• HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
Saturday, September 6, 2025
BIOENGINEER.ORG
No Result
View All Result
  • Login
  • HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
  • HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
No Result
View All Result
Bioengineer.org
No Result
View All Result
Home Headlines

Starving cancer cells of sugar — does it work?

Bioengineer.org by Bioengineer.org
January 26, 2018
in Headlines, Health, Science News
Reading Time: 2 mins read
0
Share on FacebookShare on TwitterShare on LinkedinShare on RedditShare on Telegram
IMAGE

Credit: Duke-NUS Medical School

Previous research have shown that rapidly dividing cancer cells require higher levels of sugar than healthy cells. This dependency on sugar distinguishes cancer cells from normal cells and is often used as a treatment option to kill cancer cells. In reality, the results have not been encouraging. Not all cancer cell types are sensitive to the removal of sugar, and even for the cancers that are sensitive, sugar depletion only slows down the rate of cancer progression. The pathways that sensitise cancer cells to sugar deprivation remains poorly understood.

In the research led by Singapore team under Duke-NUS Associate Professor Koji Itahana, along with a team of collaborators led by Dr. Egon Ogris of the Max F. Perutz Laboratories (MFPL), in Austria, they have demonstrated for the first time a novel cell death pathway that describes how depletion of sugar caused cancer cell death. The article was published in Science Signaling's January issue [1].

Novel role of glucose

It was long believed that sugar served as one of the main energy sources for cancer cells. However, the team discovered that in some cancer cells, tiny levels of sugar that were incapable of providing sufficient energy ensured the survival of the cancer cells. This meant that there is a previously undiscovered role of sugar for survival, besides providing energy. The team subsequently found that sugar has a novel signalling function in cancer cells whereby its deprivation would trigger voltage differences across cancer cell membrane, leading to a flowing of calcium ions into the cells and subsequently cell death.

Novel therapeutic approach

The team speculated that this unique property of sugar in cancer cells could be manipulated for a novel therapeutic approach. By combining the inhibition of sugar intake and the increase of calcium levels in cancer cells, they managed to kill cancer cells while leaving healthy cells intact. Itahana and colleagues also found that certain cancer cells lost the ability to sustain intracellular sugar levels after sugar deprivation and speculated this to be the primary reason why not all cancer cells are sensitive to sugar deprivation. By applying the combination treatment to the suitable cancer cell types, this could be a novel treatment combination against cancer. The team aims to extend their results to develop a new cancer treatment in the future.

The new combination therapy based on this finding are on international patent application no. PCT/SG2017/050208 for "A potential combination therapy using an inhibitor of glucose transport and an intracellular calcium inducer to target cancer metabolism."

###

References

1. Lee HY, Itahana Y, Schuechner S, et al. Ca2+-dependent demethylation of phosphatase PP2Ac promotes glucose deprivation-induced cell death independently of inhibiting glycolysis. Science Signal 2018, 11(512):456. DOI: 10.1126/scisignal.aam7893

Media Contact

Serene Ong
[email protected]
65-660-13272
@dukenus

http://www.duke-nus.edu.sg

Original Source

http://stke.sciencemag.org/content/11/512/eaam7893 http://dx.doi.org/10.1126/scisignal.aam7893

Share12Tweet7Share2ShareShareShare1

Related Posts

Mecp2 Mutation Elevates Anxiety in Zebrafish, No Social Change

September 6, 2025
Mitochondrial Genomes of Prototheca: Insights and Comparisons

Mitochondrial Genomes of Prototheca: Insights and Comparisons

September 6, 2025

The Impact of Mendelian Randomization on Ischemic Stroke

September 6, 2025

Hippo-vgll3 Influences Atlantic Salmon’s Maturation by Sex

September 6, 2025
Please login to join discussion

POPULAR NEWS

  • blank

    Breakthrough in Computer Hardware Advances Solves Complex Optimization Challenges

    150 shares
    Share 60 Tweet 38
  • Molecules in Focus: Capturing the Timeless Dance of Particles

    142 shares
    Share 57 Tweet 36
  • New Drug Formulation Transforms Intravenous Treatments into Rapid Injections

    116 shares
    Share 46 Tweet 29
  • First Confirmed Human Mpox Clade Ib Case China

    54 shares
    Share 22 Tweet 14

About

We bring you the latest biotechnology news from best research centers and universities around the world. Check our website.

Follow us

Recent News

Mecp2 Mutation Elevates Anxiety in Zebrafish, No Social Change

Mitochondrial Genomes of Prototheca: Insights and Comparisons

The Impact of Mendelian Randomization on Ischemic Stroke

  • Contact Us

Bioengineer.org © Copyright 2023 All Rights Reserved.

Welcome Back!

Login to your account below

Forgotten Password?

Retrieve your password

Please enter your username or email address to reset your password.

Log In
No Result
View All Result
  • Homepages
    • Home Page 1
    • Home Page 2
  • News
  • National
  • Business
  • Health
  • Lifestyle
  • Science

Bioengineer.org © Copyright 2023 All Rights Reserved.