, clinical features, immune infiltration, and DNA methylation in pan-cancer. Single-cell sequencing data from TISCH complemented this by resolving DLD expression at the cellular level. Experimental validation in KIRC was conducted via IHC, western blot, and qRT-PCR. Together, these approaches aimed to define the oncogenic role of DLD, particularly in KIRC. The Wilcoxon rank sum test, Pearson correlation test are used to teste differences among groups and correlations. The Kaplan–Meier method is used to estimate the relationship between patient prognosis and DLD expression levels. DLD exhibits elevated expression across multiple malignancies, and its high expression consistently correlates with improved clinical prognosis (p < 0.05). Bioinformatic analyses further show significant correlations between DLD expression and the activity of cancer-related pathways, as well as immunological interactions including cancer-associated fibroblasts, immune cell infiltration, and immune checkpoint genes. Single-cell analysis suggests DLD likely participates in angiogenesis, cell cycle regulation, differentiation, DNA damage, DNA repair, and hypoxia responses. Notably, experimental validation confirms significantly lower DLD expression in KIRC tissues. Moreover, DLD expression correlates significantly with TNM stage, pathological stage, histologic grade, and primary therapy outcome (all p < 0.05). The cuproptosis-related gene DLD may be a potential diagnostic and prognostic biomarker for pan-cancer. Furthermore, it may serve as an independent risk factor for poor outcomes of KIRC patients.

Cardamomin has been widely studied in cancer, but its role in cancer bladder cancer has not been mentioned. In this study, we validated the anti-cancer effect of cardamom and whether its potential mechanism is related to the PI3K/AKT pathway. After treating with different doses of cardamomin, the cytotoxicity was studied by CCK8. Secondly, we analyzed the effect of cardamomin on the proliferation, apoptosis and cell movement. Next, we analyzed the regulation of ESR1 by western blot and its impact on the PI3K/AKT pathway. We also transfected ESR1 overexpression and silencing vectors, and verified the transfection efficiency through RT-qPCR. Further, the specific mechanism of the drug's inhibitory effect on bladder cancer was also determined. We constructed the subcutaneous tumor model in vivo. After cardamomin administration, we mainly analyzed the positive expression of KI67 in tumor tissues by immunohistochemistry, and the apoptotic cells in tumor tissues by TUNEL, and related proteins in PI3K/AKT pathway by western blot. In this paper, cardamomin inhibited cell proliferation and invasion ability, blocked the transition of G0/G1 phase to S phase, and increased apoptotic rate of 5637 and HT1376 cells, as well as raised ESR1 expression. Cardamomin exerted anti-tumor effect through PI3K/AKT pathway. In vivo animal experiments indicated the inhibitory effect of cardamomin on subcutaneous implanted tumor. Cardamomin inhibited the positive expression of KI67 and promoted the TUNEL-positive cells in tumor tissues. Consistent with in vitro assay, cardamomin increased the expression of ESR1 and downregulated the PI3K/AKT pathway. Cardamomin has a significant inhibitory effect on bladder cancer, and upregulate the expression of ESR1 in bladder cancer through PI3K/AKT.

Background: Circular RNAs (circRNAs) have emerged as critical mediators in various cancers, including renal cell carcinoma (RCC). In the present research, the functions of circ_0000069 in RCC were explored.Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) assay, western blot assay and immuno-histochemistry (IHC) assay were performed for the expression of circ_0000069, microRNA-125a-5p (miR-125a-5p) and solute carrier family 1 member 5 (SLC1A5). Cell Counting Kit-8 (CCK-8) assay and 5 '-ethynyl-2 '-deox-yuridine (EdU) assay were performed for cell proliferation. Flow cytometry assay was manipulated for cell apoptosis. Transwell assay and wound-healing assay were utilized for cell invasion and migration. Glutamine metabolism level was evaluated by examining glutamine consumption, alpha-ketoglutarate production and gluta-mate production. Dual-luciferase reporter assay was used to analyze the relationships of circ_0000069, miR-125a-5p and SLC1A5. Murine xenograft model assay was conducted to analyze the function of circ_0000069 in vivo.Results: Circ_0000069 level was abnormally upregulated in RCC tissues and cells. Knockdown of circ_0000069 inhibited the proliferation, invasion, migration and glutamine metabolism and promoted the apoptosis in RCC cells in vitro and restrained tumor growth in vivo. Circ_0000069 served as the sponge for miR-125a-5p. MiR-125a-5p inhibition ameliorated the effects of circ_0000069 knockdown on RCC cell malignant behaviors. SLC1A5 was identified as the target gene of miR-125a-5p. Moreover, miR-125a-5p overexpression repressed the pro-gression of RCC cells, while SLC1A5 elevation abrogated the effect.Conclusion: Circ_0000069 knockdown inhibited the carcinogenesis of RCC by regulating miR-125a-5p/SLC1A5 axis.

