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A second place for a student of Silesian University of Technology in an international competition
Jakub Pawlikowski, a 4th year biotechnology student the at the Faculty of Automatic Control, Electronics and Computer Science of the Silesian University of Technology, took part in the Skin Ageing & Challenges Malta 2024 conference in November, where he took second place in the competition for the best poster presentation.
Silver poster
Jakub Pawlikowski and his colleague Łukasz Cienciała, together with their mentors, Dr Eng. Małgorzata Adamiec-Organiściok and MSc Eng. Magdalena Węgrzyn, represented the Student Science Club of Systems Engineering and Biology in the 15th edition of the international conference Skin Ageing & Challenges, which took place in Malta.
- “The conference brings together leading scientists and researchers to explore the latest developments in skin health, anti-aging, and cell rejuvenation. The main topics include cellular aging, mitochondrial function, microbiota influence, and iron regulation, each of which has significant implications for delaying or reversing skin aging,” explains Jakub Pawlikowski. “I was honoured to present my results on a poster entitled ‘Suppression of Thioredoxin reductase 1 in Keratinocyte Cell Line as a Key Regulator of the NRF2 Pathway’. The work reveals how TXNRD1 inhibition activates the NRF2 pathway, which plays a key role in protecting skin cells from oxidative damage. This work provides new insights into potential skin aging therapies and conditions associated with oxidative stress, including skin cancer.

Alarm in the building
The student of Silesian University of Technology took second place in the competition for the best poster and its presentation. This is a great success! He admits that his research is about a mechanism in cells, such as skin cells, which works a little on the principle of an alarm and protective system. He tries to explain his subject using the example of an alarm system in a building.
The key characters in this story are two “characters.” The first is TXNRD1, an enzyme that acts as a "guardian" of the chemical balance in the cell. It protects the cell from stress, but at the same time it can block the activation of the alarm system a little. The second is NRF2, a transcription protein, the commander of the protection system in the cell. When it receives a signal of danger, it activates repair mechanisms and protects the cell from destruction – explains the winner of the competition. - What happens when we stop TXNRD1? Turn off the "guard". The cell begins to feel stress – it’s a bit like turning off an alarm in a building. The chemical balance is disturbed, and the level of reactive molecules begins to rise. NRF2 activates in response to this stress and says: “We have to act!” It then triggers a series of defence processes that help the cell survive in these difficult conditions.

Jakub Pawlikowski explains that blocking the activation of the alarm system is a simplified but accurate statement. TXNRD1, through its antioxidant activity, can reduce the level of oxidative stress, which is a signal for NRF2 activation. When TXNRD1 is inhibited, the level of reactive oxygen species (RFT) increases, leading to the activation of NRF2, which helps the cell cope with oxidative stress – a type of “rusting” of the cell.
“However, if the stress is too high and the level of reactive molecules exceeds a certain threshold, the cell cannot cope. Ferroptosis is a controlled form of death of cells associated with uncontrolled damage to cell membranes by free radicals. It’s a bit like a decision to demolish a damaged building so that it doesn’t pose a threat to the environment. Throughout the process, it acts as a kind of catalyst that drives chemical reactions leading to damage in the cell. How is it proven? There is a technique whose author received the Nobel Prize. This is CRISPR/Cas9. I call it the molecular scissors method, because with it we can cut out the interesting fragment of the gene in the cell. In this way, we examined our control cells as well as cells after the gene was cut, a special substance erastin that initiates the process of ferroptosis.” – explains the fourth-year student. “This is a fairly new technique, and the very subject of ferroptosis, or cell death, is just coming into force in Poland. Perhaps in the future we will be able to modify cells in such a way as to create a kind of new cancer therapy. Thanks to this, there is a chance to reduce the side effects of chemotherapy and radiation. It would be a therapy that would only “kill” cancer cells.”