Arja Katrina Lea Arnesen Løchen

• Løchen, Arja Katrina Lea Arnesen; Søreng, Kristiane; Veroni, Chiara; Moncho, Laura Cristina Trachsel; Asp, Nagham Theres & Gaupset, Robin [Show all 10 contributors for this article] (2026). Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy. Molecular Oncology. ISSN 1574-7891. doi: 10.1002/1878-0261.70248. Full text in Research Archive Show summary

  The HCLS1-Binding Protein 3 (HS1BP3) interacts with the SH3 domain of cortactin (CTTN), a protein that contributes to a malignant phenotype in cancers. Here, we demonstrate that high expression of HS1BP3 is associated with reduced survival for gastric adenocarcinoma and triple negative breast carcinoma patients and that HS1BP3 is specifically upregulated in these cancers. We mapped the HS1BP3-cortactin interaction site to the third proline-rich region (PRR3.1) of HS1BP3 and show that this interaction is important for cancer cell proliferation, extracellular matrix degradation and secretion. HS1BP3 expression was found to correlate with expression of the invadopodia scaffold protein TKS5 and we show that the localisation of TKS5 inside multivesicular endosomes is increased in cells expressing an HS1BP3 PRR3.1 mutant. Overall, our results highlight the importance of the direct interaction between HS1BP3 and cortactin in cancer development by regulating cell proliferation, secretion and invasion, which may provide an explanation for the negative correlation between HS1BP3 levels and the survival of gastric adenocarcinoma and triple negative breast cancer patients.

• Collard, France; Strøm, Hallvard; Fayet, Marie-Océane; Gudmundsson, Fannar Theyr; Herzke, Dorte & Hotvedt, Ådne [Show all 10 contributors for this article] (2023). Evaluation of meso- and microplastic ingestion by the northern fulmar through a non-lethal sampling method. Marine Pollution Bulletin. ISSN 0025-326X. 196. doi: 10.1016/j.marpolbul.2023.115646. Full text in Research Archive Show summary

  An increasing number of organisms from the polar regions are reported contaminated by plastic. Rarely a non-killing sampling method is used. In this study we wanted to assess plastic levels using stomach flushing and evaluate the method suitability for further research and monitoring. The stomach of 22 fulmars from Bjørnøya, Svalbard, were flushed with water in the field. On return to the laboratory, the regurgitated content was digested using potassium hydroxide. The extracted plastics were visually characterised and analysed with spectroscopy. Only three birds had plastics in their stomach, totaling 36 particles, most of them microplastics (< 5 mm). The plastic burdens are much lower than previously reported in Svalbard. The stomach flushing is assumed not to allow the collection of the gizzard content. This is a major limitation as most of the plastics accumulate in the fulmar's gizzard. However, the method is still useful for studies investigating plastic ingestion dynamics, allowing to sample the same individuals over time.

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• Løchen, Arja Katrina Lea Arnesen (2026). Identification and characterisation of autophagy regulators in health and disease. Universitetet i Oslo. ISSN 9788234808845. Full text in Research Archive Show summary

  Autophagy is the eukaryotic cell’s renovation and degradation system and is essential for cellular homeostasis. In brief, this process is regulated by a core autophagy machinery that promotes the biogenesis of a double-membraned vesicle that isolates cellular content destined for degradation in the lysosome. The selective autophagy of mitochondria, known as mitophagy, involves specific mitochondrial determinants that interact with the core autophagy machinery for efficient mitochondrial degradation. The major aims of this thesis were to characterise the molecular mechanisms of hypoxia-induced mitophagy, with a specific focus on how discrete mitochondrial subdomains may be differentially targeted to this pathway. Furthermore, an aim was to identify novel mitophagy regulators and characterise the role of autophagy and mitophagy regulators in a cancer setting. In conclusion, the work done across the three articles in this thesis demonstrated the fascinating diversity of autophagy molecular mechanisms. The two first articles included comprehensive high-throughput analyses on original datasets and identified novel mitophagy regulators in hypoxia. Further cell biological characterisations illustrated that there are differential mechanisms and paths of hypoxia-induced mitophagy. The third article characterised an autophagy regulator in cancer conditions and demonstrated its importance in cancer development via interactions to non-autophagy pathways. Overall, this work contributes to the unravelling of autophagy molecular mechanisms and may be important in further developing a fundamental understanding of cellular health and disease.

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