J 2020

A Lipidomic Signature Complements Stemness Features Acquisition in Liver Cancer Cells

SERNA, I. M. R., I. ROMITO, A. MAUGERI, Oriana LO RE, Sebastiano GIALLONGO et. al.

Basic information

Original name

A Lipidomic Signature Complements Stemness Features Acquisition in Liver Cancer Cells

Authors

SERNA, I. M. R., I. ROMITO, A. MAUGERI, Oriana LO RE (380 Italy), Sebastiano GIALLONGO (380 Italy, belonging to the institution), G. MAZZOCCOLI, J. A. OBEN, G. LI VOLTI, T. MAZZA, A. ALISI and Manlio VINCIGUERRA (380 Italy, guarantor)

Edition

International Journal of Molecular Sciences, Basel, Multidisciplinary Digital Publishing Institute, 2020, 1422-0067

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10608 Biochemistry and molecular biology

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 5.923

RIV identification code

RIV/00216224:14110/20:00117463

Organization unit

Faculty of Medicine

DOI

UT WoS

000594195100001

Keywords in English

FAK; HCC; stemness; cancer stem cells

Tags

Tags

International impact, Reviewed
Změněno: 21/7/2021 10:27, Mgr. Tereza Miškechová

Abstract

V originále

Lipid catabolism and anabolism changes play a role in stemness acquisition by cancer cells, and cancer stem cells (CSCs) are particularly dependent on the activity of the enzymes involved in these processes. Lipidomic changes could play a role in CSCs' ability to cause disease relapse and chemoresistance. The exploration of lipid composition and metabolism changes in CSCs in the context of hepatocellular cancer (HCC) is still incomplete and their lipidomic scenario continues to be elusive. We aimed to evaluate through high-throughput mass spectrometry (MS)-based lipidomics the levels of the members of the six major classes of sphingolipids and phospholipids in two HCC cell lines (HepG2 and Huh-7) silenced for the expression of histone variant macroH2A1 (favoring stemness acquisition), or silenced for the expression of focal adhesion tyrosine kinase (FAK) (hindering aggressiveness and stemness). Transcriptomic changes were evaluated by RNA sequencing as well. We found definite lipidomic and transcriptomic changes in the HCC lines upon knockdown (KD) of macroH2A1 or FAK, in line with the acquisition or loss of stemness features. In particular, macroH2A1 KD increased total sphingomyelin (SM) levels and decreased total lysophosphatidylcholine (LPC) levels, while FAK KD decreased total phosphatidylcholine (PC) levels. In conclusion, in HCC cell lines knocked down for specific signaling/epigenetic processes driving opposite stemness potential, we defined a lipidomic signature that hallmarks hepatic CSCs to be exploited for therapeutic strategies.