Loss of histone macroH2A1 in hepatocellular carcinoma cells
promotes paracrine-mediated chemoresistance and
CD4(+)CD25(+)FoxP3(+) regulatory T cells activation

J 2020

Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4(+)CD25(+)FoxP3(+) regulatory T cells activation

LO RE, Oriana; Tommaso MAZZA; Sebastiano GIALLONGO; Paola SANNA; Francesca RAPPA et. al.

Základní údaje

Originální název

Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4(+)CD25(+)FoxP3(+) regulatory T cells activation

Autoři

Vydání

THERANOSTICS, LAKE HAVEN, IVYSPRING INT PUBL, 2020, 1838-7640

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10601 Cell biology

Stát vydavatele

Austrálie

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 11.556

Kód RIV

RIV/00216224:14110/20:00116196

Organizační jednotka

Lékařská fakulta

DOI

https://doi.org/10.7150/thno.35045

UT WoS

000498874200028

EID Scopus

2-s2.0-85077480426

Klíčová slova anglicky

hepatocellular carcinoma; histone macroH2A1; adaptive immune system; chemoresistance

Štítky

14110513, podil, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 17. 3. 2021 13:47, Mgr. Tereza Miškechová

Anotace

V originále

Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive human HCC for macroH2A1 and CD44 CSC marker expression. We also knocked down (KD) macroH2A1 in HCC cells, and performed integrated transcriptomic and secretomic analyses. Results: Human HCC showed low macroH2A1 and high CD44 expression compared to control tissues. MacroH2A1 KD CSC-like cells transferred paracrinally their chemoresistant properties to parental HCC cells. MacroH2A1 KD conditioned media transcriptionally reprogrammed parental HCC cells activated regulatory CD4(+)/CD25(+)/FoxP3(+) T cells (Tregs). Conclusions: Loss of macroH2A1 in HCC cells drives cancer stem-cell propagation and evasion from immune surveillance.

Návaznosti

LM2015091, projekt VaV

Název: Národní centrum lékařské genomiky (Akronym: NCLG)

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Národní centrum lékařské genomiky

MUNI/A/0951/2019, interní kód MU

Název: Buněčná a molekulární biologie pro Biomedicínské vědy

Investor: Masarykova univerzita, Buněčná a molekulární biologie pro Biomedicínské vědy, DO R. 2020_Kategorie A - Specifický výzkum - Studentské výzkumné projekty

Citovat

LO RE, Oriana; Tommaso MAZZA; Sebastiano GIALLONGO; Paola SANNA; Francesca RAPPA; Tu Vinh Luong LUONG; Giovanni VOLTI; Adéla DVOŘÁKOVÁ; Tania ROSKAMS; Matthias VAN HAELE; Emmanuel TSOCHATZIS a Manlio VINCIGUERRA. Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4(+)CD25(+)FoxP3(+) regulatory T cells activation. THERANOSTICS. LAKE HAVEN: IVYSPRING INT PUBL, 2020, roč. 10, č. 2, s. 910-924. ISSN 1838-7640. Dostupné z: https://doi.org/10.7150/thno.35045.

@article{1674038,
   author = {Lo Re, Oriana and Mazza, Tommaso and Giallongo, Sebastiano and Sanna, Paola and Rappa, Francesca and Luong, Tu Vinh Luong and Volti, Giovanni and Dvořáková, Adéla and Roskams, Tania and Van Haele, Matthias and Tsochatzis, Emmanuel and Vinciguerra, Manlio},
   article_location = {LAKE HAVEN},
   article_number = {2},
   doi = {https://doi.org/10.7150/thno.35045},
   keywords = {hepatocellular carcinoma; histone macroH2A1; adaptive immune system; chemoresistance},
   language = {eng},
   issn = {1838-7640},
   journal = {THERANOSTICS},
   title = {Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4(+)CD25(+)FoxP3(+) regulatory T cells activation},
   url = {https://www.thno.org/v10p0910.htm},
   volume = {10},
   year = {2020}
}

TY  - JOUR
ID  - 1674038
AU  - Lo Re, Oriana - Mazza, Tommaso - Giallongo, Sebastiano - Sanna, Paola - Rappa, Francesca - Luong, Tu Vinh Luong - Volti, Giovanni - Dvořáková, Adéla - Roskams, Tania - Van Haele, Matthias - Tsochatzis, Emmanuel - Vinciguerra, Manlio
PY  - 2020
TI  - Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4(+)CD25(+)FoxP3(+) regulatory T cells activation
JF  - THERANOSTICS
VL  - 10
IS  - 2
SP  - 910-924
EP  - 910-924
PB  - IVYSPRING INT PUBL
SN  - 18387640
KW  - hepatocellular carcinoma
KW  - histone macroH2A1
KW  - adaptive immune system
KW  - chemoresistance
UR  - https://www.thno.org/v10p0910.htm
L2  - https://www.thno.org/v10p0910.htm
N2  - Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive human HCC for macroH2A1 and CD44 CSC marker expression. We also knocked down (KD) macroH2A1 in HCC cells, and performed integrated transcriptomic and secretomic analyses. Results: Human HCC showed low macroH2A1 and high CD44 expression compared to control tissues. MacroH2A1 KD CSC-like cells transferred paracrinally their chemoresistant properties to parental HCC cells. MacroH2A1 KD conditioned media transcriptionally reprogrammed parental HCC cells activated regulatory CD4(+)/CD25(+)/FoxP3(+) T cells (Tregs). Conclusions: Loss of macroH2A1 in HCC cells drives cancer stem-cell propagation and evasion from immune surveillance.
ER  -

LO RE, Oriana; Tommaso MAZZA; Sebastiano GIALLONGO; Paola SANNA; Francesca RAPPA; Tu Vinh Luong LUONG; Giovanni VOLTI; Adéla DVOŘÁKOVÁ; Tania ROSKAMS; Matthias VAN HAELE; Emmanuel TSOCHATZIS a Manlio VINCIGUERRA. Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4(+)CD25(+)FoxP3(+) regulatory T cells activation. \textit{THERANOSTICS}. LAKE HAVEN: IVYSPRING INT PUBL, 2020, roč.~10, č.~2, s.~910-924. ISSN~1838-7640. Dostupné z: https://doi.org/10.7150/thno.35045.

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