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THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS

Yıl 2025, Cilt: 27 Sayı: 1, 111 - 119, 26.04.2025

Eser Çakmak , Birşen Bilgici

https://doi.org/10.24938/kutfd.1607213

Öz

The endoplasmic reticulum (ER) plays a central role in critical cellular processes such as protein synthesis, folding, and lipid biosynthesis. ER stress is triggered by the accumulation of misfolded proteins and activates the Unfolded Protein Response (UPR) pathways to ensure cell survival. The UPR attempts to restore ER homeostasis through sensors such as PKR-like ER Kinase (PERK), Inositol-Requiring Enzyme 1 (IRE1), and Activating Transcription Factor 6 (ATF6). However, prolonged or severe ER stress can lead to cell death by triggering apoptosis. In cancer cells, factors such as hypoxia, nutrient deprivation, and oxidative stress in the tumor microenvironment contribute to chronic ER stress. Under these conditions, activation of the UPR supports cancer cell survival, while excessive ER stress can induce apoptosis. The role of ER stress and the UPR in cancer progression is complex due to their dual effects in both promoting tumor growth and triggering apoptosis. For instance, the IRE1α-X-Box Binding Protein 1 (XBP1) and PERK-Eukaryotic Translation Initiation Factor 2α (eIF2α)- Activating Transcription Factor 4 (ATF4) pathways can enhance survival and chemoresistance in cancer cells, while pro-apoptotic signals such as C/EBP Homologous Protein (CHOP) and c-Jun N-Terminal Kinase (JNK) can trigger cell death. Understanding this balance offers new targets for cancer therapy. Proteasome inhibitors and other agents that increase ER stress have therapeutic potential by inducing apoptosis in cancer cells. This review examines the molecular mechanisms of ER stress, the UPR, and ER stress-induced apoptosis, discussing how these processes can be manipulated in cancer cells and how new treatment strategies can be developed. Targeting ER stress pathways may represent a promising approach, particularly for chemoresistant tumors.

Anahtar Kelimeler

Endoplasmic reticulum stress unfolded protein response apoptosis cell survival cancer