Background: PD-1 blockade has been shown to have promising efficacy and acceptable safety profiles in advanced and metastatic gastric cancer; however, the efficacy and safety of neoadjuvant PD-1 blockade-based immunotherapy plus chemotherapy in locally advanced gastric cancer (LAGC) remain uncertain. Methods: We performed a retrospective review of patients with LAGC who received neoadjuvant treatment followed by D2 radical resection at the Affiliated Hospital of Qingdao University from 2019 to 2021. The primary aim was to investigate the difference in pathological response rates between neoadjuvant PD-1 immunotherapy plus chemotherapy and neoadjuvant chemotherapy alone. Multivariable models for pathological complete response (pCR) were constructed to investigate the factors that facilitate pCR. Trial registration: QYFYWZLL27406. Results: A total of 77 patients were included in the analysis, among whom 34 (44.2%) received neoadjuvant PD-1 blockade immunotherapy plus chemotherapy. A higher pCR rate was observed in the neoadjuvant PD-1 blockade immunotherapy plus chemotherapy group (8 of 34, 23.5% vs. 2 of 43, 4.7%, P=0.019). Multivariate logistic regression analysis of pCR revealed neoadjuvant PD-1 blockade plus chemotherapy regimen promoted pCR (OR 12.95, P=0.016). Regarding safety, 76.5% (26 of 34) of patients in the PD-1 blockade plus chemotherapy group and 76.7% (33 of 43) of patients in the chemotherapy group experienced treatment-related adverse events (TRAEs), and grade 3 or worse adverse events were 29.4% (10 of 34) and 34.9% (15 of 43), respectively. Conclusion: Neoadjuvant PD-1 blockade plus chemotherapy induced a higher pCR rate than neoadjuvant chemotherapy, and the combined therapy was tolerable in LAGC patients.

