[en] Background and Objective
The receptor-interacting protein 3 (RIP3) has recently been outlined as a key necrosis mediator but is also thought to participate in the regulation of apoptosis. The aim of this study is to compare the cell death profile induced by 5-aminolevulic acid (5-ALA)-mediated photodynamic therapy (PDT) in the RIP3-deficient cell line U2OS and in U2OS cells in which the expression of RIP3 was restored.
Materials and Methods
RIP3-expressing U2OS cells (RIP3-U2OS) were obtained after transfection and antibiotic selection. Wild type and RIP3-U2OS cells were treated by 5-ALA-PDT. Overall cell viability was evaluated and different parameters characteristic of apoptosis, autophagy, and necrosis were studied.
Results
Surprisingly, the survival of RIP3-U2OS cells was higher compared to that of the wild type cells. In addition, RIP3-U2OS cell death was decreased by a zVAD-fmk pre-treatment. A higher cleavage of caspase-3, 7, 8, 9, and PARP was also detected in these cells, pointing out to the activation of caspase-dependent apoptosis. In parallel, a thrust of autophagy was clearly identified in the RIP3-U2OS cells. Conversely, RIP3-U2OS exhibited a lower level of necrosis than the wild types. Interestingly, necrostatin-1 efficiently decreased necrosis level in RIP3-U2OS but not in wild type cells.
Conclusion
Expression of RIP3 in U2OS cells led to a better survival but also to a death profile change in response to PDT. The apoptotic and autophagic pathways were clearly up-regulated compared to the RIP3-deficient wild type cells. However, induction of necrosis was weaker in the RIP3-U2OS cells. In this context, autophagy is likely to play a protective role against PDT-induced cell death and to allow a better survival of RIP3-U2OS cells. This work also highlights the important role played by RIP3 in the apoptotic pathway, although the modalities are still widely unknown.
scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.
Bibliography
Yu PW, Huang BC, Shen M, Quast J, Chan E, Xu X, Nolan GP, Payan DG, Luo Y,. Identification of RIP3, a RIP-like kinase that activates apoptosis and NFkappaB. Curr Biol 1999; 9 (10): 539-542. (Pubitemid 29257110)
Sun X, Lee J, Navas T, Baldwin DT, Stewart TA, Dixit VM,. RIP3, a novel apoptosis-inducing kinase. J Biol Chem 1999; 274 (24): 16871-16875.
Meylan E, Tschopp J,. The RIP kinases: Crucial integrators of cellular stress. Trends Biochem Sci 2005; 30 (3): 151-159. (Pubitemid 40332531)
Zhang D, Lin J, Han J,. Receptor-interacting protein (RIP) kinase family. Cell Mol Immunol 2010; 7 (4): 243-249.
Sun X, Yin J, Starovasnik MA, Fairbrother WJ, Dixit VM,. Identification of a novel homotypic interaction motif required for the phosphorylation of receptor-interacting protein (RIP) by RIP3. J Biol Chem 2002; 277 (11): 9505-9511. (Pubitemid 34953039)
Cho YS, Challa S, Moquin D, Genga R, Ray TD, Guildford M, Chan FK,. Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. Cell 2009; 137 (6): 1112-1123.
He S, Wang L, Miao L, Wang T, Du F, Zhao L, Wang X,. Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. Cell 2009; 137 (6): 1100-1111.
Zhang DW, Shao J, Lin J, Zhang N, Lu BJ, Lin SC, Dong MQ, Han J,. RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis. Science 2009; 325 (5938): 332-336.
Kaiser WJ, Upton JW, Long AB, Livingston-Rosanoff D, Daley-Bauer LP, Hakem R, Caspary T, Mocarski ES,. RIP3 mediates the embryonic lethality of caspase-8-deficient mice. Nature 2011; 471 (7338): 368-372.
Oberst A, Dillon CP, Weinlich R, McCormick LL, Fitzgerald P, Pop C, Hakem R, Salvesen GS, Green DR,. Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis. Nature 2011; 471 (7338): 363-367.
Christofferson DE, Yuan J,. Necroptosis as an alternative form of programmed cell death. Curr Opin Cell Biol 2010; 22 (2): 263-268.
Moquin D, Chan FK,. The molecular regulation of programmed necrotic cell injury. Trends Biochem Sci 2010; 35 (8): 434-441.
Vandenabeele P, Declercq W, Van Herreweghe F, Vanden Berghe T,. The role of the kinases RIP1 and RIP3 in TNF-induced necrosis. Sci Signal 2010; 3 (115): re4.
Degterev A, Huang Z, Boyce M, Li Y, Jagtap P, Mizushima N, Cuny GD, Mitchison TJ, Moskowitz MA, Yuan J,. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury. Nat Chem Biol 2005; 1 (2): 112-119.
