Researcher:
Peker, Nesibe

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Nesibe

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Peker

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Peker, Nesibe

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2021 - 20225

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Researcher Of Publications: search.filters.isAuthorOfPublication.7f51100a-22eb-487e-b8e1-f8a4865f60f6

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Now showing 1 - 5 of 5
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    Comparative analysis of autophagy in drug responses and aggressive behavior of adult versus pediatric glioma cell lines
    (Wiley, 2022) Aygun, Bera; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; Yenidoğan, İrem; Peker, Nesibe; Deveci, Gamze; Kırmızı, Döndü; Asarcıklı, Fikret; Sözmen, Banu Oflaz; Akyoldaş, Göktuğ; Kulaç, İbrahim; Solaroğlu, İhsan; Erbey, Mehmet Fatih; Gözüaçık, Devrim; Researcher; Researcher; PhD Student; Other; Doctor; Faculty Member; Faculty Member; Faculty Member; Faculty Member; Faculty Member; Faculty Member; N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; School of Medicine; N/A; Graduate School of Health Sciences; N/A; N/A; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; N/A; N/A; Koç University Hospital; N/A; N/A; N/A; N/A; N/A; 327591; N/A; N/A; N/A; N/A; 198711; 203677; 102059; 206213; 40248
    Central nervous system tumors are the most common solid cancer and a leading cause of cancer-related deaths in children. Glioma is the most challenging pediatric CNS tumor with therapy resistance and poor prognosis in pediatric patients. Although histopathological analyses revealed similarities with adult brain glioma, emerging evidence suggests that the deregulated molecular pathways in pediatric glioma (p-GM) are different from that of adults. Autophagy, a cellular clearance system and a drug resistance mechanism, has been implicated in glioma progression, invasion, and relapse, yet its role in pediatric patients is not well documented. In this study, we compared the autophagic capacity of adult versus p-GM cell lines and evaluated the effect of autophagy manipulation on drug responses. In addition, migration, extracellular matrix invasion ability, and the metabolism of pediatric and adult gliomas were compared and the contribution of autophagy to the aggressive phenotype was evaluated.
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    PublicationOpen Access
    Autophagy and cancer dormancy
    (Frontiers, 2021) Akçay, Arzu; Akkoç, Yunus; Peker, Nesibe; Gözüaçık, Devrim; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; N/A; N/A; 40248
    Metastasis and relapse account for the great majority of cancer-related deaths. Most metastatic lesions are micro metastases that have the capacity to remain in a non-dividing state called "dormancy" for months or even years. Commonly used anticancer drugs generally target actively dividing cancer cells. Therefore, cancer cells that remain in a dormant state evade conventional therapies and contribute to cancer recurrence. Cellular and molecular mechanisms of cancer dormancy are not fully understood. Recent studies indicate that a major cellular stress response mechanism, autophagy, plays an important role in the adaptation, survival and reactivation of dormant cells. In this review article, we will summarize accumulating knowledge about cellular and molecular mechanisms of cancer dormancy, and discuss the role and importance of autophagy in this context.
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    PublicationOpen Access
    Parkin deficiency exacerbates fasting-induced skeletal muscle wasting in mice
    (Nature Portfolio, 2022) Sharma, Mridula; Kambadur, Ravi; Peker, Nesibe; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM)
    Parkinson's Disease (PD) is a chronic and progressive neurodegenerative disease manifesting itself with tremors, muscle stiffness, bradykinesia, dementia, and depression. Mutations of mitochondria! E3 ligase, PARKIN, have been associated with juvenile PD. Previous studies have characterized muscle atrophy and motor deficits upon loss of functional Parkin in fly and rodent models. However, the mechanisms behind pathophysiology of Parkin deficient muscle remains to be elusive. Here, results suggested that knock down of Parkin significantly increases proteolytic activities in skeletal muscle cell line, the C2C12 myotubes. However, the atrogene levels increase moderately in Parkin deficient cell line. To further investigate the role of Parkin in skeletal muscle atrophy, Parkin knock out (KO) and wild type mice were subjected to 48 h starvation. After 48 h fasting, a greater reduction in skeletal muscle weights was observed in Parkin KO mice as compared to age matched wild type control, suggesting elevated proteolytic activity in the absence of Parkin. Subsequent microarray analyses revealed further enhanced expression of FOXO and ubiquitin pathway in fasted Parkin KO mice. Furthermore, a greater reduction in the expression of cytoskeleton genes was observed in Parkin KO mice following 48 h fasting. Collectively, these results suggest that Parkin deficiency exacerbates fasting-induced skeletal muscle wasting, through upregulating genes involved in catabolic activities in skeletal muscle.
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    PublicationOpen Access
    Novel protein complexes containing autophagy and UPS components regulate proteasome-dependent PARK2 recruitment onto mitochondria and PARK2-PARK6 activity during mitophagy
    (Springer Nature, 2022) Kocatürk, Nur Mehpare; Eberhart, Karin; Deveci, Gamze; Dengjel, Joern; Akkoç, Yunus; Peker, Nesibe; Gözüaçık, Devrim; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; N/A; N/A; 40248
    Autophagy is an evolutionarily conserved eukaryotic cellular mechanism through which cytosolic fragments, misfolded/aggregated proteins and organelles are degraded and recycled. Priming of mitochondria through ubiquitylation is required for the clearance the organelle by autophagy (mitophagy). Familial Parkinson's Disease-related proteins, including the E3-ligase PARK2 (PARKIN) and the serine/threonine kinase PARK6 (PINK1) control these ubiquitylation reactions and contribute to the regulation of mitophagy. Here we describe, novel protein complexes containing autophagy protein ATG5 and ubiquitin-proteasome system (UPS) components. We discovered that ATG5 interacts with PSMA7 and PARK2 upon mitochondrial stress. Results suggest that all three proteins translocate mitochondria and involve in protein complexes containing autophagy, UPS and mitophagy proteins. Interestingly, PARK2 and ATG5 recruitment onto mitochondria requires proteasome components PSMA7 and PSMB5. Strikingly, we discovered that subunit of 20 S proteasome, PSMA7, is required for the progression of PARK2-PARK6-mediated mitophagy and the proteasome activity following mitochondrial stress. Our results demonstrate direct, dynamic and functional interactions between autophagy and UPS components that contribute to the regulation of mitophagy.
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    PublicationOpen Access
    Transcriptional landscape of cellular networks reveal interactions driving the dormancy mechanisms in cancer
    (Nature Publishing Group (NPG), 2021) Uzuner, Dilara; Pir, Pınar; Çakır, Tunahan; Akkoç, Yunus; Peker, Nesibe; Gözüaçık, Devrim; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; N/A; N/A; 40248
    Primary cancer cells exert unique capacity to disseminate and nestle in distant organs. Once seeded in secondary sites, cancer cells may enter a dormant state, becoming resistant to current treatment approaches, and they remain silent until they reactivate and cause overt metastases. To illuminate the complex mechanisms of cancer dormancy, 10 transcriptomic datasets from the literature enabling 21 dormancy-cancer comparisons were mapped on protein-protein interaction networks and gene-regulatory networks to extract subnetworks that are enriched in significantly deregulated genes. The genes appearing in the subnetworks and significantly upregulated in dormancy with respect to proliferative state were scored and filtered across all comparisons, leading to a dormancy-interaction network for the first time in the literature, which includes 139 genes and 1974 interactions. The dormancy interaction network will contribute to the elucidation of cellular mechanisms orchestrating cancer dormancy, paving the way for improvements in the diagnosis and treatment of metastatic cancer.