scholarly journals AGTR1 promotes lymph node metastasis in breast cancer by upregulating CXCR4/SDF-1α and inducing cell migration and invasion

Aging ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 3969-3992 ◽  
Author(s):  
Yuxi Ma ◽  
Zihan Xia ◽  
Chunmei Ye ◽  
Chong Lu ◽  
Sheng Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Node Metastasis

The study on functions and mechanisms of miR-106b in the metastasis of colorectal cancer.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e14685-e14685
Author(s):  
Shujuan Ni ◽  
Qifeng WANG ◽  
Cong Tan ◽  
Xiang Du
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Molecular Mechanisms ◽  
Tumour Progression ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Node Metastasis ◽  
Study Results

e14685 Background: Emerging evidence has shown that aberrantly expressed microRNAs (miRNAs) are highly associated with tumour initiation, development and progression. However, little is known about the potential role of miRNAs in colorectal cancer (CRC) metastasis. Methods: The miR-106b expression levels in CRC tissues were deteted by quantitative reverse transcription polymerase chain reaction (qRT-PCR) to investigate its relationship with clinical characteristics or survival of CRC patients. Using the CRC cell lines ectopically expressing miR-106b conducted by lentivirus transduction as experimental material, cell culture, cell growth analysis and transwell used to analyze the potential influence of miR-106b on CRC metastasis. In addition, luciferase assays and western blot were used for the target gene study. Results: In this study, we firstly investigate the role and related mechanism of miR-106b in CRC metastasis. We found that miR-106b expression was lower than in CRC compared with their corresponding non-tumorous tissues (P=0.009), and the downregulated miR-106b was negatively associated with lymph-node metastasis. Functional assays demonstrated that overexpression of miR-106b suppressed CRC cell migration and invasion in vitro. In addition, we confirmed that ATAD2 was a direct and functional target of miR-106b. Overexpression of miR-106b in CRC cells could reduce the mRNA and protein levels of ATAD2, whereas miR-106b silencing significantly increased ATAD2 expression. Luciferase assays confirmed that miR-106b could directly bind to 3′ untranslated region of ATAD2. Knockdown of ATAD2 significantly inhibited CRC cell migration and invasion. We further found that ATAD2 was involved in miR-106b-induced suppression of CRC cell migration and invasion. Conclusions: By understanding the functions and molecular mechanisms of miR-106b in CRC, we found mir-106b through targeting ATAD2 inhibited CRC cell migration and invasion. These results suggest that patients with downregulated miR-106b are prone to lymph node metastasis and tumour progression. miR-106b may have a therapeutic potential to suppress CRC metastasis.

scholarly journals CCL18 Induces EMT via CEP192 Down-Regulation in Breast Cancer

2020 ◽  
Author(s):  
Zichao Wu ◽  
Xinrong Ke ◽  
Yanli Liu ◽  
Yihong Dong ◽  
Jingqi Chen
Keyword(s):  
Breast Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Western Blot ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Critical Role ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Mesenchymal Transformation

Abstract Background: Chemokine (C-C motif) ligand 18 (CCL18) secreted by TAMs induces epithelial-mesenchymal transformation (EMT) in breast cancer cells. Centrosome scaffold protein KDA192 (CEP192) ,as the important pericentriolar material (PCM), plays a critical role in microtubule nucleation and centrosome replication. Decreased expression of CEP192 will cause tumor cell polarization and elevated motility. Whether CEP192 is involved in the process of breast cancer EMT induced by CCL18 has not been reported.Methods: CEP192 mRNA level in Lymph node metastasis and non-lymph node metastasis breast cancer was evaluated by bioinformatics analysis. CCL18 and CEP192 expressions in breast tissues were examined using immunochemistry, CEP192 expression in breast cancer cells was examined using qPCR and Western blot. CEP192 was silenced using siRNA. EMT phenotype proteins were examined using Western blot. Statistical analysis was performed using GraphPad Prism 8.0 (GraphPad Software Inc).Results: CEP192 expression was decreased in lymph node metastasis breast cancer tissues compared with non-lymph node metastasis. CEP192 expression was down-regulated by CCL18 in breast cancer cells and silencing CEP192 promoted the migration and invasion of cancer cells. Based on the promotion of breast cancer EMT by CCL18, silencing CEP192 in breast cancer further increased E-cadherin and decreased KRT-8which are both EMT phenotype proteins in vitro.Conclusions: Our study elucidates that CCL18 promotes breast cancer EMT by down-regulating CEP192 expression. Down-regulated CEP192 plays a key role in invasion and migration of breast cancer cells. CEP192 is a potential new marker for tumor metastasis induced by CCL18.

scholarly journals Association of CASC18/miR-20a-3p/TGFB2 ceRNA axis with occult lymph node metastasis in tongue squamous cell carcinoma

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Bo Zhou ◽  
Yue Zhou ◽  
Ying Liu ◽  
Hailin Zhang ◽  
Huangxing Mao ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Cell Carcinoma ◽  
Molecular Mechanism ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Occult Lymph Node Metastasis

Abstract Background Tongue squamous cell carcinoma (TSCC) ranks as the most prevalent malignancy in the oral cavity. TSCC patients with occult lymph node metastasis (OLNM) are thought to be at risk of worse outcome. However, regulatory mechanisms underlying OLNM remain less investigated. Methods In the present study, CASC18/miR-20a-3p/TGFB2 axis was identified and evaluated by bioinformatic and qRT-PCR analyses. Effects of CASC18 knockdown on cell migration and invasion were determined by wound healing and transwell assays. Western blot, ELISA, RNA pulldown and luciferase reporter assays were performed for mechanism verification. Results CASC18 was identified up-regulating in TSCC tumours, and especially in those from patients with OLNM. Importantly, we found higher CASC18 expression was positively correlated with the presence of OLNM and worse outcome of TSCC patients. Furthermore, we demonstrated that CASC18 knockdown repressed cell migration and invasion through inhibiting epithelial-mesenchymal transition, which could be partly rescued by miR-20a-3p inhibitor. Regarding the molecular mechanism, we further confirmed that CASC18 functioned as a ceRNA to sponge miR-20a-3p to enhanceTGFB2 expression and secretion. Conclusion In conclusion, we have reported a novel CASC18/miR-20a-3p/TGFB2 ceRNA axis in OLNM of TSCC. Our findings will contribute to a deeper understanding of the molecular mechanism of OLNM in TSCC, and facilitate the development of diagnostic methods for assisting treatment decision-making.

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