Objective: To investigate the predictive value of platelet-to-lymphocyte ratio (PLR), red blood cell distribution width to platelet count ratio (RPR) and systemic immune inflammation index (SII) in the staging and postoperative recurrence of ovarian endometrial cysts. Methods: Retrospective analysis was made on the clinical data of patients who underwent laparoscopic surgery for ovarian cysts in the Affiliated Hospital of Qingdao University from January 2018 to January 2020. The patients with ovarian endometriosis cyst confirmed by pathology after surgery were the observation group (n=350), and the patients with other benign ovarian cyst were the control group (n=150). The preoperative platelet count, platelet distribution width, absolute number of neutrophils, lymphocyte absolute number, absolute number of monocytes, red blood cell distribution width, and serum cancer antigen 125 (CA125) of the patients in two groups were recorded, and PLR, neutrophil-to-lymphocyte ratio (NLR), RPR, SII, and systemic inflammation response index (SIRI) were calculated and analyzed. The general data of all patients and the follow-up data within 2 years after the operation of the observation group were statistically recorded to evaluate the diagnostic value of PLR, RPR and SII for ovarian endometrial cyst, and the predictive value of staging and recurrence within 2 years after the operation. Results: PLR, NLR, SII (median: 147.53, 1.86, and 488.70 respectively) and CA125 (median: 59.41 kU/L) in the observation group were significantly higher than those in the control group, while RPR (median: 0.16) was lower than that in the control group, with significant differences (all P<0.01). There was no significant difference in SIRI between the two groups (P>0.05). The PLR and SII (median: 122.73, 345.00) of the observation group at stage Ⅲ and Ⅳ were higher than those of patients at stage Ⅰ and Ⅱ, and the RPR was lower than that of patients with stage Ⅰ and Ⅱ, with significant differences (all P<0.001). The PLR, NLR, SII, SIRI (median: 179.63, 2.75, 762.96, and 1.06 respectively) and CA125 (median: 108.83 kU/L) in patients with recurrence were significantly higher than those in patients without recurrence 2 years after the operation, and the differences were statistically significant (all P<0.001). The area under curve (AUC) of CA125 in the diagnosis of ovarian endometriosis cyst was 0.951, the sensitivity was 85.7%, and the specificity was 93.0%, which were higher than those of PLR and SII; the AUC of PLR+SII+CA125 in the diagnosis of ovarian endometriosis cyst was 0.952. The AUC of RPR predicting the stage of ovarian endometriosis cyst was 0.713, higher than PLR and SII, lower than CA125; the AUC of RPR+SII+CA125 in predicting the stage of ovarian endometriotic cyst was 0.825, with sensitivity of 68.7% and specificity of 85.7%. The AUC predicted by SII for recurrence of ovarian endometriotic cyst within 2 years after the operation was 0.803, higher than NLR, PLR, SIRI and CA125; the AUC of PLR+SII+CA125, sensitivity, specificity was 0.813, 81.5% and 73.0%, higher than SII. Conclusion: PLR, RPR and SII are related to the staging of ovarian endometriotic cyst, and SII has a certain predictive value for the recurrence of ovarian endometriotic cyst after surgery.

Programmed cell death (PCD), a common modality of cell death, affects tumor development and acts as a target for tumor therapeutics. Many modalities of PCD regulate genesis, progression and metastasis of cancers, thus affecting the patients' prognosis, but the comprehensive molecular mechanisms of PCD in tumors are lacking, especially in renal cancer. Here, seventeen PRPCDGs were identified from 1257 genes associated with thirteen PCD modalities, which were highly differentially expressed and significantly affected patients' prognosis. Then, LASSO regression analysis of these PRPCDGs screened the 9-gene PRPCDGs risk signature in TCGA-KIRC database. The PRPCDGs risk signature was closely associated with the patients' prognosis and presented stable prediction efficacy for 5- and 7-year overall survival (OS) in three different cohorts of renal cancer. Immune cell infiltration, immune checkpoint expression and pathway enrichment (including GO, KEGG pathway, tumor-associated pathways and metabolism-associated pathways) were significantly different in the high- or low-PRPCDGs-risk group. Finally, we illustrated that TRIB3 might be a protumor factor responsible for the elevated proliferation and invasion capacities of renal cell carcinoma (RCC) cells. In summary, the PRPCDGs risk signature was developed and showed stable prediction efficacy for the prognosis of patients and that (such as TRIB3) could be a potential target for RCC management.

