scholarly journals In vivo imaging of lymph node metastasis with telomerase-specific replication-selective adenovirus

2006 ◽  
Vol 12 (10) ◽  
pp. 1213-1219 ◽  
Author(s):  
Hiroyuki Kishimoto ◽  
Toru Kojima ◽  
Yuichi Watanabe ◽  
Shunsuke Kagawa ◽  
Toshiya Fujiwara ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
In Vivo Imaging ◽  
Node Metastasis

scholarly journals The levels of NF-κB p50 and NF-κB p65 play a role in thyroid carcinoma malignancy in vivo

2018 ◽  
Vol 46 (10) ◽  
pp. 4092-4099 ◽  
Author(s):  
Fei Le ◽  
Jing-Yu Zhang ◽  
Wei Liu ◽  
Xian-Ming Huang ◽  
Wen-Zheng Luo
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Thyroid Carcinoma ◽  
Negative Group ◽  
Positive Group ◽  
Node Metastasis ◽  
Tumour Diameter ◽  
Tumour Characteristics ◽  
The Relationship

Background To investigate the relationship between the levels of nuclear factor (NF)-κB p50 and NF-κB p65 and tumour characteristics in patients with thyroid carcinoma. Methods This prospective study enrolled consecutive patients with thyroid carcinoma. Tumour samples were collected and the levels of NF-κB p50 and NF-κB p65 protein and mRNA were measured using immunohistochemistry and quantitative real-time reverse transcription–polymerase chain reaction (qRT–PCR). Results A total of 73 patients with thyroid carcinoma were included in the study (20 males; 53 females; mean ± SD age, 44.8 ± 12.7 years, range, 18–76 years). There were no significant differences in sex, age and pathological type between the NF-κB p50 positive group and the NF-κB p50 negative group, but tumour diameter and lymph node metastasis were significantly higher in the NF-κB p50 positive group compared with the NF-κB p50 negative group. Similar findings were observed for NF-κB p65. The levels of NF-κB p50 were positively correlated with NF-κB p65 in samples of thyroid carcinoma ( rs = 0.653). Conclusion The levels of NF-κB p50 and NF-κB p65 in samples of thyroid carcinoma were positively associated with tumour diameter and the presence of lymph node metastasis.

scholarly journals Cir-ITCH inhibits gastric cancer migration, invasion and proliferation by regulating the Wnt/β-catenin pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yang Peng ◽  
Hong Hong Wang
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Cancer Prognosis ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Node Metastasis ◽  
Cancer Tissues

Abstract Circular RNAs (circRNAs) are differentially expressed in various tumours, but the expression and regulatory mechanisms of circular RNA ITCH (cir-ITCH) in gastric cancer remain unclear. For this reason, in the present study, we assessed the expression of cir-ITCH and the associated regulatory mechanism of cir-ITCH in gastric cancer. Through RTq-PCR assays, we observed that cir-ITCH expression was attenuated in gastric cancer cell lines and tissues, with cir-ITCH expression in gastric cancer tissues with lymph node metastasis being considerably lower than that observed in gastric cancer tissues without lymph node metastasis. In addition, we demonstrated that cir-ITCH or linear ITCH may be a useful marker for gastric cancer prognosis by Kaplan–Meier survival analysis. We also showed that cir-ITCH overexpression could increase linear ITCH expression through miR-17 via RNA immunoprecipitation (RIP) and luciferase reporter assays. Moreover, in vivo and in vitro experimental results showed that cir-ITCH can act as a tumour suppressor to prevent gastric cancer tumourgenesis by sponging miR-17. The Wnt/β-catenin pathway plays a crucial role during the carcinogenesis of cancers, and we observed that cir-ITCH could negatively regulate Wnt/β-catenin signalling, which could be restored by miR-17. In summary, cir-ITCH was shown to prevent gastric cancer tumourgenesis through the Wnt/β-catenin signalling pathway by sequestering miR-17.

scholarly journals TOPK promotes metastasis of esophageal squamous cell carcinoma by activating the Src/GSK3β/STAT3 signaling pathway via γ-catenin

