Effect of PHAP1 and SUMO2 on biological characteristics of Cervical squamous cell carcinoma

2019 ◽  
Author(s):  
Qian Liu ◽  
Xiaohong Li ◽  
Song Qin
Keyword(s):  
Expression Patterns ◽  
Cervical Squamous Cell Carcinoma ◽  
Biological Characteristics ◽  
Tumor Promoter ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Tissue Samples ◽  
Normal Tissues ◽  
The Relationship ◽  
Hpv16 Infection

Abstract Background This study aimed to investigate the biological characteristics of PHAP1 and SUMO2 in CSCC and the relationship between the expression of the 2 genes and HPV16 infection. Method To detect the function of PHAP1 and SUMO2 in the occurrence and development of CSCC, we first compared their expression patterns in CSCC tissue samples, CIN and matched normal tissues through IHC, and RT-PCR. In addition, we carried on WB assay to test the expression of PHAP1 and SUMO2 in the SiHa, C33A and Ect1 cell lines. We analyzed the relationship between the expression of PHAP1 and SUMO2 and HPV16 infection. Result The results demonstrated that PHAP1 and SUMO2 expression at both the protein and mRNA levels was elevated in CSCC tissues compared with CIN and normal tissues. The expression of SUMO2 was significantly associated with lymph node metastasis (P=0.02), AJCC stage(p=0.024), but not other clinicopathological factors. The expression of PHAP1 and SUMO2 protein in SiHa, C33A cells was obviously higher than that in Ect1 cells. The expression of PHAP1 and SUMO2 was associated with a susceptibility to HPV16 infections. Conclusion Our results imply that PHAP1 and SUMO2 may be potential tumor promoter genes and may provide the biological basis for diagnosis, prognosis and treatment for CSCC.

scholarly journals Altered Expression of Three EGFR Posttranslational Regulators MDGI, MIG6, and EIG121 in Invasive Breast Carcinomas

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Didier Meseure ◽  
Kinan Drak Alsibai ◽  
Sophie Vacher ◽  
Rana Hatem ◽  
Andre Nicolas ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Prognostic Significance ◽  
Growth Factor Receptor ◽  
Growth Inhibitor ◽  
Receptor Activation ◽  
Mrna Levels ◽  
Breast Carcinomas ◽  
Rt Pcr ◽  
Altered Expression ◽  
Invasive Breast Carcinomas

Epidermal growth factor receptor (EGFR) signalling is a highly regulated process with a tight balance between receptor activation and inactivation in invasive breast carcinomas (IBCs) particularly in triple-negative carcinomas (TNC). Clinical trials using anti-EGFR therapies are actually performed although no activating alterations (mutations, amplifications, or rearrangements) of EGFR have been clearly recognized in order to identify new targeted modalities for IBCs. We explored mammary-derived growth inhibitor (MDGI), estrogen-induced gene-121 (EIG121), and mitogen-induced gene-6 (MIG6), three posttranslational EGFR trafficking molecules implicated in EGFR spatiotemporal regulatory pathway. We quantified MDGI, EIG121, and MIG6 at mRNA levels by using real-time quantitative RT-PCR in a series of 440 IBCs and at protein levels by using immunohistochemistry in a series of 88 IBCs. Results obtained by RT-PCR showed that in IBCs, MDGI, MIG6, and EIG121 mRNA were mainly underexpressed (25.7%, 45.0%, and 16.1%, respectively) particularly in the TNC subtype for EIG121 (60.3%). We also observed mRNA overexpression of MDGI and EIG121, respectively, in 12.7% and 22.3% of IBCs. These altered mRNA expressions were confirmed at the protein level. Some links were found between expression patterns of these three genes and several classical pathological and clinical parameters. Only EIG121 was found to have a prognostic significance (p=0.0038). Altered expression of these three major EGFR posttranslational negative regulators could create an aberrant EGFR-mediated oncogenic signalling pathway in IBCs. MDGI, MIG6, and EIG121 expression status also may be potential useful biomarkers (sensitivity or resistance) in targeted EGFR therapy.