Objective: To investigate the expression levels and clinical significance of glioma-associated oncogene homolog 1 (GLI1) and sonic hedgehog signaling molecule (Shh) in the malignant transformation of ovarian endometriosis (EM). Methods: The expressions of GLI1 and Shh were detected by real-time reverse transcription (RT)-polymerase chain reaction (PCR) and EnVision method in 50 cases of ovarian EM tissues, 35 cases of atypical endometriosis (aEM) and 50 cases of endometriosis-associated ovarian cancer (EAOC). The expression differences of two molecular markers in the malignant transformation of ovarian EM were compared, and the relationships between two molecular markers and the clinicopathological features and prognosis of EAOC were analyzed. Results: (1) RT-PCR showed that the expression levels of GLI1 mRNA in EM, aEM and EAOC group were 1.77±0.40, 3.54±0.44, and 7.80±0.24, respectively. The expression levels of Shh mRNA were 0.95±0.21, 3.14±0.35, and 5.41±0.31, respectively. GLI1 and Shh mRNA in EAOC group were significantly higher than those in EM and aEM group (all P<0.01), and there were statistically significant differences between EM and aEM group (all P<0.01). The percentages of GLI1 in ovarian EM, aEM and EAOC were 32% (16/50), 57% (20/35), and 66% (33/50), respectively, meanwhile, the positive expression rates of Shh were 20% (10/50), 49% (17/35), and 54% (27/50), respectively (all P<0.01). GLI1 mRNA expression was positively correlated with Shh mRNA expression in EAOC tissues (r=0.721, P<0.01). The expressions of GLI1 protein were proportionated to Shh protein in EAOC tissues (r=0.608,P=0.001). (2) The expression of GLI1 was significantly related to the International Federation of Gynecology and Obstetrics (FIGO) stage, cancer antigen 125 (CA125) levels, lymph node metastasis, and Platinum resistance in EAOC patients (all P<0.05). The expression of Shh were related to FIGO stage and lymph node metastasis in EAOC patients (all P<0.05). Logistic regression analysis showed that GLI1 expression was an independent risk factor for poor prognosis in EAOC patients (P<0.05). Kaplan-meier survival analysis showed that the overall survival rate of EAOC patients with high GLI1 expression and low GLI1 expression was 12.1% and 35.3%, respectively, with statistical significance (χ²=10.73, P<0.01). The overall survival rate of EAOC patients with high and low expression of Shh protein was 11.1% and 30.4%, in which there was statistically significant difference (χ²=3.96, P=0.047). Conclusion: GLI1 and Shh are highly associated with the malignant transformation of ovarian EM, which may play a role in promoting malignant degeneration of ovarian EM, and the high expression of GLI1 and Shh indicates a poor prognosis in EAOC patients.

The 5-minute frequency domain method was used to examine the effects of polysomnography (PSG)-guided acute selective sleep deprivation (REM/SWS) on the cardiovascular autonomic nervous system, heart rate, and rhythm in healthy volunteers to understand the relationship between cardiac neuro regulatory homeostasis and cardiovascular system diseases in healthy subjects. The study included 30 healthy volunteers selected through the randomized-controlled method, randomly divided into REM sleep deprivation and SWS sleep deprivation groups. PSG analyses and dynamic electrocardiogram monitoring were done at night, during slow wave sleep or REM sleep. An all-night sleep paradigm, without any interruptions, was tested 3 times for comparison. The frequency domain parameter method was further used to monitor the volunteers 5 min before and after a period of sleep deprivation. According to the characteristics of the all-night sleep scatter plot, healthy volunteers were divided into abnormal and normal scatter plot groups. When compared with the period before sleep deprivation, high frequency (HF) and normalized high-frequency component (HFnu) were found to be decreased. Normalized low-frequency component (LFnu) increased in the abnormal scatter plot group after sleep deprivation, and this difference was statistically significant (P < 0.05). The scatter plot also showed that very low frequency (VLF) increased only in the normal group after deprivation and this difference, as well, was statistically significant (P < 0.05). The increase in diastolic blood pressure in the abnormal group was statistically significant (P < 0.05), but the change in blood pressure in the normal group was not statistically significant (P > 0.05). There are 62.5% of the patients and 20% of the employees that were observed to have abnormal whole-night sleep patterns during the uninterrupted whole-night sleep regime. Patients with atrial or ventricular premature beats (more than 0.1%), and those with ST-t changes during sleep, were all ascertained as abnormal. We concluded that some healthy people could face unstable autonomic nervous functioning related to their long-term tension, anxiety, time urgency, hostility, and other chronic stress states. In the face of acute sleep deprivation selectivity, mild stress based excitability of the vagus nerve is reduced, which diminishes the protective function, making them susceptible to conditions such as premature ventricular arrhythmia.