Kaynakça

  • Szegezdi E, Logue SE, Gorman AM, Samali A. Mediators of endoplasmic reticulum stress-induced apoptosis. EMBO Rep. 2006;7(9):880-885.
  • Celik C, Lee SYT, Yap WS, Thibault G. Endoplasmic reticulum stress and lipids in health and diseases. Prog Lipid Res. 2023;89:101198.
  • Hussain SG, Ramaiah KVA. Endoplasmic reticulum: Stress, signalling and apoptosis. Current Sci. 2007;93:1684-1696.
  • Rasheva VI, Domingos PM. Cellular responses to endoplasmic reticulum stress and apoptosis. Apoptosis. 2009;14(8):996-1007.
  • Kim I, Xu W, Reed JC. Cell death and endoplasmic reticulum stress: Disease relevance and therapeutic opportunities. Nat Rev Drug Discov. 2008;7(12):1013- 1030.
  • Giampietri C, Petrungaro S, Conti S, Facchiano A, Filippini A, Ziparo E. Cancer microenvironment and endoplasmic reticulum stress response. Mediators Inflamm. 2015;2015:417281.
  • Patra D, Bhavya K, Ramprasad P, Kalia M, Pal D. Anti- cancer drug molecules targeting cancer cell cycle and proliferation. Adv Protein Chem Struct Biol. 2023;135:343-395.
  • Brown JM, Attardi LD. The role of apoptosis in cancer development and treatment response. Nat Rev Cancer. 2005;5(3):231-237.
  • Chen X, Cubillos-Ruiz JR. Endoplasmic reticulum stress signals in the tumour and its microenvironment. Nat Rev Cancer. 2021;21(2):71-88.
  • Oakes SA. Endoplasmic reticulum stress signaling in cancer cells. Am J Pathol. 2020;190(5):934-946.
  • Koumenis C. ER stress, hypoxia tolerance and tumor progression. Curr. Mol. Med. 2006;6:55-69.
  • Young RM, Ackerman D, Quinn ZL et al. Dysregulated mTORC1 renders cells critically dependent on desaturated lipids for survival under tumor-like stress. Genes Dev. 2013;27(10):1115-1131.
  • Koumenis C, Wouters BG. "Translating" tumor hypoxia: Unfolded protein response (UPR)-dependent and UPR- independent pathways. Mol Cancer Res. 2006;4(7):423- 436.
  • Denzel MS, Antebi A. Hexosamine pathway and (ER) protein quality control. Curr Opin Cell Biol. 2015;33:14- 18.
  • Pakos-Zebrucka K, Koryga I, Mnich K, Ljujic M, Samali A, Gorman AM. The integrated stress response. EMBO Rep. 2016;17(10):1374-1395.
  • Park J, Morley TS, Kim M, Clegg DJ, Scherer PE. Obesity and cancer -- mechanisms underlying tumour progression and recurrence. Nat. Rev. Endocrinol. 2014;10:455-465
  • Wei Y, Wang D, Topczewski F, Pagliassotti MJ. Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells. Am J Physiol Endocrinol Metab. 2006;291(2):E275- E281.
  • Görlach A, Bertram K, Hudecova S, Krizanova O. Calcium and ROS: A mutual interplay. Redox Biol. 2015;6:260-271.
  • Vladykovskaya E, Sithu SD, Haberzettl P et al. Lipid peroxidation product 4-hydroxy-trans-2-nonenal causes endothelial activation by inducing endoplasmic reticulum stress. Biol Chem. 2012;287(14):11398-11409.
  • Babour A, Bicknell AA, Tourtellotte J, Niwa M. A surveillance pathway monitors the fitness of the endoplasmic reticulum to control its inheritance. Cell. 2010;142(2):256-269.
  • Walter P, Ron D. The unfolded protein response: From stress pathway to homeostatic regulation. Science. 2011;334(6059):1081-1086.
  • Lai E, Teodoro T, Volchuk A. Endoplasmic reticulum stress: Signaling the unfolded protein response. Physiology. 2007;22:193-201.
  • Ghobrial IM, Witzig TE, Adjei AA. Targeting apoptosis pathways in cancer therapy. CA Cancer J Clin. 2005;55(3):178-194.
  • Fulda S, Debatin KM. Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy. Oncogene. 2006;25(34):4798-4811.
  • Hetz C, Zhang K, Kaufman RJ. Mechanisms, regulation and functions of the unfolded protein response. Nat Rev Mol Cell Biol. 2000;21(8):421-438.
  • Schroder M, Kaufman RJ. The mammalian unfolded protein response. Annu Rev Biochem. 2005;74,739-789.
  • Colgan SM, Hashimi AA, Austin RC. Endoplasmic reticulum stress and lipid dysregulation. Expert Rev Mol Med. 2011;13:e4.
  • Harding HP, Zhang Y, Zeng H et al. An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. Mol Cell. 2003;11:619-633.
  • Harding HP, Novoa I, Zhang Yet al. Regulated translation initiation controls stress-induced gene expression in mammalian cells. Mol Cell. 2000;6:1099- 1108.
  • Hollien J, Lin JH, Li H, Stevens N, Walter P, Weissman JS. Regulated Ire1-dependent decay of messenger RNAs in mammalian cells. J Cell Biol. 2009;186:323-331.
  • Lee AH, Iwakoshi NN, Glimcher LH. XBP-1 regulates a subset of endoplasmic reticulum resident chaperone genes in the unfolded protein response. Mol Cell Biol. 2003;23:7448-7459.
  • Urano F, Wang X, Bertolotti A et al. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Science. 2000;287:664-666.
