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Evaluation of anticancer potentials ofphysciosporin, a lichen-originated compound,in colorectal and breast cancer

Başlık çevirisi mevcut değil.

  1. Tez No: 719814
  2. Yazar: ISA TAS
  3. Danışmanlar: PROF. JAE-SEOUN, HUR, PROF. HANGUN KİM
  4. Tez Türü: Doktora
  5. Konular: Göğüs Hastalıkları, Onkoloji, Chest Diseases, Oncology
  6. Anahtar Kelimeler: Belirtilmemiş.
  7. Yıl: 2020
  8. Dil: İngilizce
  9. Üniversite: Sunchon National University
  10. Enstitü: Yurtdışı Enstitü
  11. Ana Bilim Dalı: Belirtilmemiş.
  12. Bilim Dalı: Belirtilmemiş.
  13. Sayfa Sayısı: 115

Özet

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Özet (Çeviri)

Lichens, which represent symbiotic associations of fungi and algae, are potential sources of numerous natural products. Physciosporin (PHY) is a potent secondary metabolite found in lichens and was recently reported to inhibit the motility of lung cancer cells via novel mechanisms. The present study investigated the anticancer potential of PHY on colorectal and breast cancer cells. PHY was isolated from lichen extract by preparative TLC. The effect of PHY on cell viability, motility and tumorigenicity was elucidated by MTT assay, hoechst staining, flow cytometric analysis, transwell invasion and migration assay, soft agar colony formation assay, Western blotting, qRT-PCR and PCR array in vitro as well as xi tumorigenicity study in vivo. In the first chapter, PHY decreased the viability of various colorectal cancer (CRC) cell lines (Caco2, CT26, DLD1, HCT116 and SW620). Moreover, PHY elicited cytotoxic effects by inducing apoptosis at toxic concentrations. At non-toxic concentrations, PHY dose-dependently suppressed the invasion, migration, and colony formation of CRC cells. PHY inhibited the motility of CRC cells by suppressing epithelial-mesenchymal transition and downregulating actin-based motility markers. In addition, PHY downregulated βcatenin and its downstream target genes cyclin-D1 and c-Myc. Moreover, PHY modulated KAI1 C-terminal-interacting tetraspanin and KAI1 expression and downregulated the downstream transcription factors c-jun and c-fos. Finally, PHY administration showed considerable bioavailability and effectively decreased the growth of CRC xenografts in mice without causing toxicity. Therefore, PHY suppresses the growth and motility of CRC cells via novel mechanisms. In the second chapter, effect of PHY was evaluated on breast cancer (BC) cells. we investigated the effects of PHY on growth, and metabolism of BC cells MCF-7 and MDA-MB-231. Our results indicated that PHY markedly inhibits BC cell growth. Cell cycle analysis and Annexin V-FITC/PI double staining showed that the toxic concentration of PHY induced the apoptosis on BC cells through the mitochondrial apoptotic pathway via the regulation of Bcl-2 family proteins BAX and Bcl-xL. In non-toxic concentration, PHY potently decreased the ability of migration, proliferation, and tumorigenesis in BC cells. Metabolic investigation xii revealed that PHY treatment significantly diminished the bioenergetic profile by reducing the glucose uptake, ATP generation, and lactate production. Moreover, PHY alters glucose metabolism-related gene expressions such as Glut1 and PKM2 and downregulated transcription factors and oncogenes related with PKM2 including β-catenin, c-Myc, HIF-1, NF-κB and STAT3. Orthotopic implantation mouse model of BC further confirmed that PHY treatment suppressed BC growth. In conclusion, present results indicated that PHY possessed significant anticancer activity against BC and CRC cell lines in vitro. Furthermore, PHY inhibited tumor growth in orthotopic and skin xenograft mouse models, respectively. Together, these findings suggest that PHY has a potential further in vivo application as an anti-proliferative, anti-glycolytic and anti-tumorigenic agent

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