Mechanisms and consequences of entosis

Krishna, Shefali; Overholtzer, Michael

doi:10.1007/s00018-016-2207-0

Cited by 89 publications

(88 citation statements)

References 65 publications

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“…Upon glu cose star va tion, can cer cells rely on their high meta bolic plas tic ity to ex ploit other re sources orig i nat ing from their mi croen vi ron ment, such as glu t a mine, lipids, var i ous amino acids and even nearby host and can cer cells that can be en gulfed to gen er ate meta bolic in ter me di ates and pre cur sors in the process of cel lu lar can ni bal ism [66][67][68]. Upon per sis tent nu tri ent star va tion, can cer cells can fur ther sur vive on au tophagy, a process by which cells re cy cle dis pens able com po nents (such as pro teins and or ganelles) for short to medium term sur vival un der star va tion [69].…”

Section: Metabolic Cooperation In Cancermentioning

confidence: 99%

See 1 more Smart Citation

Cancer metabolism in space and time: Beyond the Warburg effect

Danhier

Bański

Payen

et al. 2017

Biochimica et Biophysica Acta (BBA) - Bioenergetics

177

139

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Available online xxx Keywords:Can cer Me tab o lism Mi to chon dria Het ero gene ity Metas ta sis A B S T R A C T Al tered me tab o lism in can cer cells is piv otal for tu mor growth, most no tably by pro vid ing en ergy, re duc ing equiv a lents and build ing blocks while sev eral metabo lites ex ert a sig nal ing func tion pro mot ing tu mor growth and pro gres sion. A can cer tis sue can not be sim ply re duced to a bulk of pro lif er at ing cells. Tu mors are in deed com plex and dy namic struc tures where sin gle cells can het ero ge neously per form var i ous bi o log i cal ac tiv i ties with dif fer ent meta bolic re quire ments. Be cause tu mors are com posed of dif fer ent types of cells with meta bolic ac tiv i ties af fected by dif fer ent spa tial and tem po ral con texts, it is im por tant to ad dress me tab o lism tak ing into ac count cel lu lar and bi o log i cal het ero gene ity. In this re view, we de scribe this het ero gene ity also in meta bolic fluxes, thus show ing the rel a tive con tri bu tion of dif fer ent meta bolic ac tiv i ties to tu mor pro gres sion ac cord ing to the cel lu lar con text. This ar ti cle is part of a Spe cial Is sue en ti tled Res pi ra tory com plex I, edited by Giuseppe Gas parre, Ro drigue Rossig nol and Pierre Son veaux. Abbreviations: ACL, ATP cit rate lyase; AMPK, adeno sine monophos phate ki nase; ARG1, L argi nine me tab o liz ing en zyme arginase 1; BCAA, branched chain amino acid; Bcl2, B cell lym phoma 2; CAF, can cer as so ci ated fi brob last; CIC, can cer ini ti at ing cell; COX2, cy tochrome ox i dase; CSC, can cer stem cell; CREB, cyclic adeno sine monophos phate re sponse el e ment bind ing pro tein; DEC1, dif fer en tially ex pressed in chon dro cytes 1; EMT, ep ithe lial to mes enchy mal tran si tion; FAK, fo cal ad he sion ki nase; FAS, fatty acid syn thase; FBP, fruc tose 1,6 bis pho s phate; FDG PET, [ F] flu o rodeoxyglu cose positron emis sion to mog ra phy; GAPDH, glyc er alde hyde 3 phos phate de hy dro ge nase; HIF 1, hy poxia ac ti vated fac tor 1; HK2, hex ok i nase 2; HMGB1, high mo bil ity group box 1; HU VEC, hu man um bil i cal vein en dothe lial cell; IFN γ, in ter feron gamma; LDH, lac tate de hy dro ge nase; MEF, murine em bry onic fi brob last; MET, mes enchy mal to ep ithe lial tran si tion; MRI, mag netic res o nance imag ing; mTORC1, mam malian tar get of ra pamycin com plex 1; NSCLC, non small cell lung can cer; OX PHOS, ox ida tive phos pho ry la tion; PDAC, pan cre atic duc tal ade no car ci noma; PHD, pro lyl hy drox y lase; pHe, ex tra cel lu lar pH; pHi, in tra cel lu lar pH; PK, pyru vate ki nase; PPP, pen tose phos phate path way; REDD1, reg u lated in de vel op ment and DNA dam age re sponse 1; RhoA, Ras ho molog gene fam ily, mem ber A; ROS, re ac tive oxy gen species; SASP, senes cence as so ci ated se cre tory phe no type; SCO2, syn the sis of cy tochrome ox i dase 2; SGK 1, serum and glu co cor ti coid reg u lated ki nase 1 Sirt1, sir tuin 1; TAM, tu mor as so ci ated macrophage; TIGAR, TP53 in duced gly col y ...