  • Qu L, Liu Z, Zhang HM, Su Y, Ye X. Endoplasmic reticulum stress-induced cell survival and apoptosis. JCCM. 2009;8:1-4.
  • Chen X, Shi C, He M, Xiong S, Xia X. Endoplasmic reticulum stress: Molecular mechanism and therapeutic targets. Signal Transduct Target Ther. 2023;8(1):352.
  • Novoa I, Zeng H, Harding HP, Ron D. Feedback inhibition of the unfolded protein response by GADD34- mediated dephosphorylation of eIF2alpha. J Cell Biol. 2001;153:1011-1022.
  • Sevier CS, Kaiser CA. Ero1 and redox homeostasis in the endoplasmic reticulum. Biochim Biophys Acta. 2008;1783(4):549-556.
  • Tabas I, Ron D. Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress. Nat Cell Biol. 2011;13(3):184-190.
  • Vandewynckel YP, Laukens D, Geerts A et al. The paradox of the unfolded protein response in cancer. Anticancer Res. 2013;33(11):4683-4694.
  • Leibowitz B, Yu J. Mitochondrial signaling in cell death via the Bcl-2 family. Cancer Biol Ther. 2010;9(6):417- 422.
  • Germain M, Mathai JP, McBride HM, Shore GC. Endoplasmic reticulum BIK initiates DRP1-regulated remodelling of mitochondrial cristae during apoptosis. EMBO J. 2005;24(8):1546-1556.
  • Degterev A, Boyce M, Yuan J. A decade of caspases.Oncogene. 2003;22(53):8543-8567.
  • Parrish AB, Freel CD, Kornbluth S. Cellular mechanisms controlling caspase activation and function. Cold Spring Harb Perspect Biol. 2013;5(6):a008672.
  • Szegezdi E, Fitzgerald U, Samali A. Caspase-12 and ER- stress-mediated apoptosis: The story so far. Ann N Y Acad Sci. 2003;1010:86-194.
  • Baliga B, Kumar S. Apaf-1/cytochrome c apoptosome: An essential initiator of caspase activation or just a sideshow? Cell Death Differ. 2003;10(1):16-18.
  • Zhang W, Shi Y, Oyang L et al. Endoplasmic reticulum stress-a key guardian in cancer. Cell Death Discov. 2024;10(1):343.
  • Bi M, Naczki C, Koritzinsky M et al. ER stress-regulated translation increases tolerance to extreme hypoxia and promotes tumor growth. EMBO J. 2005;24(19):3470- 3481.
  • Moenner M, Pluquet O, Bouchecareilh M, Chevet E. Integrated endoplasmic reticulum stress responses in cancer. Cancer Res. 2007;67(22):10631-10634.
  • Fernandez PM, Tabbara SO, Jacobs LK et al. Overexpression of the glucose-regulated stress gene GRP78 in malignant but not benign human breast lesions. Breast Cancer Resch Treat. 2000;59(1):15-26.
  • Sheng X, Nenseth HZ, Qu S et al. IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling. Nat Commun. 2019;10(1):323.
  • Chen X, Iliopoulos D, Zhang Q et al. XBP1 promotes triple-negative breast cancer by controlling the HIF1α pathway. Nature. 2014;508(7494):103-107.
  • Auf G, Jabouille A, Guérit S et al. Inositol-requiring enzyme 1alpha is a key regulator of angiogenesis and invasion in malignant glioma. Proc Natl Acad Sci USA. 2010;107(35):15553-15558.
  • Bobrovnikova-Marjon E, Grigoriadou C, Pytel D et al. PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage. Oncogene. 2010;29(27):3881-3895.
  • Salaroglio IC, Panada E, Moiso E et al. PERK induces resistance to cell death elicited by endoplasmic reticulum stress and chemotherapy. Mol Cancer. 2017;16(1):91.
  • Benedetti R, Romeo MA, Arena A et al. ATF6 prevents DNA damage and cell death in colon cancer cells undergoing ER stress. Cell Death Discov. 2022;8(1):295.
  • Hanaoka M, Ishikawa T, Ishiguro M et al. Expression of ATF6 as a marker of pre-cancerous atypical change in ulcerative colitis-associated colorectal cancer: A potential role in the management of dysplasia. J Gastroenterol. 2018;53(5):631-641.
  • Cusack JC, Jr Liu R, Houston M et al. Enhanced chemosensitivity to CPT-11 with proteasome inhibitor PS-341: Implications for systemic nuclear factor-kappaB inhibition. Cancer Res. 2001;61(9):3535-3540.
  • Yeung BH, Huang DC, Sinicrope FA. PS-341 (bortezomib) induces lysosomal cathepsin B release and a caspase-2-dependent mitochondrial permeabilization and apoptosis in human pancreatic cancer cells. The J Biol Chem. 2006;281(17):11923-11932.
  • Fribley A, Wang CY. Proteasome inhibitor induces apoptosis through induction of endoplasmic reticulum stress. Cancer Biol Ther. 2006;5(7),745-748.
  • Kim AD, Madduma Hewage SR, Piao MJ, Kang KA, Cho SJ, Hyun JW. Esculetin induces apoptosis in human colon cancer cells by inducing endoplasmic reticulum stress. Cell Biochem Func. 2015;33(7):487-494.
  • Banerjee A, Ahmed H, Yang P, Czinn SJ, Blanchard TG. Endoplasmic reticulum stress and IRE-1 signaling cause apoptosis in colon cancer cells in response to andrographolide treatment. Oncotarget. 2016;7(27):41432-41444.

