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We are analyzing https://link.springer.com/article/10.1007/s13277-016-5021-2.

Title:
Discoidin domain receptor 1 (DDR1), a promising biomarker, induces epithelial to mesenchymal transition in renal cancer cells | Tumor Biology
Description:
Discoidin domain receptor I (DDR1) is confirmed as a receptor tyrosine kinase (RTK), which plays a consequential role in a variety of cancers. Nevertheless, the influence of DDR1 expression and development in renal clear cell carcinoma (RCCC) are still not well corroborated. In our research, we firstly discovered that the expression level of DDR1 was remarkable related to TNM stage (p = 0.032), depth of tumor invasion (p = 0.047), and lymph node metastasis (p = 0.034) in 119 RCCC tissue samples using tissue microarray. The function of DDR1 was then evaluated in vitro using collagen I and DDR1 small interfering RNA (siRNA) to regulate the expression of DDR1 in OS-RC-2 and ACHN renal cancer cells (RCC). DDR1 expression correlated with increased RCC cell migration, invasion, and angiogenesis. Further study revealed that high expression of DDR1 can result in epithelial to mesenchymal transition (EMT) activation. Western blot assay showed that the N-cadherin protein and vimentin were induced while E-cadherin was reduced after DDR1 over expression. Our results suggest that DDR1 is both a prognostic marker for RCCC and a potential functional target for therapy.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,932 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We don't see any clear sign of profit-making.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {πŸ”}

pubmed, article, google, scholar, cas, cancer, receptor, cell, discoidin, ddr, domain, expression, central, tyrosine, biol, renal, cells, kinase, carcinoma, matrix, tumor, transition, metastasis, invasion, clin, exp, jiangsu, development, collagen, epithelialmesenchymal, vogel, res, human, privacy, cookies, content, research, liu, junnian, zheng, kinases, receptors, int, mol, med, xuzhou, function, information, publish, search,

Topics {βœ’οΈ}

month download article/chapter zoledronate-treated pc3 cells discoidin domain receptors jak2-erk1/2-mediated mechanism triple-negative breast cancer renal cell carcinoma receptor tyrosine kinase membrane-type matrix metalloproteinases renal cancer cells breast carcinoma cells full article pdf nonintegrin collagen receptors epithelial-mesenchymal transition er hepatocellular carcinoma cells privacy choices/manage cookies extracellular discoidin i postdoctoral research funds related subjects kinase-deficient variants published randomised trials n-cadherin protein article song assoc cancer res human gastric cancer mol cell biol sensing extracellular matrix clin cancer res pancreatic ductal adenocarcinoma angiogenic growth factors soc exp biol human brain tumors tumor biology junnian zheng promotes cell invasion european economic area retroviral insertional mutagenesis rat hippocampal neurons distinct structural characteristics arterial wound repair talent peaks project ethics declarations conflicts article log cancer metastasis rev conditions privacy policy exp ther med vogel wf small molecule inhibitors collagen i-mediated jiangsu planned projects potential functional target

Schema {πŸ—ΊοΈ}

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         description:Discoidin domain receptor I (DDR1) is confirmed as a receptor tyrosine kinase (RTK), which plays a consequential role in a variety of cancers. Nevertheless, the influence of DDR1 expression and development in renal clear cell carcinoma (RCCC) are still not well corroborated. In our research, we firstly discovered that the expression level of DDR1 was remarkable related to TNM stage (p = 0.032), depth of tumor invasion (p = 0.047), and lymph node metastasis (p = 0.034) in 119 RCCC tissue samples using tissue microarray. The function of DDR1 was then evaluated in vitro using collagen I and DDR1 small interfering RNA (siRNA) to regulate the expression of DDR1 in OS-RC-2 and ACHN renal cancer cells (RCC). DDR1 expression correlated with increased RCC cell migration, invasion, and angiogenesis. Further study revealed that high expression of DDR1 can result in epithelial to mesenchymal transition (EMT) activation. Western blot assay showed that the N-cadherin protein and vimentin were induced while E-cadherin was reduced after DDR1 over expression. Our results suggest that DDR1 is both a prognostic marker for RCCC and a potential functional target for therapy.
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      headline:Discoidin domain receptor 1 (DDR1), a promising biomarker, induces epithelial to mesenchymal transition in renal cancer cells
      description:Discoidin domain receptor I (DDR1) is confirmed as a receptor tyrosine kinase (RTK), which plays a consequential role in a variety of cancers. Nevertheless, the influence of DDR1 expression and development in renal clear cell carcinoma (RCCC) are still not well corroborated. In our research, we firstly discovered that the expression level of DDR1 was remarkable related to TNM stage (p = 0.032), depth of tumor invasion (p = 0.047), and lymph node metastasis (p = 0.034) in 119 RCCC tissue samples using tissue microarray. The function of DDR1 was then evaluated in vitro using collagen I and DDR1 small interfering RNA (siRNA) to regulate the expression of DDR1 in OS-RC-2 and ACHN renal cancer cells (RCC). DDR1 expression correlated with increased RCC cell migration, invasion, and angiogenesis. Further study revealed that high expression of DDR1 can result in epithelial to mesenchymal transition (EMT) activation. Western blot assay showed that the N-cadherin protein and vimentin were induced while E-cadherin was reduced after DDR1 over expression. Our results suggest that DDR1 is both a prognostic marker for RCCC and a potential functional target for therapy.
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