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Section: Metabolic Cooperation In Cancermentioning

confidence: 99%

“…Upon nu tri ent star va tion, can cer cells can sur vive on au tophagy. [67]. How ever, if nu tri ent and oxy gen de liv ery are per sis tently low, au tophagy ul ti mately leads to necrotic cell death.…”

Section: Metabolic Regulation Of Cancer Cell Deathmentioning

confidence: 99%

Cancer metabolism in space and time: Beyond the Warburg effect

Danhier

Bański

Payen

et al. 2017

Biochimica et Biophysica Acta (BBA) - Bioenergetics

177

139

View full text Add to dashboard Cite

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“…However, in the process of entosis or emperipolesis, most invader cells are eventually killed by the receiver cells through lysosomal digestion, and some cells even escape from the receiver cells 1. We found that cells that were forced to invade target cells by the synthetic cell invasion system met the same fate (Figure S4, Supporting Information).…”

mentioning

confidence: 82%

Engineering Whole Mammalian Cells for Target‐Cell‐Specific Invasion/Fusion

Kojima

Fussenegger

2018

Advanced Science

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Live mammalian cells are equipped with a synthetic cell invasion system that enables their target‐specific insertion into other live mammalian cells. By conjugating RhoA activator to a transmembrane protein that is segregated from cell–cell interface when specific cell contact occurs, polarization of RhoA activity is synthetically induced inside the cells in response to specific cell contact. This polarization is a sufficient condition for invader cells to selectively penetrate cells expressing a target antigen. Further, when an acid‐responsive fusogenic protein is expressed on invader cells, invader/receiver cell fusion occurs after invasion, and the invader's intracellular contents are released into the recipient's cytosol. It is shown that this system can be used for specific cell ablation. This synthetic‐biology‐inspired cell invasion/fusion system might open the door to using whole mammalian cells for cargo delivery purposes or for ablation of a specific cell type.

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“…Perhaps cell death in the blastocyst stage embryo is simply not critical for development or may not follow classic routes. Excess cells in BAX/BAK DKO blastocysts have not yet been demonstrated but might be cleared by other means; for example, cell cannibalization via entosis (Krishna and Overholtzer 2016) or nonprofessional phagocytosis by neighboring cells upon exposure of "eat me" signals (Arandjelovic and Ravichandran 2015). Certainly, a failure to clear dying cells from embryoid bodies-e.g., observed in the context of ATG5 or Beclin-1 deficiency-blocks cavitation (Qu et al 2007), suggesting that lack of cell death and accumulation of cells at that stage should do the same.…”

Section: Mitochondrial Apoptosis and Its Role In Early Embryogenesismentioning

confidence: 99%

Interrogating the relevance of mitochondrial apoptosis for vertebrate development and postnatal tissue homeostasis

Tuzlak

Kaufmann

2016

Genes Dev.

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“Programmed cell death or ‘apoptosis’ is critical for organogenesis during embryonic development and tissue homeostasis in the adult. Its deregulation can contribute to a broad range of human pathologies, including neurodegeneration, cancer, or autoimmunity…” These or similar phrases have become generic opening statements in many reviews and textbooks describing the physiological relevance of apoptotic cell death. However, while the role in disease has been documented beyond doubt, facilitating innovative drug discovery, we wonder whether the former is really true. What goes wrong in vertebrate development or in adult tissue when the main route to apoptotic cell death, controlled by the BCL2 family, is impaired? Such scenarios have been mimicked by deletion of one or more prodeath genes within the BCL2 family, and gene targeting studies in mice exploring the consequences have been manifold. Many of these studies were geared toward understanding the role of BCL2 family proteins and mitochondrial apoptosis in disease, whereas fewer focused in detail on their role during normal development or tissue homeostasis, perhaps also due to an irritating lack of phenotype. Looking at these studies, the relevance of classical programmed cell death by apoptosis for development appears rather limited. Together, these many studies suggest either highly selective and context-dependent contributions of mitochondrial apoptosis or significant redundancy with alternative cell death mechanisms, as summarized and discussed here.

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Mechanisms and consequences of entosis

Cited by 89 publications

References 65 publications

Cancer metabolism in space and time: Beyond the Warburg effect

Cancer metabolism in space and time: Beyond the Warburg effect

Engineering Whole Mammalian Cells for Target‐Cell‐Specific Invasion/Fusion

Interrogating the relevance of mitochondrial apoptosis for vertebrate development and postnatal tissue homeostasis

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