CO suppresses prostate cancer cell growth by directly targeting LKB1/AMPK/mTOR pathway in vitro and in vivo

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Updated: Feb 12, 2026

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
07:16

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Published on: March 14, 2014

14.7K

Yutao Yan1, Caiqi Du2, Guohao Li3

  • 1Institute of Organ, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan China; Key Laboratory of Organ Transplantation, Ministry of Health, China; Key Laboratory of Organ Transplantation, Ministry of Education, China.

Urologic Oncology
|March 24, 2018
PubMed
Abstract

Insights

Carbon monoxide (CO) demonstrates significant anticancer effects in prostate cancer cells by inhibiting proliferation and invasion. This action is primarily mediated through the LKB1-AMPK-mTOR signaling pathway, impacting tumor growth both in vitro and in vivo.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Carbon monoxide (CO) is a gasotransmitter with known anticancer properties in various cancer types.
  • The specific effects and underlying mechanisms of CO on prostate cancer remain largely unexplored.
  • This study investigates the antitumor potential of CO in prostate cancer models.

Purpose of the Study:

  • To evaluate the anticancer activities of CO in human prostate cancer cell lines (LNCaP and PC-3) in vitro.
  • To elucidate the molecular mechanisms by which CO exerts its antitumor effects, focusing on the LKB1 signaling pathway.
  • To assess the efficacy of CO in suppressing prostate cancer growth in a preclinical in vivo model.

Main Methods:

  • Cell viability and ATP production assays (CCK-8) were used to assess proliferation.
  • Flow cytometry and Western blotting were employed to evaluate apoptosis and related protein expression (Caspases).
  • In vitro invasion assays and in vivo xenograft tumor models were utilized to determine CO's impact on tumor invasion and growth.

Main Results:

  • CO significantly inhibited prostate cancer cell proliferation and invasion while inducing apoptosis.
  • CO treatment upregulated LKB1 expression, increased p-AMPK levels, and decreased p-mTOR.
  • LKB1 knockdown diminished CO's antitumor effects, and CO suppressed tumor growth in vivo.

Conclusions:

  • Carbon monoxide exhibits potent anticancer effects against human prostate cancer cells.
  • The observed antitumor activity is largely mediated by the LKB1-AMPK-mTOR signaling pathway.
  • CO represents a promising therapeutic agent for prostate cancer treatment.
Keywords:
ApoptosisCOInvasionLKB1Prostate cancer

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