The aim of the present study was to investigate the effects of microRNA (miR)-29b-3p gene promoter methylation on angiogenesis, invasion, and migration in human pancreatic cancer. Prediction of promoter methylation of miR-29b-3p was performed through the MethPrimer tool. Then the methylation levels of miR-29b-3p in human pancreatic cancer tissues and cell lines were detected by pyrosequencing, and the relative expression of miR-29b-3p was assessed in pancreatic cancer tissues by qPCR. The results were analyzed by linear regression. Western blot analysis was used to detect expression of DNA methyltransferases (DNMTs) in pancreatic cancer tissues and adjacent tissues. The Transwell assay was used to detect the ability of cell migration and invasion. Cells were co-cultured with human umbilical vein endothelial cells (HUVECs) to detect the ability of angiogenesis. The results revealed that DNMT1 expression in pancreatic cancer tissues was higher than that in adjacent tissues. Further results showed that expression of miR-29b was negatively correlated with the methylation level of the miR-29b promoter. Bxpc3 and Capan-2 cells had higher methylation levels, and the expression level of miR-29b-3p in Bxpc3 and Capan-2 cells was found to be lower than that of other cell lines. Expression of zonula occludens-1 (ZO-1) and occludin was significantly increased, and the migration of cancer cells was decreased after cells were treated with siRNA DNMT1. Further results showed that miR-29b reversed the promotive effect of DNMT1 overexpression on tumor cell malignant properties. Methylation of the miR-29b-3p promoter contributes to angiogenesis, invasion, and migration in pancreatic cancer. This study indicated that the alteration of methylation of mR-19b may be a potential approach for inhibiting the progression of pancreatic cancer.

OBJECTIVE: Bladder cancer is the most frequent tumor of the urinary system. Despite variety of new treatment options, bladder cancer remains a main global medical problem. Our purpose was to explore the potential molecular and therapeutic targets of bladder cancer diagnosis. PATIENTS AND METHODS: The qRT-PCR was used to assess the expression of miR-20a in tissues and cell lines. Counting Cell Kit-8 (CCK-8) assay was carried out to evaluate cell proliferation. Cell migration was calculated using the transwell assay. RESULTS: The expression of miR-20a increased and PDCD4 decreased in bladder cancer tissues compared with normal tissues. Over-expression of miR-20a promoted T24 cell proliferation and migration, while miR-20a inhibitor suppressed cell proliferation and migration. MiR-20a targeted PDCD4 to regulate its expression in T24 cells. MiR-20a is inversely related to PDCD4 and PTENPL in bladder cancer tissues. Upregulation of PDCD4 suppressed T24 cell proliferation and migration. CONCLUSIONS: The PTENP1/miR-20a/PTEN axis was involved in the progression of bladder cancer. Our study investigated the function of miR-20a in bladder cancer and provided new insights into the treatment of bladder cancer.

MicroRNAs (miRNAs) have been validated to play prominent roles in the occurrence and development of anaplastic thyroid carcinoma (ATC). miR-199a-5p was previously reported to act as a tumor suppressor or oncomiRNA in various types of cancer. However, its accurate expression, function, and mechanism in ATC remain unclear. Here, we find that miR-199a-5p is significantly downregulated in ATC tissues compared with adjacent non-cancerous tissues. Overexpression of miR-199a-5p significantly inhibits migration and invasion of ATC cells in vitro, and lung metastasis in vivo. Importantly, miR-199a-5p suppresses epithelial-mesenchymal transition (EMT) both in vitro and in vivo by targeting Snail. Taken together, this study reveals that miR-199a-5p is critical to the EMT progression in ATC cells. Targeting the pathway described here may be a novel approach for inhibiting metastasis of ATC.

The different advantages of laparoscopic gastrectomy (LG) and robotic gastrectomy (RG), two new minimally invasive surgical techniques for gastric cancer, remain controversial.

