Periprostatic adipocytes act as a driving force for prostate cancer progression in obesity

Laurent, Victor; Guérard, Adrien; Mazerolles, Catherine; Gonidec, Sophie Le; Toulet, Aurélie; Nieto, Laurence; Zaïdi, Falek; Majed, Bilal; Garandeau, David; Socrier, Y; Golzio, Muriel; Cadoudal, Thomas; Chaoui, Karima; Dray, Cédric; Monsarrat, Bernard; Burlet‐Schiltz, Odile; Wang, Yuan Yuan; Couderc, Bettina; Valet, Philippe; Malavaud, Bernard; Müller, Cathérine

doi:10.1038/ncomms10230

Cited by 222 publications

(216 citation statements)

References 66 publications

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“…For ex am ple, stroma as so ci ated pan cre atic stel late cells (my ofi brob last like cells) pro duce non es sen tial amino acids, in par tic u lar ala nine that sup port pan cre atic tu mor me tab o lism [96]. In an other ex am ple, adipocytes, which are abun dant in the tu mor mi croen vi ron ment of re nal, breast, prostate and ovar ian can cers and have been for long con sid ered as pas sive by standers to can cer de vel op ment [97][98][99], usu ally dis play fewer lipid droplets com pared to nor mal adipocytes, sug gest ing that they sup ply fatty acids to nearby can cer cells [78]. Nie man et al [99] showed that hu man omen tal adipocytes pro mote the in va sion, mi gra tion and metas ta sis of SKOV3ip1 hu man ovar ian can cer cells to ward the omen tum.…”

Section: Metabolic Cooperation In Cancermentioning

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

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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%

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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“…In cell line models, lipids taken up by prostate cancer cells can drive proliferation (Nieman et al 2013) and potentially invasiveness (Sacca et al 2012). Moreover, a recent report has demonstrated enhanced migration of prostate cancer cells induced by coculture with periprostatic-derived adipocytes from obese compared with lean mice (Laurent et al 2016). Given that the antitumor effects of inhibiting lipogenesis can be overcome by providing exogenous fatty acids (Kuemmerle et al 2011, Griffiths et al 2013, uptake of fatty acids by prostate tumor cells may be an important mechanism of clinical resistance to inhibitors of lipid synthesis (e.g.…”

Section: Androgens Stimulate Lipid Synthesis Uptake and Storagementioning

confidence: 99%

Androgen control of lipid metabolism in prostate cancer: novel insights and future applications

Butler

Centenera

Swinnen

2016

Endocrine-Related Cancer

113

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One of the most typical hallmarks of prostate cancer cells is their exquisite dependence on androgens, which is the basis of the widely applied androgen deprivation therapy. Among the variety of key cellular processes and functions that are regulated by androgens, lipid metabolism stands out by its complex regulation and its many intricate links with cancer cell biology. Here, we review our current knowledge on the links between androgens and lipid metabolism in prostate cancer, and highlight recent developments and insights into the links between key oncogenic stimuli and altered lipid synthesis and/or uptake that may hold significant potential for biomarker development and provide new vulnerabilities for therapeutic intervention.

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“…The crosstalk between fat cells and cancer cells plays an important role in driving cancer survival and metabolism for several tumor types such as ovarian, breast, prostate and pancreatic cancers. [1][2][3] This is particularly important in the case of ovarian cancer since, unlike other tumors, it rarely metastasizes outside the abdominal cavity. The main cause of death from ovarian cancer is malnutrition secondary to intestinal obstruction because of metastasis-induced adhesion formation.…”

Section: Editorials: Cell Cycle Featuresmentioning

confidence: 99%