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  • 1.
    Lazarczyk, Marzena
    et al.
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, PL-05552 Jastrzebiec, Poland..
    Kurzejamska, Ewa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Neurooncology and neurodegeneration.
    Mickael, Michel-Edwar
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, PL-05552 Jastrzebiec, Poland..
    Poznanski, Piotr
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, PL-05552 Jastrzebiec, Poland..
    Skiba, Dominik
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, PL-05552 Jastrzebiec, Poland..
    Sacharczuk, Mariusz
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, PL-05552 Jastrzebiec, Poland.;Med Univ Warsaw, Ctr Preclin Res & Technol, Dept Pharmacodynam, PL-02091 Warsaw, Poland..
    Gaciong, Zbigniew
    Med Univ Warsaw, Dept Internal Med Hypertens & Vasc Dis, PL-02091 Warsaw, Poland..
    Religa, Piotr
    Karolinska Inst, Dept Med, S-17176 Stockholm, Sweden..
    Mouse CCL9 Chemokine Acts as Tumor Suppressor in a Murine Model of Colon Cancer2023In: Current Issues in Molecular Biology, ISSN 1467-3037, E-ISSN 1467-3045, Vol. 45, no 4, p. 3446-3461Article in journal (Refereed)
    Abstract [en]

    Colorectal cancer is the third most frequently diagnosed cancer in the world. Despite extensive studies and apparent progress in modern strategies for disease control, the treatment options are still not sufficient and effective, mostly due to frequently encountered resistance to immunotherapy of colon cancer patients in common clinical practice. In our study, we aimed to uncover the CCL9 chemokine action employing the murine model of colon cancer to seek new, potential molecular targets that could be promising in the development of colon cancer therapy. Mouse CT26.CL25 colon cancer cell line was used for introducing lentivirus-mediated CCL9 overexpression. The blank control cell line contained an empty vector, while the cell line marked as CCL9+ carried the CCL9-overexpressing vector. Next, cancer cells with empty vector (control) or CCL9-overexpressing cells were injected subcutaneously, and the growing tumors were measured within 2 weeks. Surprisingly, CCL9 contributed to a decline in tumor growth in vivo but had no effect on CT26.CL25 cell proliferation or migration in vitro. Microarray analysis of the collected tumor tissues revealed upregulation of the immune system-related genes in the CCL9 group. Obtained results suggest that CCL9 reveals its anti-proliferative functions by interplay with host immune cells and mediators that were absent in the isolated, in vitro system. Under specific study conditions, we determined unknown features of the murine CCL9 that have so far bee reported to be predominantly pro-oncogenic.

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  • 2.
    Lazarczyk, Marzena
    et al.
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, Postepu 36A, PL-05552 Garbatka, Poland..
    Mickael, Michel Edwar
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, Postepu 36A, PL-05552 Garbatka, Poland..
    Skiba, Dominik
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, Postepu 36A, PL-05552 Garbatka, Poland..
    Kurzejamska, Ewa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Neurooncology and neurodegeneration. Karolinska Inst, Dept Lab Med, Div Pathol, SE-14186 Stockholm, Sweden.
    Lawinski, Michal
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, Postepu 36A, PL-05552 Garbatka, Poland.;Med Univ Warsaw, Dept Gen Surg Gastroenterol & Oncol, PL-02091 Warsaw, Poland..
    Horbanczuk, Jaroslaw Olav
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Postepu 36A, PL-05552 Garbatka, Poland..
    Radziszewski, Jakub
    Siedlce Univ Nat Sci & Humanities, Fac Med & Hlth Sci, Stanislawa Konarskiego 2, PL-08110 Siedlce, Poland.;Jan Pawel II Mem Prov Mazov Hosp, Dept Oncol Surg, 26, Ksiec Jozefa Poniatowskiego, PL-08110 Siedlce, Poland..
    Fraczek, Karolina
    Med Univ Warsaw, Fac Pharm, Dept Pharmacodynam, Banacha 1B, PL-02091 Warsaw, Poland..
    Wolinska, Renata
    Med Univ Warsaw, Fac Pharm, Dept Pharmacodynam, Banacha 1B, PL-02091 Warsaw, Poland..
    Paszkiewicz, Justyna
    John Paul II Univ Appl Sci Biala Podlaska, Dept Hlth, Sidorska 95-97, PL-21500 Biala Podlaska, Poland..
    Religa, Piotr
    Karolinska Inst, Dept Med, SE-17177 Solna, Sweden..
    Sacharczuk, Mariusz
    Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Expt Genom, Postepu 36A, PL-05552 Garbatka, Poland.;Med Univ Warsaw, Fac Pharm, Dept Pharmacodynam, Banacha 1B, PL-02091 Warsaw, Poland..
    The Journey of Cancer Cells to the Brain: Challenges and Opportunities2023In: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 24, no 4, article id 3854Article, review/survey (Refereed)
    Abstract [en]

