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miR-143 decreases COX-2 mRNA stability and expression in pancreatic cancer cells

Hung Pham1, C Ekaterina Rodriguez, Graham W Donald

  • 1Department of Surgery, UCLA Center of Excellence in Pancreatic Diseases, UCLA David Geffen School of Medicine, University of California - Los Angeles, Los Angeles, CA 90095, United States; Department of Medicine, Veterans Affair Greater Los Angeles Healthcare System, Los Angeles, CA 90073, United States.

Biochemical and Biophysical Research Communications
|August 27, 2013
PubMed

Insights

Restoring microRNA-143 (miR-143) in pancreatic cancer cells suppresses tumor growth by inhibiting cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2). This study reveals miR-143 as a key regulator in pancreatic cancer progression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by targeting messenger RNAs (mRNAs).
  • Dysregulated miRNA expression is implicated in various cancers, including pancreatic cancer (PaCa).
  • PaCa is characterized by decreased miRNA, elevated cyclooxygenase-2 (COX-2), and increased prostaglandin E2 (PGE2), promoting tumor growth and metastasis.

Purpose of the Study:

  • To investigate the role of miRNA-143 (miR-143) in regulating COX-2 and cell proliferation in pancreatic cancer.
  • To explore the relationship between miR-143, COX-2, PGE2, and MEK/MAPK signaling in PaCa.

Main Methods:

  • Utilized human PaCa cell lines to assess miR-143 levels and its correlation with COX-2, PGE2, and MEK/MAPK activation.
  • Administered MEK inhibitors (U0126, PD98059) to observe effects on miR-143 expression.
  • Performed miR-143 transfection to evaluate its impact on COX-2 mRNA stability, COX-2 expression, cell proliferation, and PGE2 levels.

Main Results:

  • Restoration of miR-143 in PaCa cells significantly inhibited cell proliferation and decreased COX-2 and PGE2 levels.
  • miR-143 transfection reduced COX-2 mRNA stability and suppressed MEK/MAPK activation.
  • Low miR-143 levels correlated with elevated MEK/MAPK activation in specific PaCa cell lines.

Conclusions:

  • Restoring miR-143 expression in pancreatic cancer cells effectively suppresses tumor growth, proliferation, and metastasis.
  • miR-143 acts as a tumor suppressor by downregulating COX-2, PGE2, and MEK/MAPK signaling pathways.
  • These findings highlight miR-143 as a potential therapeutic target for pancreatic cancer treatment.
Keywords:
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromideCOX-2CREBCyclooxygenase-2MAPKMAPK kinaseMEKMTTPGE(2)PKAPaCaPancreatic cancerProstaglandin E(2)RREB1cyclic AMP responsive element binding proteincyclooxygenase-2miR-143microRNA-143mitogen-activated protein kinasepancreatic cancerprostaglandin E(2)protein kinase Aras responsive element binding protein

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