Kanser ve Endoplazmik Retikulum Stres İndüklü Apoptoz Arasındaki İlişki

Yıl 2025, Cilt: 27 Sayı: 1, 111 - 119, 26.04.2025

Eser Çakmak , Birşen Bilgici

https://doi.org/10.24938/kutfd.1607213

Öz

Endoplazmik retikulum (ER); protein sentezi, katlanması ve lipid biyosentezi gibi kritik hücresel süreçlerde merkezi bir rol oynar. ER stres, yanlış katlanmış proteinlerin birikmesiyle tetiklenir ve hücrenin hayatta kalmasını sağlamak için Unfolded Protein Response (UPR) yolaklarını aktive eder. UPR; PRKR benzeri ER Kinaz (PERK), İnozitol Gerektiren Enzim 1 (IRE1) ve Aktive edici transkripsiyon faktör 6 (ATF6) gibi sensörler aracılığıyla ER homeostazını restore etmeye çalışır. Ancak, uzun süreli veya şiddetli ER stres, apoptozu tetikleyerek hücre ölümüne yol açabilir. Kanser hücrelerinde, tümör mikroçevresindeki hipoksi, besin yetersizliği ve oksidatif stres gibi faktörler kronik ER strese neden olur. Bu koşullar altında, UPR'nin aktivasyonu kanser hücrelerinin hayatta kalmasını desteklerken, aşırı ER stres apoptozu indükleyebilir. ER stres ve UPR'nin kanser progresyonundaki rolü, hem tümör büyümesini destekleyici hem de apoptozu tetikleyici etkileri nedeniyle karmaşıktır. Örneğin, IRE1α- X-Box Bağlayıcı Protein 1 (XBP1) ve PERK- Ökaryotik Translasyon Başlatma Faktörü 2α (eIF2α)- Aktive edici transkripsiyon faktör 4 (ATF4) yolakları, kanser hücrelerinde hayatta kalma ve kemorezistansı artırabilirken, C/EBP Homolog Protein (CHOP) ve C-Jun N-Terminal Kinaz (JNK) gibi pro-apoptotik sinyaller hücre ölümünü tetikleyebilir. Bu dengenin anlaşılması, kanser tedavisi için yeni hedefler sunmaktadır. Proteazom inhibitörleri ve ER stresini artıran diğer ajanlar, kanser hücrelerinde apoptozu indükleyerek terapötik potansiyele sahiptir. Bu derleme, ER stres, UPR ve ER strese bağlı apoptozun moleküler mekanizmalarını inceleyerek, kanser hücrelerinde bu süreçlerin nasıl manipüle edilebileceğini ve yeni tedavi stratejilerinin nasıl geliştirilebileceğini tartışmaktadır. ER stres yolaklarının hedeflenmesi, özellikle kemorezistan tümörler için umut verici bir yaklaşım olabilir.

Anahtar Kelimeler

Endoplazmik retikulum stresi katlanmamış protein yanıtı apoptoz hücrenin hayatta kalması kanser

