Effects of L-Selenocystine on Mutual Crosstalk between Autophagy, Oxidative Stress and Inflammatory Responses in Human Colorectal Adenocarcinoma Cells

Project Details


Selenium (Se) is an essential and unique trace element that plays a vital role in health and disease. It is generally believed that Se turn into a pro-oxidant at lower concentrations in preneoplastic or tumor cells than those of in benign cells, hence tumor cells are more sensitive to Se supplementation. However, the precise molecular targets and mechanisms engaged following Se compounds treatment in various cancer models not in normal cells are still inconclusive. In Taiwan, colorectal cancer is one of the greatest frequently diagnosed cancers in recent years. It is in urgent need of discovery effective chemotherapy for colorectal cancer. ROS may mediate the colorectal carcinogenesis through gene mutations, redox related signaling pathways and redox related transcription factors. Interestingly, mechanistic studies showed that selenocystine time- and dose-dependently increased intracellular reactive oxygen species (ROS) in various susceptible cancer cells. It is worth to investigate whether selenocompound (L-selenocystine) act as effective chemotherapy and clarify precise molecular targets and mechanisms in colorectal cancer. Autophagy plays a dual role in tumorigenesis, which act as both tumor suppressor and tumor promoter. It has been proposed for the complexity of autophagy effects during cancer therapy, which involving vital roles of ROS, cell death or inflammations. Autophagy, ROS and inflammations may exist mutual crosstalk in tumor cell. Anti-autophagy therapy is an entirely new approach to cancer treatment. Our preliminary results show that L-selenocystine inhibited several autophagy associated proteins expression. Oxidative stress and inflammations occur after L-selenocystine treatment. In this study, we would like to determine the effects of L-Selenocystine on mutual crosstalk between autophagy, oxidative stress and inflammatory responses in human colorectal adenocarcinoma cells.
Effective start/end date1/08/2031/07/21

UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This project contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being
  • SDG 16 - Peace, Justice and Strong Institutions
  • SDG 17 - Partnerships for the Goals


  • L-Selenocystine
  • human colorectal adenocarcinoma cells
  • autophagy
  • oxidative stress
  • inflammatory responses


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