    Cancer metastases into the brain constitute one of the most severe, but not uncommon, manifestations of cancer progression. Several factors control how cancer cells interact with the brain to establish metastasis. These factors include mediators of signaling pathways participating in migration, infiltration of the blood-brain barrier, interaction with host cells (e.g., neurons, astrocytes), and the immune system. Development of novel therapies offers a glimpse of hope for increasing the diminutive life expectancy currently forecasted for patients suffering from brain metastasis. However, applying these treatment strategies has not been sufficiently effective. Therefore, there is a need for a better understanding of the metastasis process to uncover novel therapeutic targets. In this review, we follow the journey of various cancer cells from their primary location through the diverse processes that they undergo to colonize the brain. These processes include EMT, intravasation, extravasation, and infiltration of the blood-brain barrier, ending up with colonization and angiogenesis. In each phase, we focus on the pathways engaging molecules that potentially could be drug target candidates.

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  • 3.
    Mader, Theresa
    et al.
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden..
    Chaillou, Thomas
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden.;Örebro Univ, Sch Hlth Sci, Örebro, Sweden..
    Alves, Estela Santos
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden..
    Jude, Baptiste
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden..
    Cheng, Arthur J.
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden.;York Univ, Muscle Hlth Res Ctr, Sch Kinesiol & Hlth Sci, Fac Hlth Toronto, Toronto, ON, Canada..
    Kenne, Ellinor
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden..
    Mijwel, Sara
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden.;Karolinska Inst, Dept Neurobiol Care Sci & Soc, Stockholm, Sweden..
    Kurzejamska, Ewa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Vincent, Clara Theresa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. NYU, Dept Microbiol, Grossman Sch Med, New York, NY 10016 USA..
    Rundqvist, Helene
    Karolinska Inst, Dept Lab Med, Clin Physiol, Stockholm, Sweden..
    Lanner, Johanna T.
    Karolinska Inst, Dept Physiol & Pharmacol Mol Muscle Physiol & Pat, Solnavagen 9, SE-17177 Stockholm, Sweden..
    Exercise reduces intramuscular stress and counteracts muscle weakness in mice with breast cancer2022In: Journal of Cachexia, Sarcopenia and Muscle, ISSN 2190-5991, E-ISSN 2190-6009, Vol. 13, no 2, p. 1151-1163Article in journal (Refereed)
    Abstract [en]

    Background Patients with breast cancer exhibit muscle weakness, which is associated with increased mortality risk and reduced quality of life. Muscle weakness is experienced even in the absence of loss of muscle mass in breast cancer patients, indicating intrinsic muscle dysfunction. Physical activity is correlated with reduced cancer mortality and disease recurrence. However, the molecular processes underlying breast cancer-induced muscle weakness and the beneficial effect of exercise are largely unknown. Methods Eight-week-old breast cancer (MMTV-PyMT, PyMT) and control (WT) mice had access to active or inactive in-cage voluntary running wheels for 4 weeks. Mice were also subjected to a treadmill test. Muscle force was measured ex vivo. Tumour markers were determined with immunohistochemistry. Mitochondrial biogenesis and function were assessed with transcriptional analyses of PGC-1 alpha, the electron transport chain (ETC) and antioxidants superoxide dismutase (Sod) and catalase (Cat), combined with activity measurements of SOD, citrate synthase (CS) and beta-hydroxyacyl-CoA-dehydrogenase (beta HAD). Serum and intramuscular stress levels were evaluated by enzymatic assays, immunoblotting, and transcriptional analyses of, for example, tumour necrosis factor-alpha (TNF-alpha) and p38 mitogen-activated protein kinase (MAPK) signalling. Results PyMT mice endured shorter time and distance during the treadmill test (similar to 30%, P < 0.05) and ex vivo force measurements revealed similar to 25% weaker slow-twitch soleus muscle (P < 0.001). This was independent of cancer-induced alteration of muscle size or fibre type. Inflammatory stressors in serum and muscle, including TNF-alpha and p38 MAPK, were higher in PyMT than in WT mice (P < 0.05). Cancer-induced decreases in ETC (P < 0.05, P < 0.01) and antioxidant gene expression were observed (P < 0.05). The exercise intervention counteracted the cancer-induced muscle weakness and was accompanied by a less aggressive, differentiated tumour phenotype, determined by increased CK8 and reduced CK14 expression (P < 0.05). In PyMT mice, the exercise intervention led to higher CS activity (P = 0.23), enhanced beta-HAD and SOD activities (P < 0.05), and reduced levels of intramuscular stressors together with a normalization of the expression signature of TNF alpha-targets and ETC genes (P < 0.05, P < 0.01). At the same time, the exercise-induced PGC-1 alpha expression, and CS and beta-HAD activity was blunted in muscle from the PyMT mice as compared with WT mice, indicative that breast cancer interfere with transcriptional programming of mitochondria and that the molecular adaptation to exercise differs between healthy mice and those afflicted by disease. Conclusions Four-week voluntary wheel running counteracted muscle weakness in PyMT mice which was accompanied by reduced intrinsic stress and improved mitochondrial and antioxidant profiles and activities that aligned with muscles of healthy mice.

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