Kaynakça

  • Szegezdi E, Logue SE, Gorman AM, Samali A. Mediators of endoplasmic reticulum stress-induced apoptosis. EMBO Rep. 2006;7(9):880-885.
  • Celik C, Lee SYT, Yap WS, Thibault G. Endoplasmic reticulum stress and lipids in health and diseases. Prog Lipid Res. 2023;89:101198.
  • Hussain SG, Ramaiah KVA. Endoplasmic reticulum: Stress, signalling and apoptosis. Current Sci. 2007;93:1684-1696.
  • Rasheva VI, Domingos PM. Cellular responses to endoplasmic reticulum stress and apoptosis. Apoptosis. 2009;14(8):996-1007.
  • Kim I, Xu W, Reed JC. Cell death and endoplasmic reticulum stress: Disease relevance and therapeutic opportunities. Nat Rev Drug Discov. 2008;7(12):1013- 1030.
  • Giampietri C, Petrungaro S, Conti S, Facchiano A, Filippini A, Ziparo E. Cancer microenvironment and endoplasmic reticulum stress response. Mediators Inflamm. 2015;2015:417281.
  • Patra D, Bhavya K, Ramprasad P, Kalia M, Pal D. Anti- cancer drug molecules targeting cancer cell cycle and proliferation. Adv Protein Chem Struct Biol. 2023;135:343-395.
  • Brown JM, Attardi LD. The role of apoptosis in cancer development and treatment response. Nat Rev Cancer. 2005;5(3):231-237.
  • Chen X, Cubillos-Ruiz JR. Endoplasmic reticulum stress signals in the tumour and its microenvironment. Nat Rev Cancer. 2021;21(2):71-88.
  • Oakes SA. Endoplasmic reticulum stress signaling in cancer cells. Am J Pathol. 2020;190(5):934-946.
  • Koumenis C. ER stress, hypoxia tolerance and tumor progression. Curr. Mol. Med. 2006;6:55-69.
  • Young RM, Ackerman D, Quinn ZL et al. Dysregulated mTORC1 renders cells critically dependent on desaturated lipids for survival under tumor-like stress. Genes Dev. 2013;27(10):1115-1131.
  • Koumenis C, Wouters BG. "Translating" tumor hypoxia: Unfolded protein response (UPR)-dependent and UPR- independent pathways. Mol Cancer Res. 2006;4(7):423- 436.
  • Denzel MS, Antebi A. Hexosamine pathway and (ER) protein quality control. Curr Opin Cell Biol. 2015;33:14- 18.
  • Pakos-Zebrucka K, Koryga I, Mnich K, Ljujic M, Samali A, Gorman AM. The integrated stress response. EMBO Rep. 2016;17(10):1374-1395.
  • Park J, Morley TS, Kim M, Clegg DJ, Scherer PE. Obesity and cancer -- mechanisms underlying tumour progression and recurrence. Nat. Rev. Endocrinol. 2014;10:455-465
  • Wei Y, Wang D, Topczewski F, Pagliassotti MJ. Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells. Am J Physiol Endocrinol Metab. 2006;291(2):E275- E281.
  • Görlach A, Bertram K, Hudecova S, Krizanova O. Calcium and ROS: A mutual interplay. Redox Biol. 2015;6:260-271.
  • Vladykovskaya E, Sithu SD, Haberzettl P et al. Lipid peroxidation product 4-hydroxy-trans-2-nonenal causes endothelial activation by inducing endoplasmic reticulum stress. Biol Chem. 2012;287(14):11398-11409.
  • Babour A, Bicknell AA, Tourtellotte J, Niwa M. A surveillance pathway monitors the fitness of the endoplasmic reticulum to control its inheritance. Cell. 2010;142(2):256-269.
  • Walter P, Ron D. The unfolded protein response: From stress pathway to homeostatic regulation. Science. 2011;334(6059):1081-1086.
  • Lai E, Teodoro T, Volchuk A. Endoplasmic reticulum stress: Signaling the unfolded protein response. Physiology. 2007;22:193-201.
  • Ghobrial IM, Witzig TE, Adjei AA. Targeting apoptosis pathways in cancer therapy. CA Cancer J Clin. 2005;55(3):178-194.
  • Fulda S, Debatin KM. Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy. Oncogene. 2006;25(34):4798-4811.
  • Hetz C, Zhang K, Kaufman RJ. Mechanisms, regulation and functions of the unfolded protein response. Nat Rev Mol Cell Biol. 2000;21(8):421-438.
  • Schroder M, Kaufman RJ. The mammalian unfolded protein response. Annu Rev Biochem. 2005;74,739-789.
  • Colgan SM, Hashimi AA, Austin RC. Endoplasmic reticulum stress and lipid dysregulation. Expert Rev Mol Med. 2011;13:e4.
  • Harding HP, Zhang Y, Zeng H et al. An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. Mol Cell. 2003;11:619-633.
  • Harding HP, Novoa I, Zhang Yet al. Regulated translation initiation controls stress-induced gene expression in mammalian cells. Mol Cell. 2000;6:1099- 1108.
  • Hollien J, Lin JH, Li H, Stevens N, Walter P, Weissman JS. Regulated Ire1-dependent decay of messenger RNAs in mammalian cells. J Cell Biol. 2009;186:323-331.
  • Lee AH, Iwakoshi NN, Glimcher LH. XBP-1 regulates a subset of endoplasmic reticulum resident chaperone genes in the unfolded protein response. Mol Cell Biol. 2003;23:7448-7459.
  • Urano F, Wang X, Bertolotti A et al. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Science. 2000;287:664-666.