scholarly journals Reciprocal interplay between asporin and decorin: Implications in gastric cancer prognosis

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255915
Author(s):  
Dipjit Basak ◽  
Zarqua Jamal ◽  
Arnab Ghosh ◽  
Pronoy Kanti Mondal ◽  
Priyanka Dey Talukdar ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Western Blot ◽  
Interaction Analysis ◽  
Cancer Prognosis ◽  
Gastric Epithelium ◽  
Tumor Promoter ◽  
Physical Interaction ◽  
Mrna Levels ◽  
Normal Tissues ◽  
Tgfβ Pathway

Effective patient prognosis necessitates identification of novel tumor promoting drivers of gastric cancer (GC) which contribute to worsened conditions by analysing TCGA-gastric adenocarcinoma dataset. Small leucine-rich proteoglycans, asporin (ASPN) and decorin (DCN), play overlapping roles in development and diseases; however, the mechanisms underlying their interplay remain elusive. Here, we investigated the complex interplay of asporin, decorin and their interaction with TGFβ in GC tumor and corresponding normal tissues. The mRNA levels, protein expressions and cellular localizations of ASPN and DCN were analyzed using real-time PCR, western blot and immunohistochemistry, respectively. The protein-protein interaction was predicted by in-silico interaction analysis and validated by co-immunoprecipitation assay. The correlations between ASPN and EMT proteins, VEGF and collagen were achieved using western blot analysis. A significant increase in expression of ASPN in tumor tissue vs. normal tissue was observed in both TCGA and our patient cohort. DCN, an effective inhibitor of the TGFβ pathway, was negatively correlated with stages of GC. Co-immunoprecipitation demonstrated that DCN binds with TGFβ, in normal gastric epithelium, whereas in GC, ASPN preferentially binds TGFβ. Possible activation of the canonical TGFβ pathway by phosphorylation of SMAD2 in tumor tissues suggests its role as an intracellular tumor promoter. Furthermore, tissues expressing ASPN showed unregulated EMT signalling. Our study uncovers ASPN as a GC-promoting gene and DCN as tumor suppressor, suggesting that ASPN can act as a prognostic marker in GC. For the first time, we describe the physical interaction of TGFβ with ASPN in GC and DCN with TGFβ in GC and normal gastric epithelium respectively. This study suggests that prevention of ASPN-TGFβ interaction or overexpression of DCN could serve as promising therapeutic strategies for GC patients.

scholarly journals Comprehensive analysis of ceRNA network of ERCC4 in colorectal cancer

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12647
Author(s):  
Huixin Hu ◽  
Songyi Liu ◽  
Aining Chu ◽  
Jing Chen ◽  
Chengzhong Xing ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Regulatory Network ◽  
Drug Sensitivity ◽  
Hazard Ratio ◽  
High Expression ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Normal Tissues ◽  
Cerna Network ◽  
Kaplan Meier

