Clinical and experimental role of ring finger protein 180 on lymph node metastasis and survival in gastric cancer

2016 ◽  
Vol 103 (4) ◽  
pp. 407-416 ◽  
Author(s):  
J. Deng ◽  
H. Liang ◽  
R. Zhang ◽  
Y. Hou ◽  
Y. Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Ring Finger ◽  
Ring Finger Protein ◽  
Node Metastasis ◽  
Finger Protein

Role of intraoperative assessment of lymph node metastasis and serosal invasion in patients with gastric cancer

1994 ◽  
Vol 55 (4) ◽  
pp. 250-254 ◽  
Author(s):  
Daisuke Korenaga ◽  
Toshiro Okuyama ◽  
Hiroyuki Orita ◽  
Hideaki Anai ◽  
Hideo Baba ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Serosal Invasion ◽  
Node Metastasis ◽  
Intraoperative Assessment

scholarly journals circCOL6A3_030 is involved in the metastasis of gastric cancer by encoding polypeptide

2020 ◽  
Author(s):  
Wensheng Pan ◽  
Xiaoge Geng ◽  
Jingya Wang ◽  
Chenjing Zhang ◽  
Xiaolu Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Cell Lines ◽  
Human Life ◽  
Pcr Analysis ◽  
Small Peptide ◽  
Node Metastasis ◽  
Distant Lymph Node Metastasis

Abstract Background Gastric cancer (GC) is a serious digestive tract disease that threatens human life worldwide, and the prognosis of gastric cancer accompanied by distant lymph node or the distant metastasis organs is worse. The purpose of this study was to investigate the role of circular RNA COL6A3_030 (circBase ID: hsa_circ_0006401; circRNADb ID: hsa_circ_28198; circBank ID: hsa_circCOL6A3_030) in GC metastasis. Methods qRT-PCR analysis using back-splicing primers and Sanger sequencing of PCR products were performed to identify circCOL6A3_030 in GC tissues and cell lines; RNA-FISH assay was performed to validate the subcellular localization of circCOL6A3_030. Transwell and wound-healing assays were carried out to evaluate the migration ability of GC cells. Western blot was conducted to detect the polypeptide encoded by circCOL6A3_030 in cells. Results circCOL6A3_030 was down-regulated in GC tissues and cell lines, while circCOL6A3_030 was up-regulated in GC with distant lymph node metastasis. The migration of circCOL6A3_030 silenced GC cells was significantly inhibited in both SGC-7901 and BGC-823 cell lines. Importantly, in vivo assay, silencing circCOL6A3_030 could reduce liver metastases from gastric cancer cells. Meanwhile, further studies suggested that circCOL6A3_030 encoded a small peptide that had a function as a tumor-promoting metastasis factor and immunohistochemistry confirmed the presence of this polypeptide. Conclusions To sum up, our study showed that circCOL6A3_030 promoted GC cell migration by encoding a small peptide called circCOL6A3_030_198aa. Therefore, our results highlight the potential role of circCOL6A3_030 for clinical diagnosis and treatment of GC with distant lymph node metastasis.

scholarly journals Long noncoding RNA CCAT1 rs67085638 SNP contribution to the progression of gastric cancer in a Polish population

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tomasz Olesiński ◽  
Anna Lutkowska ◽  
Adam Balcerek ◽  
Anna Sowińska ◽  
P Piotrowski ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Insertion Site ◽  
Leukaemia Virus ◽  
Node Metastasis ◽  
Melting Analysis

AbstractThe role of the long noncoding RNA CCAT1 NC_000008.10:g.128220661C > T (rs67085638) in the development of colon cancer has been reported. Therefore, we assessed the prevalence of rs67085638 in patients with gastric cancer (GC). We also evaluated the effect of rs67085638 on B-cell-specific Moloney leukaemia virus insertion site 1 (BMI1) transcripts in primary GC and counterpart histopathologically confirmed disease-free margin tissue. Using high-resolution melting analysis, we evaluated rs67085638 frequency in patients with the GC genotype (n = 214) and controls (n = 502) in a Polish Caucasian population. qRT-PCR was used to determine BMI1 transcripts. We observed the trend of rs67085638 association in all patients with GC (ptrend = 0.028), a strong risk of the GC genotype in male (ptrend = 0.035) but not female (ptrend = 0.747) patients, and the association with non-cardia GC (ptrend = 0.041), tumour stages T3 (ptrend = 0.014) and T4 (ptrend = 0.032), differentiation grading G3 (ptrend = 0.009), lymph node metastasis stage N3 (ptrend = 0.0005) and metastasis stage M0 (ptrend = 0.027). We found that significantly increased BMI1 transcripts were associated with the primary GC genotype classified as grade G3 (p = 0.011) and as lymph node metastasis N3 (p = 0.010) and counterpart marginal tissues (p = 0.026, p = 0.040, respectively) from carriers of the T/T versus C/C genotypes. rs67085638 may contribute to increased BMI1 transcripts and the progression and rapid growth of GC.