  • Qu L, Liu Z, Zhang HM, Su Y, Ye X. Endoplasmic reticulum stress-induced cell survival and apoptosis. JCCM. 2009;8:1-4.
  • Chen X, Shi C, He M, Xiong S, Xia X. Endoplasmic reticulum stress: Molecular mechanism and therapeutic targets. Signal Transduct Target Ther. 2023;8(1):352.
  • Novoa I, Zeng H, Harding HP, Ron D. Feedback inhibition of the unfolded protein response by GADD34- mediated dephosphorylation of eIF2alpha. J Cell Biol. 2001;153:1011-1022.
  • Sevier CS, Kaiser CA. Ero1 and redox homeostasis in the endoplasmic reticulum. Biochim Biophys Acta. 2008;1783(4):549-556.
  • Tabas I, Ron D. Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress. Nat Cell Biol. 2011;13(3):184-190.
  • Vandewynckel YP, Laukens D, Geerts A et al. The paradox of the unfolded protein response in cancer. Anticancer Res. 2013;33(11):4683-4694.
  • Leibowitz B, Yu J. Mitochondrial signaling in cell death via the Bcl-2 family. Cancer Biol Ther. 2010;9(6):417- 422.
  • Germain M, Mathai JP, McBride HM, Shore GC. Endoplasmic reticulum BIK initiates DRP1-regulated remodelling of mitochondrial cristae during apoptosis. EMBO J. 2005;24(8):1546-1556.
  • Degterev A, Boyce M, Yuan J. A decade of caspases.Oncogene. 2003;22(53):8543-8567.
  • Parrish AB, Freel CD, Kornbluth S. Cellular mechanisms controlling caspase activation and function. Cold Spring Harb Perspect Biol. 2013;5(6):a008672.
  • Szegezdi E, Fitzgerald U, Samali A. Caspase-12 and ER- stress-mediated apoptosis: The story so far. Ann N Y Acad Sci. 2003;1010:86-194.
  • Baliga B, Kumar S. Apaf-1/cytochrome c apoptosome: An essential initiator of caspase activation or just a sideshow? Cell Death Differ. 2003;10(1):16-18.
  • Zhang W, Shi Y, Oyang L et al. Endoplasmic reticulum stress-a key guardian in cancer. Cell Death Discov. 2024;10(1):343.
  • Bi M, Naczki C, Koritzinsky M et al. ER stress-regulated translation increases tolerance to extreme hypoxia and promotes tumor growth. EMBO J. 2005;24(19):3470- 3481.
  • Moenner M, Pluquet O, Bouchecareilh M, Chevet E. Integrated endoplasmic reticulum stress responses in cancer. Cancer Res. 2007;67(22):10631-10634.
  • Fernandez PM, Tabbara SO, Jacobs LK et al. Overexpression of the glucose-regulated stress gene GRP78 in malignant but not benign human breast lesions. Breast Cancer Resch Treat. 2000;59(1):15-26.
  • Sheng X, Nenseth HZ, Qu S et al. IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling. Nat Commun. 2019;10(1):323.
  • Chen X, Iliopoulos D, Zhang Q et al. XBP1 promotes triple-negative breast cancer by controlling the HIF1α pathway. Nature. 2014;508(7494):103-107.
  • Auf G, Jabouille A, Guérit S et al. Inositol-requiring enzyme 1alpha is a key regulator of angiogenesis and invasion in malignant glioma. Proc Natl Acad Sci USA. 2010;107(35):15553-15558.
  • Bobrovnikova-Marjon E, Grigoriadou C, Pytel D et al. PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage. Oncogene. 2010;29(27):3881-3895.
  • Salaroglio IC, Panada E, Moiso E et al. PERK induces resistance to cell death elicited by endoplasmic reticulum stress and chemotherapy. Mol Cancer. 2017;16(1):91.
  • Benedetti R, Romeo MA, Arena A et al. ATF6 prevents DNA damage and cell death in colon cancer cells undergoing ER stress. Cell Death Discov. 2022;8(1):295.
  • Hanaoka M, Ishikawa T, Ishiguro M et al. Expression of ATF6 as a marker of pre-cancerous atypical change in ulcerative colitis-associated colorectal cancer: A potential role in the management of dysplasia. J Gastroenterol. 2018;53(5):631-641.
  • Cusack JC, Jr Liu R, Houston M et al. Enhanced chemosensitivity to CPT-11 with proteasome inhibitor PS-341: Implications for systemic nuclear factor-kappaB inhibition. Cancer Res. 2001;61(9):3535-3540.
  • Yeung BH, Huang DC, Sinicrope FA. PS-341 (bortezomib) induces lysosomal cathepsin B release and a caspase-2-dependent mitochondrial permeabilization and apoptosis in human pancreatic cancer cells. The J Biol Chem. 2006;281(17):11923-11932.
  • Fribley A, Wang CY. Proteasome inhibitor induces apoptosis through induction of endoplasmic reticulum stress. Cancer Biol Ther. 2006;5(7),745-748.
  • Kim AD, Madduma Hewage SR, Piao MJ, Kang KA, Cho SJ, Hyun JW. Esculetin induces apoptosis in human colon cancer cells by inducing endoplasmic reticulum stress. Cell Biochem Func. 2015;33(7):487-494.
  • Banerjee A, Ahmed H, Yang P, Czinn SJ, Blanchard TG. Endoplasmic reticulum stress and IRE-1 signaling cause apoptosis in colon cancer cells in response to andrographolide treatment. Oncotarget. 2016;7(27):41432-41444.
Toplam 60 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Sağlık Hizmetleri ve Sistemleri (Diğer)
Bölüm Derleme
Yazarlar