Objective ERCC4 is one of the most significant molecules of Nucleotide Excision Repair (NER), which has been researched due to its high expression in colorectal cancer (CRC). This study aimed to find out the ceRNA (competitive endogenous RNA) network of ERCC4 in CRC. Methods and Materials Pan cancer mRNA expression of ERCC4 was evaluated using TCGA database. The protein expression of ERCC4 was evaluated based on the Human Protein Atlas (HPA). We screened DElncRNAs and DEmiRNAs in two groups of ERCC4high and ERCC4low expression in CRC. Then a lncRNA-miRNA-ERCC4 regulatory network was constructed based on DElncRNAs and DEmiRNAs using Starbase database and visualized by Cytoscape software. Kaplan-Meier analysis was performed to evaluate the prognostic value of the ceRNA network. Further, RT-PCR was performed to validate the expression of the representative molecules in the ceRNA network in CRC and normal tissues. The relationship between drug sensitivity and these molecules were also evaluated using RNAactDrug database. Results ERCC4 was overexpressed in a variety of tumors at mRNA levels, including CRC. High expression of ERCC4 was also observed on protein level in CRC. A total of 1,885 DElncRNAs and 68 DEmiRNAs were identified from CRC samples in ERCC4high and ERCC4low expression groups. Predicted by the Starbase database, we got interacting miRNAs and lncRNAs of ERCC4 from the DEmiRNAs and DElncRNAs, and a lncRNA-miRNA-ERCC4 regulatory network was constructed. Kaplan-Meier survival curves results showed that miR-200c-3p (hazard ratio [HR] = 0.62, P = 0.032), MALAT1 (HR = 1.54, P = 0.016), and AC005520.2 (hazard ratio [HR] = 1.75, P = 0.002) were significantly associated with the prognosis of CRC. After validation by RT-PCR, we found that ERCC4 and MALAT1 were up-regulated in CRC compared with normal tissues, while miR-200c-3p was down-regulated. A strong negative correlation was observed between MALAT1 and miR-200c-3p. Drug sensitivity analysis showed that ERCC4, miR-200c and MALAT1 were all associated with Cisplatin. Conclusion We constructed a ceRNA network of ERCC4 in CRC, of which the MALAT1-miR-200c-3p-ERCC4 axis may be involved in the development, prognosis and chemotherapy sensitivity of CRC. These findings might provide novel clues and insights on the molecular mechanisms of ERCC4 and NER pathway in CRC.

Expression of a KCC1 Splice Variant Is Suppressed by NF-ΚB in Erythroid Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1669-1669
Author(s):  
Kathleen P. Anderson ◽  
Scott C. Crable ◽  
Suzan M. Hammond ◽  
Patrick G. Gallagher ◽  
Clinton H. Joiner
Keyword(s):  
Sickle Cell ◽  
Splice Variant ◽  
Expression Patterns ◽  
K562 Cells ◽  
Regulatory Elements ◽  
Mrna Levels ◽  
Red Cell ◽  
Rt Pcr ◽  
Erythroid Precursor

Abstract The K+Cl- cotransporter (KCC) plays a significant role in the maintenance of red cell volume. Activity of the cotransporter is higher in sickle (SS) compared to normal (AA) reticulocytes, and contributes to SS dehydration. Thus, KCC is considered a potential modifier gene for sickle cell disease (SCD). We have demonstrated the presence of transcripts for KCC1, KCC3, and KCC4 in human reticulocytes (Exp.Hem.2005;33:624–31) and shown that one splice variant of KCC1 (KCC1ex1b), which codes for a protein with a small (7aa) alternative N-terminal exon, is detected in AA, but not SS reticulocytes. Studies with murine KCC1 have demonstrated that proteins produced by N-terminal truncation are inactive for K+Cl- cotransport, and function as dominant negative regulators of full-length KCC1 and KCC3 proteins. Since high level expression of this variant in AA cells compared to SS cells might explain the relatively low KCC activity in AA reticulocytes, we have identified the promoter for the KCC1ex1b transcript and investigated the regulatory elements that control its expression. Here we report the involvement of TNFα and NF-ΚB in the transcriptional regulation of the KCC1ex1b variant. Although KCC1ex1b is not expressed in reticulocytes isolated from sickle cell patients, we found that SS erythroid precursor cells cultured in vitro express this variant. SS and AA peripheral blood mononuclear cells were cultured in semi-liquid media with stem cell factor and erythropoietin, and collected after 5, 10, and 14 days in culture. Cells harvested at 14 days and isolated by binding to micromagnetic beads coated with transferrin receptor antibody were 95–98% positive for glycophorin A. RNA was extracted and analyzed by semi-quantitative RT-PCR, using primers for KCC1ex1 and KCC1ex1b. In both AA and SS cells, the transcript level for KCC1ex1b rose over the time in culture, while the KCC1ex1 transcript was constant. This difference between the in vitro and in vivo expression patterns for the KCC1ex1b variant could be explained by regulation via an external factor, such as a cytokine present in the blood of sickle cell patients, but absent in the in vitro culture system. The levels of numerous cytokines, including TNF, VEGF, and various interleukins, are elevated in SCD. We therefore assayed the effect of TNFα on endogenous KCC1ex1b expression in K562 cells by RT-PCR analysis at 24 and 48 hours after the addition of TNFα to the tissue culture medium. The steady-state mRNA levels of the KCC1ex1b variant decreased approximately 40% in response to TNF treatment. The transcription factor NF-ΚB is activated by TNF signaling, and an NF-ΚB consensus site is present in the KCC1ex1b promoter region. We assayed the effect of co-expressing NF-ΚB and our KCC1ex1b promoter constructs in K562 cells. NF-ΚB expression produced an 8-fold decrease in luciferase activity from these promoter constructs indicating NF-ΚB transcriptionally represses this promoter, either directly or indirectly. Our current model proposes that induction or modulation of the expression of the KCC1ex1bvariant could be an important factor in the control of red cell hydration.