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yanan Jiang ◽  
Jing Zhang ◽  
Jimin Zhao ◽  
Zhenzhen Li ◽  
Hanyong Chen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Lymph Node ◽  
Protein Kinase ◽  
Lymph Node Metastasis ◽  
Esophageal Squamous Cell Carcinoma ◽  
Erk Signaling ◽  
Node Metastasis

Abstract Background Esophageal squamous cell carcinoma (ESCC) is a fatal disease with poor prognosis. The predominant reason for ESCC-related death is distal metastasis. A comprehensive understanding of the molecular mechanism underlying metastasis is needed for improving patient prognosis. T-LAK cell-originated protein kinase (TOPK) is a MAPKK-like kinase, which plays a vital role in various physiological and pathophysiological processes. However, the role of TOPK in ESCC metastasis is unclear. Methods Tissue array was used to evaluate the correlation between TOPK expression and ESCC lymph node metastasis. Wound healing assay, transwell assay, and lung metastasis mice model were used to examine the role of TOPK in the migration of ESCC cells in vitro and in vivo. Protein kinase array, mass spectrometry (MS), and molecular modeling were used to examine the pathways and direct target proteins of TOPK that are involved in ESCC metastasis. Additionally, immunofluorescence and western blotting analyses were performed to verify these findings. Results The enhanced expression of TOPK was correlated with lymph node metastasis in the ESCC tissues. TOPK knockdown or treatment with the TOPK inhibitor (HI-TOPK-032) decreased the invasion and migration of ESCC cells in vitro. HI-TOPK-032 also inhibited the lung metastasis in ESCC cell xenograft in vivo model. Moreover, TOPK promoted the invasion of ESCC cells by activating the Src/GSK3β/STAT3 and ERK signaling pathways via γ-catenin. Conclusion The findings of this study reveal that TOPK is involved in ESCC metastasis and promoted the ESCC cell mobility by activating the Src/GSK3β/STAT3 and ERK signaling pathways. This indicated that TOPK may be a potential molecular therapeutic target for ESCC metastasis.

scholarly journals CXCR7 promotes migration and invasion in head and neck squamous cell carcinoma by upregulating TGF-β1/Smad2/3 signaling

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nayoung Kim ◽  
Hyewon Ryu ◽  
Solbi Kim ◽  
Mina Joo ◽  
Heung Jin Jeon ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Tgf Β1

AbstractThe chemokine receptor CXCR7 has been suggested to play important roles in the progression of several types of cancers. However, few studies have investigated the biological roles of CXCR7 in head and neck squamous cell carcinoma (HNSCC). CXCR7 expression and its clinical implications were examined in 103 HNSCC tissues using immunohistochemistry (IHC). The biological roles and mechanisms of CXCR7-mediated signaling pathways were investigated in HNSCC cells through CXCR7 overexpression in vitro and in vivo. High expression of CXCR7 was significantly associated with tumor size (P = 0.007), lymph node metastasis (P = 0.004), and stage (P = 0.020) in HNSCC. Overexpression of CXCR7 in HNSCC cells enhanced cell migration and invasion in vitro and promoted lymph node metastasis in vivo. CXCR7 also induced epithelial–mesenchymal transition through PI3K/AKT. CXCR7 increased secretion of transforming growth factor-β1 (TGF-β1) and promoted EMT through phosphorylated Smad2/3. Taken together, our results provide functional and mechanistic roles of CXCR7 as a master regulator of oncogenic TGF-β1/Smad2/3 signaling in HNSCC, suggesting that CXCR7 might be a therapeutic target for the treatment of HNSCC.

scholarly journals VEGF-c expression in an in vivo model of orthotopic endometrial cancer and retroperitoneal lymph node metastasis

2013 ◽  
Vol 11 (1) ◽  
pp. 49 ◽  
Author(s):  
Yong-Wen Huang ◽  
Li-Qun Xu ◽  
Rong-Zhen Luo ◽  
Xin Huang ◽  
Teng Hou ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
In Vivo Model ◽  
Retroperitoneal Lymph Node ◽  
Node Metastasis
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