Pazdernik NJ, Donner DB, Goebl MG, Harrington MA,. Mouse receptor interacting protein 3 does not contain a caspase-recruiting or a death domain but induces apoptosis and activates NF-kappaB. Mol Cell Biol 1999; 19 (10): 6500-6508. (Pubitemid 29441835)
Feng S, Ma L, Yang Y, Wu M,. Truncated RIP3 (tRIP3) acts upstream of FADD to induce apoptosis in the human hepatocellular carcinoma cell line QGY-7703. Biochem Biophys Res Commun 2006; 347 (3): 558-565. (Pubitemid 44092622)
Dolmans DE, Fukumura D, Jain RK,. Photodynamic therapy for cancer. Nat Rev Cancer 2003; 3 (5): 380-387. (Pubitemid 37328858)
Peng Q, Berg K, Moan J, Kongshaug M, Nesland JM,. 5-Aminolevulinic acid-based photodynamic therapy: Principles and experimental research. Photochem Photobiol 1997; 65 (2): 235-251. (Pubitemid 27158805)
Ohgari Y, Nakayasu Y, Kitajima S, Sawamoto M, Mori H, Shimokawa O, Matsui H, Taketani S,. Mechanisms involved in delta-aminolevulinic acid (ALA)-induced photosensitivity of tumor cells: Relation of ferrochelatase and uptake of ALA to the accumulation of protoporphyrin. Biochem Pharmacol 2005; 71 (1-2): 42-49. (Pubitemid 41713525)
Kelty CJ, Brown NJ, Reed MW, Ackroyd R,. The use of 5-aminolaevulinic acid as a photosensitiser in photodynamic therapy and photodiagnosis. Photochem Photobiol Sci 2002; 1 (3): 158-168. (Pubitemid 37069724)
Rebsamen M, Heinz LX, Meylan E, Michallet MC, Schroder K, Hofmann K, Vazquez J, Benedict CA, Tschopp J,. DAI/ZBP1 recruits RIP1 and RIP3 through RIP homotypic interaction motifs to activate NF-kappaB. EMBO Rep 2009; 10 (8): 916-922.
Coupienne I, Bontems S, Dewaele M, Rubio N, Habraken Y, Fulda S, Agostinis P, Piette J,. NF-kappaB inhibition improves the sensitivity of human glioblastoma cells to 5-aminolevulinic acid-based photodynamic therapy. Biochem Pharmacol 2011; 81 (5): 606-616.
Yang Y, Ma J, Chen Y, Wu M,. Nucleocytoplasmic shuttling of receptor-interacting protein 3 (RIP3): Identification of novel nuclear export and import signals in RIP3. J Biol Chem 2004; 279 (37): 38820-38829. (Pubitemid 39296041)
Kasof GM, Prosser JC, Liu D, Lorenzi MV, Gomes BC,. The RIP-like kinase, RIP3, induces apoptosis and NF-kappaB nuclear translocation and localizes to mitochondria. FEBS Lett 2000; 473 (3): 285-291. (Pubitemid 30249141)
Karin M,. Nuclear factor-kappaB in cancer development and progression. Nature 2006; 441 (7092): 431-436. (Pubitemid 44050137)
Karin M, Cao Y, Greten FR, Li ZW,. NF-kappaB in cancer: From innocent bystander to major culprit. Nat Rev Cancer 2002; 2 (4): 301-310. (Pubitemid 37328783)
Karin M, Lin A,. NF-kappaB at the crossroads of life and death. Nat Immunol 2002; 3 (3): 221-227.
Feng S, Yang Y, Mei Y, Ma L, Zhu DE, Hoti N, Castanares M, Wu M,. Cleavage of RIP3 inactivates its caspase-independent apoptosis pathway by removal of kinase domain. Cell Signal 2007; 19 (10): 2056-2067. (Pubitemid 47353808)
Li M, Feng S, Wu M,. Multiple roles for nuclear localization signal (NLS, aa 442-472) of receptor interacting protein 3 (RIP3). Biochem Biophys Res Commun 2008; 372 (4): 850-855.
Azad MB, Chen Y, Henson ES, Cizeau J, McMillan-Ward E, Israels SJ, Gibson SB,. Hypoxia induces autophagic cell death in apoptosis-competent cells through a mechanism involving BNIP3. Autophagy 2008; 4 (2): 195-204. (Pubitemid 351231183)
Xue LY, Chiu SM, Oleinick NL,. Atg7 deficiency increases resistance of MCF-7 human breast cancer cells to photodynamic therapy. Autophagy 2010; 6 (2): 248-255.
Apel A, Herr I, Schwarz H, Rodemann HP, Mayer A,. Blocked autophagy sensitizes resistant carcinoma cells to radiation therapy. Cancer Res 2008; 68 (5): 1485-1494. (Pubitemid 351346857)
Wu YT, Tan HL, Huang Q, Kim YS, Pan N, Ong WY, Liu ZG, Ong CN, Shen HM,. Autophagy plays a protective role during zVAD-induced necrotic cell death. Autophagy 2008; 4 (4): 457-466. (Pubitemid 351705142)
Baehrecke EH,. Autophagy: Dual roles in life and death? Nat Rev Mol Cell Biol 2005; 6 (6): 505-510. (Pubitemid 40780562)
Codogno P, Meijer AJ,. Autophagy and signaling: Their role in cell survival and cell death. Cell Death Differ 2005; 12 (Suppl 2): 1509-1518. (Pubitemid 41553987)
Klionsky DJ, Emr SD,. Autophagy as a regulated pathway of cellular degradation. Science 2000; 290 (5497): 1717-1721. (Pubitemid 32004796)
Similar publications
Sorry the service is unavailable at the moment. Please try again later.
This website uses cookies to improve user experience. Read more
Save & Close
Accept all
Decline all
Show detailsHide details
Cookie declaration
About cookies
Strictly necessary
Performance
Strictly necessary cookies allow core website functionality such as user login and account management. The website cannot be used properly without strictly necessary cookies.
This cookie is used by Cookie-Script.com service to remember visitor cookie consent preferences. It is necessary for Cookie-Script.com cookie banner to work properly.
Performance cookies are used to see how visitors use the website, eg. analytics cookies. Those cookies cannot be used to directly identify a certain visitor.
Used to store the attribution information, the referrer initially used to visit the website
Cookies are small text files that are placed on your computer by websites that you visit. Websites use cookies to help users navigate efficiently and perform certain functions. Cookies that are required for the website to operate properly are allowed to be set without your permission. All other cookies need to be approved before they can be set in the browser.
You can change your consent to cookie usage at any time on our Privacy Policy page.