scholarly journals Enhanced Bruton’s tyrosine kinase activity in the kidney of patients with IgA nephropathy

2021 ◽  
Author(s):  
Jie Wei ◽  
Yan Wang ◽  
Xiangming Qi ◽  
Yonggui Wu
Keyword(s):  
Tyrosine Kinase ◽  
Iga Nephropathy ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Bruton’S Tyrosine Kinase ◽  
Rt Pcr ◽  
Bruton's Tyrosine Kinase ◽  
Tissue Samples ◽  
Normal Tissues

Abstract Purpose Bruton’s tyrosine kinase (BTK) is a vital biological molecule that contributes to immune regulation. Previous studies have showed that BTK can be detected in patients with lupus nephritis and rheumatoid arthritis. However, the role of BTK in IgA nephropathy (IgAN) has not yet been elucidated. The purpose of this research was to investigate the role of BTK activation in macrophages in IgAN. Methods Peripheral blood and renal tissue samples were collected from 63 patients with IgAN, and peritumoral normal tissues were collected from 20 patients after surgical resection of renal tumor for use as control. Additionally, 20 healthy volunteers were recruited as control. The levels of BTK, CD68, phosphorylated BTK (pBTK), phosphorylated NF-κB (p-NF-κB p65), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and monocyte chemotactic protein (MCP)-1 were measured by immunohistochemistry (IHC), real-time polymerase chain reaction (RT-PCR), western blotting, and enzyme-linked immunosorbent assay (ELISA). Results Compared to peritumoral normal tissues, the expression levels of CD68 and BTK were significantly increased in IgAN group (p < 0.001) and the differences between M0 and M1, E0 and E1, S0 and S1, T0 and T1-2, C0 and C1-2 were statistically significant in the updated Oxford Classification (p < 0.05). Also, CD68 and BTK were positively correlated with Katafuchi semi-quantitative glomerular and tubulointerstitial scores (r = 0.580, 0.637 and 0.442, 0.489, respectively, p < 0.05). The expression of BTK was significantly higher in C3b- and C4d-positive renal tissues of patients with IgAN (p < 0.05). In addition, BTK was positively correlated with 24-h urine protein, serum creatinine levels (r = 0.456 and 0.453, respectively, p < 0.001), and negatively correlated with serum albumin (r = 0.357, p < 0.05). The intensity of expression of pBTK and p-NF-κB p65 was observably increased in renal tissues and monocytes of patients with IgAN compared to the control group. The results of IHC, RT-PCR, and ELISA indicated that the levels of TNF-ɑ, IL-1β, and MCP-1 were markedly increased in the IgAN group (p < 0.05). Conclusion The results of this study indicate that activation of BTK in macrophages may play an important role in promoting the progression of renal inflammation in IgAN.

