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Regulation of pancreatic cancer cells by suppressing KIN17 through the PI3K/AKT/mTOR signaling pathway

Qiuyan Li1, Yuxia Yang1, Xiaocong Lin2

  • 1Department of Medical Laboratory, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524000, P.R. China.

Oncology Reports
|January 10, 2025
PubMed

Insights

High KIN17 expression in pancreatic cancer correlates with poor prognosis. Inhibiting KIN17 suppresses cancer cell migration and invasion, suggesting it as a potential therapeutic target for pancreatic cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Pancreatic cancer exhibits aggressive behavior, poor prognosis, and chemotherapy resistance, necessitating novel therapeutic markers.
  • The role of the DNA- and RNA-binding protein KIN17 in pancreatic cancer progression remains largely unknown.
  • Identifying new biomarkers is crucial for improving clinical outcomes in pancreatic cancer patients.

Purpose of the Study:

  • To investigate the role of KIN17 in pancreatic cancer development and progression.
  • To determine if KIN17 can serve as a prognostic biomarker for pancreatic cancer.
  • To explore KIN17 as a potential therapeutic target in pancreatic cancer.

Main Methods:

  • Bioinformatic analysis of The Cancer Genome Atlas and Gene Expression Omnibus databases to verify KIN17 upregulation.
  • Immunohistochemistry to correlate KIN17 expression with pathological features in clinical samples.
  • In vitro experiments involving KIN17 knockdown to assess its effects on cell migration, invasion, and epithelial-mesenchymal transition (EMT).
  • Investigation of KIN17's role in the PI3K/Akt/mTOR pathway and autophagy.

Main Results:

  • KIN17 was found to be upregulated in pancreatic cancer tissues.
  • KIN17 expression correlated with patient prognosis and pathological features.
  • Knockdown of KIN17 inhibited pancreatic cancer cell migration and invasion, reversing EMT by altering Vimentin, N-cadherin, and E-cadherin levels.
  • KIN17 inhibition suppressed cell motility via PI3K/AKT/mTOR-mediated autophagy.
  • Combined KIN17 and mTOR inhibition enhanced autophagy, leading to anti-migratory and anti-invasion effects.

Conclusions:

  • KIN17 upregulation plays a role in pancreatic cancer carcinogenesis and progression.
  • KIN17 serves as a potential prognostic biomarker for pancreatic cancer due to its high expression.
  • KIN17 represents a promising therapeutic target, as its inhibition effectively reduces pancreatic cancer cell motility and invasion.
Keywords:
EMTKIN17PI3K/AKT/mTORpancreatic cancer

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