Eser Çakmak 0000-0002-2243-4489

Birşen Bilgici 0000-0001-7783-5039

Yayımlanma Tarihi 26 Nisan 2025
Gönderilme Tarihi 25 Aralık 2024
Kabul Tarihi 18 Şubat 2025
Yayımlandığı Sayı Yıl 2025 Cilt: 27 Sayı: 1

Kaynak Göster

APA Çakmak, E., & Bilgici, B. (2025). THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS. The Journal of Kırıkkale University Faculty of Medicine, 27(1), 111-119. https://doi.org/10.24938/kutfd.1607213
AMA Çakmak E, Bilgici B. THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS. Kırıkkale Üni Tıp Derg. Nisan 2025;27(1):111-119. doi:10.24938/kutfd.1607213
Chicago Çakmak, Eser, ve Birşen Bilgici. “THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS”. The Journal of Kırıkkale University Faculty of Medicine 27, sy. 1 (Nisan 2025): 111-19. https://doi.org/10.24938/kutfd.1607213.
EndNote Çakmak E, Bilgici B (01 Nisan 2025) THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS. The Journal of Kırıkkale University Faculty of Medicine 27 1 111–119.
IEEE E. Çakmak ve B. Bilgici, “THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS”, Kırıkkale Üni Tıp Derg, c. 27, sy. 1, ss. 111–119, 2025, doi: 10.24938/kutfd.1607213.
ISNAD Çakmak, Eser - Bilgici, Birşen. “THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS”. The Journal of Kırıkkale University Faculty of Medicine 27/1 (Nisan 2025), 111-119. https://doi.org/10.24938/kutfd.1607213.
JAMA Çakmak E, Bilgici B. THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS. Kırıkkale Üni Tıp Derg. 2025;27:111–119.
MLA Çakmak, Eser ve Birşen Bilgici. “THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS”. The Journal of Kırıkkale University Faculty of Medicine, c. 27, sy. 1, 2025, ss. 111-9, doi:10.24938/kutfd.1607213.
Vancouver Çakmak E, Bilgici B. THE RELATIONSHIP BETWEEN CANCER AND ENDOPLASMIC RETICULUM STRESS-INDUCED APOPTOSIS. Kırıkkale Üni Tıp Derg. 2025;27(1):111-9.
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