scholarly journals Effect of Organic and Inorganic Dietary Selenium Supplementation on Gene Expression in Oviduct Tissues and, Antioxidant Capacity of Laying Hens

2020 ◽  
Author(s):  
Aliyu Muhammad ◽  
Abdul-Alla Dalia ◽  
Teck Loh ◽  
Henny Akit ◽  
Anjas Asmara Samsudin
Keyword(s):  
Laying Hens ◽  
Selenium Supplementation ◽  
Functional Genes ◽  
Mrna Levels ◽  
Tissue Sampling ◽  
Rt Pcr ◽  
Active Growth ◽  
Tissue Samples ◽  
Inorganic Selenium ◽  
Egg Components

Abstract Some functional genes were investigated for their involvement in egg (eggshell biomineralization) formation and selenoproteins in the oviduct and liver of laying hens fed different organic and inorganic selenium source. A total of 24 hens were selected randomly from the four treatments and slaughter. Uteri and liver tissue samples were collected from hens during the active growth phase of calcification (15 - 20 h post-ovulation) for RT-PCR. The basal diets supplemented with 0.3mg/kg of different organic Se sources and sodium selenite upregulate uterine and selenoproteins mRNA levels. This research reaps the advantage of tissue sampling from specialized segments of the oviduct that consecutively form different egg components. Expression of OC-17 and OC-116, and OC-17 were significantly higher in the uterus and magnum of laying hens, respectively. Their higher expression was observed with organic Se (bacterial selenoprotein or Se-yeast) fed-hens. The results may postulate the efficacy of organic Se in enhancing the expression of functional genes involved in the egg (eggshell biomineralization) formation and selenoproteins compared to inorganic and non-Se supplemented hens. This study proposed the efficacy of bacterial selenoprotein in the upregulation of the uterine genes and hepatic selenoproteins in laying hens.

scholarly journals Comparison of expression patterns of six canonical clock genes of follicular phase and luteal phase in Small-tailed Han sheep

2021 ◽  
Vol 64 (2) ◽  
pp. 457-466
Author(s):  
Qi Han ◽  
Xiaoyun He ◽  
Ran Di ◽  
Mingxing Chu
Keyword(s):  
Gene Expression ◽  
Estrous Cycle ◽  
Luteal Phase ◽  
Clock Gene ◽  
Clock Genes ◽  
Expression Patterns ◽  
Mrna Levels ◽  
Clock Gene Expression ◽  
The Relationship ◽  
The Brain

Abstract. The circadian rhythm is a biological rhythm that is closely related to the rhythmic expression of a series of clock genes. Results from several studies have indicated that clock genes are associated with the estrous cycle in female animals. Until now, the relationship between estrus cycle transition and clock gene expression in reproductive-axis-related tissues has remained unknown in Small-tailed Han (STH) sheep. This study was conducted to analyze the expression patterns of six canonical clock genes (Clock, BMAL1, Per1, Per2, Cry1, and Cry2) in the follicle phase and luteal phase of STH sheep. We found that all six genes were expressed in the brain, cerebellum, hypothalamus, pituitary, ovary, uterus, and oviduct in follicle and luteal phases. The results indicated that Clock expression was significantly higher in the cerebellum, hypothalamus, and uterus of the luteal phase than that of the follicle phase, whereas BMAL1 expression was significantly higher in the hypothalamus of the luteal phase than that of the follicle phase. Per1 expression was significantly higher in the brain, cerebellum, hypothalamus, and pituitary of the luteal phase than that of the follicle phase, and Per2 expression was significantly higher in the hypothalamus, pituitary, and uterus of the luteal phase than that of the follicle phase. Cry1 expression was significantly higher in the brain, cerebellum, and hypothalamus of the luteal phase than that of the follicle phase, whereas Cry2 expression was significantly higher in the pituitary of the luteal phase than that of the follicle phase. The clock gene expression in all tissues was different between follicle and luteal phases, but all clock gene mRNA levels were found to exhibit higher expression among seven tissues in the luteal phase. Our results suggest that estrous cycles may be associated with clock gene expression in the STH sheep. This is the first study to systematically analyze the expression patterns of clock genes of different estrous cycle in ewes, which could form a basis for further studies to develop the relationship between clock genes and the estrous cycle.

