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Related Concept Videos

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Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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Related Experiment Video

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miRNA Expression Analyses in Prostate Cancer Clinical Tissues
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Vimentin 3 Expression in Prostate Cancer Cells.

Barbara KÖditz1, Andreas Stog2, Heike GÖbel3

  • 1University Hospital of Cologne, Faculty of Medicine and University Hospital Cologne, Department of Urology, Cologne, Germany; barbara.koeditz@uk-koeln.de.

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|January 9, 2021
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Vimentin3 (Vim3) expression increases in prostate cancer cell lines when endothelin B receptor (ETBR) is blocked or non-functional. This suggests Vim3 may serve as a novel tumor marker for prostate cancers with ETBR methylation.

Keywords:
Endothelin-1Prostate cancerVimentin 3

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Vimentin3 (Vim3) has been identified as a potential tumor marker for distinguishing between benign and malignant kidney tumors.
  • The role and regulation of Vim3 expression in prostate cancer (PCa) remain largely unexplored.
  • Endothelin receptors (ETRs) are implicated in various cancer processes, including cell proliferation and migration.

Purpose of the Study:

  • To investigate the expression of Vimentin3 (Vim3) in prostate cancer (PCa) cell lines.
  • To elucidate the regulatory role of endothelin receptors (ETRs) in Vim3 expression within PCa.
  • To assess the potential of Vim3 as a diagnostic marker for prostate cancer.

Main Methods:

  • Prostate cancer cell lines (PC3, DU145, LNCap) were treated with endothelin 1 (ET-1) and specific endothelin receptor antagonists (BQ123 for ETAR, BQ788 for ETBR).
  • Cell migration was assessed using a scratch assay.
  • Vim3 expression levels were quantified using western blotting and quantitative real-time PCR (qRT-PCR).

Main Results:

  • Endothelin 1 (ET-1) treatment led to the overexpression of Vim3 in prostate cancer cell lines.
  • Blocking the endothelin B receptor (ETBR) significantly increased cell migration rates.
  • Vim3 expression was markedly elevated in cell lines where ETBR function was inhibited or absent.

Conclusions:

  • Vim3 expression is upregulated in prostate cancer cells lacking functional endothelin B receptors (ETBRs).
  • The findings suggest a potential link between Vim3 expression and ETBR status in prostate cancer.
  • Vim3 may serve as a valuable tumor marker for identifying prostate cancers associated with ETBR methylation.