scholarly journals UHRF1 mediates cell migration and invasion of gastric cancer

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Haixia Zhang ◽  
Yanli Song ◽  
Changqing Yang ◽  
Xianzheng Wu
Keyword(s):  
Gastric Cancer ◽  
Ring Finger ◽  
Migration And Invasion ◽  
Ros Generation ◽  
Ring Finger Protein ◽  
Caspase 9 ◽  
Sgc7901 Cell ◽  
Finger Protein ◽  
Underlying Mechanisms

Gastric cancer (GC) is a common highly aggressive malignant tumor in worldwide. Ubiquitin-like with PHD and ring-finger protein 1 (UHRF1) has a key role in several kinds of cancers development. However, the biology effect of UHRF1 on the tumorigenesis of GC remains unclear. In this research, the role of UHRF1 in the growth, migration, invasion and apoptosis and the underlying mechanisms were investigated in MGC803 and SGC7901 cells. The UHRF1 knockdown MGC803 and SGC7901 cell lines were used to investigate the roles of UHRF1 on GC cell growth, migration, invasion and apoptosis. The growth, migration and invasion rate of UHRF1 knockdown cells was lower than that of the control. Moreover, ROS generation and caspase-3/caspase-9 activities increased in UHRF1 knockdown cells. And mitochondrial membrane potential decreased in UHRF1 knockdown cells. These findings indicated that UHRF1 promoted the growth, migration and invasion of MGC803 and SGC7901 cells and inhibited apoptosis via a ROS-associated pathway.

scholarly journals Role of D2 gastrectomy in gastric cancer with clinical para-aortic lymph node metastasis

2019 ◽  
Vol 25 (19) ◽  
pp. 2338-2353 ◽  
Author(s):  
Xiao-Hao Zheng ◽  
Wen Zhang ◽  
Lin Yang ◽  
Chun-Xia Du ◽  
Ning Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
D2 Gastrectomy ◽  
Node Metastasis ◽  
Aortic Lymph Node

scholarly journals Lymph node metastasis-derived gastric cancer cells educate bone marrow-derived mesenchymal stem cells via YAP signaling activation by exosomal Wnt5a

Oncogene ◽  
2021 ◽  
Vol 40 (12) ◽  
pp. 2296-2308
Author(s):  
Mei Wang ◽  
Xinxin Zhao ◽  
Rong Qiu ◽  
Zheng Gong ◽  
Feng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Metastatic Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Node Metastasis ◽  
Signaling Activation

AbstractLymph node metastasis (LNM), a common metastatic gastric-cancer (GC) route, is closely related to poor prognosis in GC patients. Bone marrow-derived mesenchymal stem cells (BM-MSCs) preferentially engraft at metastatic lesions. Whether BM-MSCs are specifically reprogrammed by LNM-derived GC cells (LNM-GCs) and incorporated into metastatic LN microenvironment to prompt GC malignant progression remains unknown. Herein, we found that LNM-GCs specifically educated BM-MSCs via secretory exosomes. Exosomal Wnt5a was identified as key protein mediating LNM-GCs education of BM-MSCs, which was verified by analysis of serum exosomes collected from GC patients with LNM. Wnt5a-enriched exosomes induced YAP dephosphorylation in BM-MSCs, whereas Wnt5a-deficient exosomes exerted the opposite effect. Inhibition of YAP signaling by verteporfin blocked LNM-GC exosome- and serum exosome-mediated reprogramming in BM-MSCs. Analysis of MSC-like cells obtained from metastatic LN tissues of GC patients (GLN-MSCs) confirmed that BM-MSCs incorporated into metastatic LN microenvironment, and that YAP activation participated in maintaining their tumor-promoting phenotype and function. Collectively, our results show that LNM-GCs specifically educated BM-MSCs via exosomal Wnt5a-elicited activation of YAP signaling. This study provides new insights into the mechanisms of LNM in GC and BM-MSC reprogramming, and will provide potential therapeutic targets and detection indicators for GC patients with LNM.

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