MiR-216a-5p inhibits tumorigenesis in Pancreatic Cancer by targeting TPT1/mTORC1 and is mediated by LINC01133

Jian Zhang1, Shuohui Gao2, Yandong Zhang1

  • 1Department of Hepatobiliary and Pancreas Surgery, Jilin University First Hospital, Changchun, China.

Insights

MicroRNA-216a-5p acts as a tumor suppressor in pancreatic cancer (PC), inhibiting growth and metastasis. Its downregulation is linked to advanced disease, suggesting potential diagnostic and therapeutic roles for the LINC01133/miR-216a-5p/TPT1 axis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • MicroRNA-216a-5p exhibits context-dependent roles in tumorigenesis.
  • Its specific function in pancreatic cancer (PC) remains largely uncharacterized.

Purpose of the Study:

  • To investigate the expression and functional role of miR-216a-5p in pancreatic cancer.
  • To elucidate the molecular mechanisms underlying miR-216a-5p's function in PC progression.

Main Methods:

  • Analysis of miR-216a-5p expression in PC tissues and cell lines.
  • In vitro and in vivo functional assays to assess cell growth and migration.
  • Bioinformatics analysis, luciferase reporter assays, and RNA pulldown assays to identify targets and regulatory interactions.

Main Results:

  • miR-216a-5p was significantly downregulated in PC tissues and correlated negatively with lymph node metastasis, perineural invasion, and TNM stage.
  • miR-216a-5p suppressed PC cell growth and migration in vitro and in vivo.
  • TPT1 was identified as a direct target of miR-216a-5p, mediating mTORC1 pathway-associated autophagy.
  • LINC01133 was confirmed to act as a competing endogenous RNA (ceRNA) sponging miR-216a-5p.

Conclusions:

  • The LINC01133/miR-216a-5p/TPT1 axis plays a critical role in the genesis and progression of pancreatic cancer.
  • miR-216a-5p functions as a tumor suppressor in PC.
  • This axis presents potential biomarkers for the clinical diagnosis and therapy of pancreatic cancer.

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