Journals / Harran Üniversitesi Tıp Fakültesi Dergisi / 2016 / Cilt: 13 - Sayı: 1

The Role in Tumor Process of Endoplasmic Reticulum Stress and Anticancer Treatments

Endoplazmik Retikulum Stresinin Tümör Sürecindeki Rolü ve Antikanser Uygulamaları

Pages
124–133
Publication Date
2016-04-28
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this review, knowledge shed light on our understanding about roles of UPR on both tumor sustaining and suppression and also new strategies targeting unfolded protein response for the treatment of cancer will be discussed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Endoplasmic reticulum stress resulted from accumulation of unfolded or misfolded proteins have a large impact on proliferation and survival of cancer cell.
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Key Findings & Data:Several studies have shown that during this process, cells could activate unfolded protein response as a survival strategy.
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Conclusion & Impact:In this review, knowledge shed light on our understanding about roles of UPR on both tumor sustaining and suppression and also new strategies targeting unfolded protein response for the treatment of cancer will be discussed.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Endoplazmik Retikulum stresi · katlanmamış protein yanıtı · kanser

Abstract

Endoplasmic reticulum stress resulted from accumulation of unfolded or misfolded proteins have a large impact on proliferation and survival of cancer cell. In order to grow, tumor cells need a hypoxic environment and stimulation of the unfolded protein response plays a key role in this response. The emergence and progression of the cancer under stressful microenvironment lead to oncogenic transformation. Several studies have shown that during this process, cells could activate unfolded protein response as a survival strategy. Recent studies have focused on relationship between unfolded protein response signal molecules and cancer development; and association between various oncogenes and tumor suppressor genes with unfolded protein response have been emerging. Detailed studies that will help us to understand the effect of signalling pathways on each other's, are very important to figure out the unfolded protein response and cancer mechanism. In this review, knowledge shed light on our understanding about roles of UPR on both tumor sustaining and suppression and also new strategies targeting unfolded protein response for the treatment of cancer will be discussed.

Özet

Katlanmamış ya da yanlış katlanmış proteinlerin birikimi sonucu ortaya çıkan Endoplazmik retikulum stresi, kanser hücre çoğalması ve sağkalımı üzerinde büyük bir etkiye sahiptir. Tümör hücreleri büyümek için etraflarında hipoksik bir çevreye ihtiyaç duyarlar ve katlanmamış protein yanıtı 'nın uyarılması bu yanıtta kilit bir rol oynar. Kanserin stresli bir mikroçevrede oluşması ve ilerlemesi sonucunda ortaya çıkan onkogenik transformasyon süresince hücrelerin sağkalım stratejisi olarak katlanmamış protein yanıtını aktive edebildiği çeşitli çalışmalarla gösterilmiştir. Son zamanlarda katlanmamış protein yanıtı sinyal moleküllerinin kanser gelişimi boyunca fonksiyonlarının belirlenmesi için çalışmalar yürütülmektedir. Elde edilen verilerle, çeşitli onkogen ve tümör baskılayıcı genlerin katlanmamış protein yanıtı ile ilişkisi ortaya çıkmaya devam etmektedir. Bu sinyal yolaklarının birbirlerini etkileyip etkilemediklerini anlamamıza fayda sağlayacak detaylı çalışmalar, katlanmamış protein yanıtı ve kanser mekanizmasının açığa çıkmasında oldukça önemlidir. Bu derlemede katlanmamış protein yanıtı aktivasyonunun hem tümörü destekleyen hem de tümörü baskılayan rollerini anlamamıza ışık tutacak bilgilerin yanında kanser tedavisi için katlanmamış protein yanıtını hedefleyen yeni stratejilerin neler olduğu tartışılacaktır.

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Cite This Article

Çetinkaya, S., Çınar, İ., Dursun, H. G. (2016). The Role in Tumor Process of Endoplasmic Reticulum Stress and Anticancer Treatments. Harran Üniversitesi Tıp Fakültesi Dergisi, Cilt: 13 - Sayı: 1, 124–133. https://ajindex.com/articles/104257

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References (17)

  1. Ackerman D, Simon MC. Hypoxia, lipids, and cancer: surviving the harsh tumor microenvironment. Trends Cell Biol. 2014; 24(8):472-8
  2. Sutherland RM, Ausserer WA, Murphy BJ, Laderoute KR. Tumor hypoxia and heterogeneity: challenges and opportunities for the future. Semin Radiat Oncol. 1996; 6:59–70
  3. Höckel M, Vaupel P. Tumor hypoxia: definitions and current clinical, biologic, and molecular aspects. J Natl Cancer Inst. 2001; 93(4):266-76
  4. Schröder M, Kaufman RJ. The mammalian unfolded protein response. Annu Rev Biochem. 2005; 74: 739–89
  5. Ratcliffe PJ, O'Rourke JF, Maxwell PH, Pugh CW. Oxygen sensing, hypoxia-inducible factor-1 and the regulation of mammalian gene expression. J. Exp. Biol. 1998; 201, 1153-1162
  6. Semenza GL. Targeting HIF-1 for cancer therapy. Nature Rev. Cancer. 2003; 3, 721–732
  7. Hill RP, De Jaeger K, Jang A, Cairns R. pH, hypoxia and metastasis. Novartis Found. Symp. 2001; 240, 154- 165
  8. Cairns RA, Hill RP. Acute hypoxia enhances spontaneous lymph node metastasis in an orthotopic murine model of human cervical carcinoma. Cancer Res. 2004; 64, 2054-2061
  9. Koumenis C. ER Stress, Hypoxia Tolerance and Tumor Progression. Current Molecular Medicine. 2006; 6, 55-69
  10. Wouters BG, Koritzinsky M. Hypoxia signalling through mTOR and the unfolded protein response in cancer. Nat Rev Cancer. 2008; 8(11):851–64
  11. Kelly CJ, Hussien K, Fokas E, Kannan P, Shipley RJ, Ashton TM, Stratford M, Pearson N, Muschel RJ. Regulation of O2 consumption by the PI3K and mTOR pathways contributes to tumor hypoxia. Radiother Oncol. 2014;111(1):72-80
  12. Edinger AL, Linardic CM, Chiang GG, Thompson CB, Abraham RT. Differential effects of rapamycin on mammalian target of rapamycin signaling functions in mammalian cells. Cancer Res. 2003; 63, 8451–8460
  13. Brugarolas J, Lei K, Hurley RL, Manning BD, Reiling JH, Hafen E, Witters LA, et al. Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. Genes Dev. 2004; 18, 2893–2904
  14. Inoki K, Zhu T, Guan K.L. TSC2 mediates cellular energy response to control cell growth and survival. Cell. 2003; 115, 577–590
  15. Walter P, Ron D. The unfolded protein response: from stres pathway to homeostatic regulation. Science. 2011; 334, 1081–1086
  16. Li XC, Raghavan M. Structure and function of major histo compatibility complex class I antigens. Curr Opin Organ Transplant. 2010; 15(4):499–504
  17. Gutiérrez T, Simmen T. Endoplasmic reticulum chaperones and oxidor