The long noncoding RNA plasmacytoma variant translocation 1 gene (LncRNA PVT1) has an important role in tumor occurrence and development, yet the role and underlying molecular mechanisms of this RNA in cervical cancer have not yet been elucidated. In the present study, three cervical cancer cell lines (HeLa, Ca Ski and SiHa) were used to verify how LncRNA PVT1 mediates cervical cancer development, and the H8 cell line was used as a control. A LncRNA PVT1 overexpression vector or small interfering RNAs targeting LncRNA PVT1 were transfected into cervical cancer cells to generate LncRNA PVT1 overexpression and silencing in these cells. LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis; increases in Cyclin D1 (CCND1) mRNA and activated Bcl‑2 protein expression levels also supported this finding. Furthermore, NF‑κB activation and expression was increased by LncRNA PVT1 overexpression. In addition, NF‑κB activation or inhibition induced changes in cell viability, accompanied by changes in CCND1 and Bcl‑2 expression. Increases or decreases in microRNA‑16 (miR‑16) expression (using miR mimics and inhibitors) also corresponded to changes in LncRNA PVT1 expression, in vitro. miR‑16 mimics and inhibitor had opposite effects to those of NF‑κB activity, and miR‑16 was demonstrated to directly interact with the NF‑κB gene as measured using the dual‑luciferase assay. In summary, LncRNA PVT1 inhibits the effect of miR‑16, promoting the cell cycle and inhibiting cellular apoptosis of cervical cancer cells, potentially via the NF‑κB pathway. The data from the present study will contribute to the current knowledge surrounding the theoretical basis of cervical cancer and provide a new perspective for the treatment of cervical cancer.

OBJECTIVE:This study aims to investigate whether long non-coding RNA (lncRNA) SNHG1 could regulate proliferative and invasive abilities of liver cancer (LC) cells via p53 and DNMT1, so as to regulate the occurrence and progression of LC.PATIENTS AND METHODS:SNHG1 expression in LC tissues and paracancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between SNHG1 expression and tumor stage of LC patients was analyzed. The regulatory effects of SNHG1 and p53 on proliferative, invasive capacities and cell cycle were accessed by CCK-8 (cell counting kit-8), transwell assay and flow cytometry, respectively. The binding condition between SNHG1 and DNMT1 was determined by RNA binding protein immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP). Western blot was conducted to determine whether SNHG1 could regulate p53 in LC cells. Finally, rescue experiments were carried out to evaluate whether SNHG1 regulates proliferative and invasive abilities of LC cells through p53.RESULTS:SNHG1 expression was higher in LC tissues than that of paracancerous tissues. LC patients with stage III-IV presented higher expression level of SNHG1 than those with stage I-II. Similarly, SNHG1 was highly expressed in LC cells than that of normal liver cells. LC cell lines SMMC-7721 and SK-HEP-1 were selected for this study. SNHG1 knockdown inhibited the proliferative and invasive abilities, and arrested the cell cycle in the G0/G1 phase of SMMC-7721 and SK-HEP-1 cells. RIP and ChIP results demonstrated that SNHG1 could bind to DNMT1 and inhibit p53 expression. Overexpression of p53 partially reversed the inhibitory effects of SNHG1 on proliferative and invasive abilities of LC cells.CONCLUSIONS:High expression of SNHG1 could promote proliferative and invasive abilities of LC cells through targeting inhibition of p53 expression by binding to DNMT1.

Based on the important functions of phosphatase and tensin homolog (PTEN)-Long for renal diseases, the present study aimed to investigate the expression of PTEN-Long in patients and mice with nephritis and its effect on nephritis. Expression levels of PTEN-Long in serum of patients with nephritis, renal cell carcinoma (RCC) as well as normal controls, and in serum and renal tissues of mice were measured by western blotting. PTEN-Long knock-in and knock-out mice were constructed via the CRISPR-Cas9 technique. Intraperitoneal injection of lipopolysaccharide+renal homogenate was performed to construct a mouse nephritis model. Mice were divided into control group, model group, knock-in group and knock-out group. A Bio-Plex system was used to detect secretion of serum inflammatory factors. Expression of inflammatory factors in renal tissues of different groups was detected by reverse transcription semi-quantitative polymerase chain reaction. Hematoxylin and eosin staining was used to observe the pathological changes of renal tissue. PTEN-Long was downregulated in patients with nephritis and RCC compared with controls, whereas the expression levels of inflammatory factors were increased. PTEN-long knock-in significantly reduced the serum content and expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-18. PTEN-long knock-out also decreased the expression levels of TNF-α and IL-6 but exhibited no effects on expression of IL-1β and IL-18. Compared with knock-out and model groups, renal tissue inflammation was significantly reduced in knock-in group. The protein level of PTEN-Long was significantly lower in serum than in renal tissue. These findings suggest that PTEN-long can inhibit the progression of nephritis by interacting with inflammatory factors to protect kidney.

