Nasi Ulam Betawi, a specialty of Betawi people of Jakarta, Indonesia prepared with kencur ginger – credit Gunawan Kartapranata CC 3.0. BY-SA

An active compound in ginger root may inhibit the growth of cancer tumors via a sabotage of their metabolic pathways.

Published in Nature Scientific Reports by a team at Osaka Metropolitan University (OMU), the study demonstrated that a ginger-derived molecule known as EMC shuts down the cells’ fat-making machinery, causing it to activate backup systems and potentially become vulnerable to detection or treatment.

Despite a century of serious innovation and research into cancer and its prevention and treatment, we still don’t fully understand a cancer tumor’s diet so to speak.

A cancer’s key characteristic is its ability to reprogram normal energy metabolism to sustain the uncontrolled proliferation that allows it to spread through the organism. This leads to distinct metabolic traits compared to normal cells, among which has been the nearly 100-year-old supposition that cancers rely on glycolysis for primary energy production—an observation known as the Warburg effect.

For readers who remembered their high school biology textbook, glycolysis is the process of turning stored energy (glycogen) into available energy (glucose).

The authors note however that cancer metabolism is subject to ongoing research, and they themselves present in their paper evidence of cancer cells relying on de novo fatty acid synthesis to sustain their growth.

Metabolically speaking, fatty acids produce more energy per molecule than sugars, but instead of using fatty acids from food, the cancer cells produce their own, hence the Latin descriptor “de novo,” or “of new creation.”

Associate Professor Akiko Kojima-Yuasa at OMU, analyzed ethyl p-methoxycinnamate or EMC, a main component of kencur ginger, found commonly in Indonesian, Chinese, and Thai cuisine, for an inhibitory effect on cancer cells—something which his team had previously uncovered.

This time, the team was specifically hoping to see if its inhibitory effect was related to cancer metabolism. Results revealed that the acid ester inhibits energy production by disrupting de novo fatty acid synthesis and fat metabolism, rather than through glycolysis as commonly theorized.

Further, the researchers discovered application of the EMC triggered increased glycolysis, which they supposed was a survival mechanism in the cells.

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“These findings not only provide new insights that supplement and expand the theory of the Warburg effect, which can be considered the starting point of cancer metabolism research, but are also expected to lead to the discovery of new therapeutic targets and the development of new treatment methods,” stated Professor Kojima-Yuasa.

A cell-cycle checkpoint is a moment in the life cycle of a cell when, following a period of growth and DNA synthesis, a control mechanism determines whether to further grow the cell or terminate it.

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Cancers need tremendous energy to fuel their growth, and the authors write that when conditions of an energy deficit are detected at a cell-cycle checkpoint, it’s a common red flag that can lead to the cell cycle being arrested or terminated altogether.

Knocking out the primary method of energy generation may help highlight an energy deficit at a cell-cycle checkpoint during the early stages of malignancy, though this was not investigated in the study.

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