200 REPROGRAMMING OF Oct-4 FOLLOWING EQUINE SOMATIC CELL NUCLEAR TRANSFER

2009 ◽  
Vol 21 (1) ◽  
pp. 198
Author(s):  
T. Xiang ◽  
S. Walker ◽  
K. Gregg ◽  
W. Zhou ◽  
V. Farrar ◽  
...  
Keyword(s):  
Somatic Cell ◽  
Somatic Cell Nuclear Transfer ◽  
Nuclear Transfer ◽  
Expression Patterns ◽  
Somatic Cells ◽  
Blastocyst Stage ◽  
Rt Pcr ◽  
Tissue Samples ◽  
Donor Cells

Oct-4, a POU domain-containing transcription factor encoded by Pou5f1, is selectively expressed in pre-implantation embryos and pluripotent stem cells, but not in somatic cells. Because of such a unique expression feature, Oct-4 can serve as a useful reprogramming indicator in somatic cell nuclear transfer (SCNT). Compared with data of Oct-4 expression in mouse and bovine cloned embryos, little is known about this gene in equine nuclear transfer. In the present study, we investigated Oct-4 expression in donor cells, oocytes, and SCNT embryos to evaluate reprogramming of equine somatic cells following nuclear transfer. Horse ovaries were obtained from a local slaughterhouse and the oocytes collected from the ovaries were matured in vitro in an M199-based medium (Galli et al. 2003 Nature 424, 635) for 24 h. Donor cells were derived from biopsy tissue samples of adult horses and cultured for 1 to 5 passages. Standard nuclear transfer procedures (Zhou et al. 2008 Mol. Reprod. Dev. 75, 744–758) were performed to produce cloned embryos derived from equine adult somatic cells. Cloned blastocysts were obtained after 7 days of in vitro culture of reconstructed embryos. Total RNA were extracted using Absolutely RNA Miniprep/Nanoprep kits (Stratagen, La Jolla, CA) from oocytes (n = 200), donor cells, and embryos (n = 5). DNase I treatment was included in the procedure to prevent DNA contamination. Semiquantitative RT-PCR was performed with optimized cycling parameters to analyze Oct-4, GDF9, and β-actin in equine donor cells, oocytes, and cloned blastocysts. The RT-PCR products were sequenced to verify identity of the genes tested. The relative expression abundance was calculated by normalizing the band intensity of Oct-4 to that of β-actin in each analysis. No transcript of Oct-4 was detected in equine somatic cells used as donor nuclei, consistent with its expression patterns in other animal species, whereas Oct-4 was abundantly expressed in equine SCNT blastocysts derived from the same donor cell line. Oct-4 transcripts were also detected in equine oocytes and whether any maternally inherited Oct-4 mRNA persisted up to the blastocyst stage was unclear in this study. We selected GDF9 to address this question; GDF9 was abundantly detected in equine oocytes, consistent with its expression pattern in mouse and bovine, but not detected in donor cells and cloned blastocysts, suggesting that the GDF9 mRNA from the oocyte was degraded at least by the blastocyst stage. The results from this study imply occurrence of Oct-4 reprogramming in equine SCNT blastocysts, and future analysis for more developmentally important genes is needed to better understand reprogramming at molecular levels in this species.