Introduction: CA125 has poor sensitivity and low specificity for detecting early ovarian cancer. Serum ferritin is elevated in many malignancies. We evaluated the performance of ferritin alone and in combination with CA125 as a diagnostic tool to detect epithelial ovarian cancer (EOC). Methods: CA125 and ferritin were detected in the serum of 50 healthy control (HC), 50 women with benign gynaecological conditions and 124 women with EOC. The relationship between serum ferritin and CA125 and each of the clinicopathological parameters was assessed, and their diagnostic accuracy for discriminating ovarian cancer determined. Results: Serum ferritin and CA125 were higher in patients with EOC compared to HCs and patients with benign conditions (both p < 0.001). There was no relationship between levels of ferritin and CA125. Both ferritin and CA125 discriminated HC from EOC (p < 0.05), but ferritin showed better diagnostic accuracy than CA125 (p = 0.048). Ferritin was superior to CA125 in discrimination early EOC (p = 0.002), but in advanced stages, CA125 was superior (p = 0.026). A combination of ferritin and CA125 marginally increases the diagnostic accuracy to discriminate EOC from HCs. Conclusion: Ferritin discriminates between HCs and EOC patients, especially in early stage disease. The combination of serum ferritin and CA125 provides the higher diagnostic accuracy to screen for EOC. Serum ferritin could serve as an EOC biomarker to complement the standard CA125 test.

Increasing evidence indicates that miR-429 is involved in tumor suppression in various human cancers. however, its role in hepatocellular carcinoma (HCC) remains unclear. In the present study, we found that miR-429 was significantly downregulated in HCC tissue samples and cell lines. Upregulation of miR-429 markedly suppressed proliferation and migration of HCC cells. Moreover, we identified TRAF6 as a direct target of miR-429. Downregulation of TRAF6 partially attenuated the oncogenic effect of anti‑miR-429 on HCC cells. Ectopic expression of miR-429 in HCC cells inhibited TCF-4 activity as well as nuclear accumulation of P65 and expression of the NF-κB targets c-Myc and phosphorylation of TAK1. In a nude xenograft model, miR-429 upregulation significantly decreased HCC growth. In conclusion, by targeting TRAF6, miR-429 is downregulated in HCC and inhibits HCC cell proliferation and motility. Our data suggest that miR-429 may serve as a potential anticancer target for the treatment of HCC.

Study on the correlation of MLCK and FAP expression with uterine fibroid cell proliferation and invasion Wei Lin, Sha Ma, Li Wang Department of Obstetrics and Gynecology,Wuhan Red Cross Hospital (Wuhan 11 Hospital) in Hubei Province, Wuhan City, Hubei Province, 430015 Department of Obstetrics and Gynecology, Wuhan Women and Children Medical Care Center in Hubei Province,Wuhan City, Hubei Province, 430016 Journal of Hainan Medical University

Long noncoding RNAs (lncRNAs) have been recently regarded as systemic regulators in multiple biological processes including tumorigenesis. In this study, we report an ultra-highly expressed lncRNA, lnc-Sox5, in tongue tumor tissues. The results imply that lnc-Sox5 may play vital role in tongue carcinoma progression. We observed that the growth of Tca8113 cells was suppressed by lnc-Sox5 downregulation. Additionally, lnc-Sox5 knockdown simultaneously increased Tca8113 cell apoptosis, but the cell cycle was arrested. RNA immunoprecipitation suggested that HuR directly bound to and stabilized lnc-Sox5 RNA. Consistently, HuR knockdown reduced the level of lnc-Sox5 in Tca8113 cells. However, overexpression of HuR induced more lnc-Sox5 in Tca8113 cells. Both lnc-Sox5 knockdown and HuR knockdown suppressed Tca8113 cell tumorigenesis in xenograft models. These results suggest that lnc-Sox5, which was stabilized by HuR, could regulate carcinogenesis of tongue cancer and may serve as a predicted target for tongue carcinoma therapies.