Prognosis, Significance and Positive Correlation of Rab1A and p-S6K/Gli1 Expression in Gastric Cancer

2019 ◽  
Vol 19 (11) ◽  
pp. 1359-1367 ◽  
Author(s):  
Xinyu Shao ◽  
Zhengwu Cheng ◽  
Menglin Xu ◽  
Jiading Mao ◽  
Junfeng Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Targeted Therapy ◽  
Tissue Samples ◽  
Normal Tissues ◽  
Positive Expression ◽  
Gli1 Expression ◽  
Single Positive ◽  
High Level ◽  
The Relationship ◽  
Worse Prognosis

Background:Gastric Cancer (GC) is a frequently common malignancy. Recent studies have reported Rab1A as an activator of mTORC1, and the mTOR1 pathway is involved in regulating Gli1 expression in several cancers. Only a few studies have been performed to explore the relationship between Rab1A and p-S6K/Gli1in GC.Methods:Immunohistochemistry (IHC) was performed to explore the association of Rab1A/p-S6K/Gli1 expression and prognosis in 117 GC tissue samples and adjacent normal tissues.Results:Our results indicated that Rab1A/p-S6K/Gli1 was significantly overexpressed in GC tissues. High expression of Rab1A was closely related to the tumor size and the depth of tumor invasion. In addition, Rab1A expression was closely related with p-S6K/Gli1 expression in GC, and high level of Rab1A/p-S6K/Gli1 caused worse prognosis of GC patients. The univariate and multivariate analysis indicated that the expression of Rab1A was an independent prognostic factor. Moreover, both high Rab1A and p-S6K expression led to a worse prognosis when compared to a single positive expression as well as both high Rab1A/Gli1 expression also led to a worse prognosis than the single positive expression of Rab1A/Gli1. Strikingly, the overexpression of p-S6K also led to a worse prognosis in Rab1A positive patients, as did Gli1.Conclusion:Our results indicate that Rab1A/mTOR/S6K/Gli1 axis played a crucial role in GC, which may provide a novel field on targeted therapy of GC, especially for mTORC1-targeted therapy-resistant cancers.

scholarly journals Levels of Soluble CD30 and CD26 and Their Clinical Significance in Patients with Primary Immune Thrombocytopenia

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Honghui Wang ◽  
Xueping Gu ◽  
Huiyuan Li ◽  
Lingmei Yin ◽  
Wei Tao ◽  
...  
Keyword(s):  
Immune Thrombocytopenia ◽  
Patient Characteristics ◽  
Mrna Levels ◽  
Healthy Controls ◽  
Medical Sciences ◽  
Rt Pcr ◽  
Soluble Cd30 ◽  
Primary Immune Thrombocytopenia ◽  
Disease Hospital ◽  
The Relationship

Background. sCD30 and sCD26 are correlated with autoimmune diseases. However, little research has been done on the relationship between them and primary immune thrombocytopenia (ITP). Methods. This study enrolled 47 patients diagnosed with ITP in the Institute of Hematology and Blood Disease Hospital, Chinese Academy of Medical Sciences (Tianjin, China), from January 2015 to August 2015. The peripheral blood of all subjects was collected. The mRNA expression of CD30 was quantified by RT-PCR, and concentrations of sCD30 and sCD26 were measured by ELISA. Patient characteristics, CD30 mRNA levels, and sCD30 and sCD26 concentrations were analyzed. Results. The concentration of sCD30 was higher in active ITP patients (median, 35.82 ng/mL) than in remission ITP patients (median, 23.12 ng/mL; P=0.021) and healthy controls (median, 25.11 ng/mL; P=0.002). Plasma sCD26 levels decreased in remission ITP patients compared with that in healthy controls (median, 599.4 ng/mL vs. 964.23 ng/mL; P=0.004). Ratios of sCD26/sCD30 in active ITP patients decreased compared with those in controls (P=0.005). Increased sCD30 was positively correlated with hemorrhage (r=0.493, P=0.017) in ITP patients while little relationship was identified between sCD26 and ITP. Conclusion. Since sCD30 levels and sCD26/sCD30 ratios may contribute to the activity of the disease, they may be used to assess ITP disease activity.

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