Knockdown of death receptor 5 antisense long noncoding RNA and cisplatin treatment modulate similar macromolecular and metabolic changes in HeLa cells.
DR5-AS
FTIR spectroscopy
HeLa cells
cancer
cisplatin
metabolism
transcriptomics
Journal
Turkish journal of biology = Turk biyoloji dergisi
ISSN: 1303-6092
Titre abrégé: Turk J Biol
Pays: Turkey
ID NLM: 9434434
Informations de publication
Date de publication:
2022
2022
Historique:
received:
17
08
2022
revised:
19
12
2022
accepted:
05
12
2022
medline:
2
8
2023
pubmed:
2
8
2023
entrez:
2
8
2023
Statut:
epublish
Résumé
Despite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells. We used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown. Cisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells. These results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular and metabolic changes in HeLa cervix cancer cells.
Sections du résumé
Background/aim
UNASSIGNED
Despite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells.
Materials and methods
UNASSIGNED
We used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown.
Results
UNASSIGNED
Cisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells.
Conclusion
UNASSIGNED
These results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular and metabolic changes in HeLa cervix cancer cells.
Identifiants
pubmed: 37529795
doi: 10.55730/1300-0152.2634
pii: turkjbiol-46-6-488
pmc: PMC10387844
doi:
Types de publication
Journal Article
Langues
eng
Pagination
488-500Informations de copyright
© TÜBİTAK.
Références
Oncogene. 2012 Oct 18;31(42):4567-76
pubmed: 22249249
Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):10988-92
pubmed: 1763013
Bioinformatics. 2012 Dec 15;28(24):3211-7
pubmed: 23071270
Spectrochim Acta A Mol Biomol Spectrosc. 2015;150:902-8
pubmed: 26119356
Oncol Lett. 2017 May;13(5):3567-3571
pubmed: 28521459
Curr Pharm Biotechnol. 2023;24(7):872-888
pubmed: 35747959
Bioinformatics. 2016 Oct 1;32(19):3047-8
pubmed: 27312411
J Oral Biol Craniofac Res. 2018 Sep-Dec;8(3):234-240
pubmed: 30191116
Spectrochim Acta A Mol Biomol Spectrosc. 2017 Oct 5;185:317-335
pubmed: 28599236
J Transl Med. 2015 Apr 02;13:108
pubmed: 25884618
J Biol Chem. 2014 Mar 21;289(12):8170-81
pubmed: 24469450
Sci Rep. 2017 Aug 21;7(1):8911
pubmed: 28827680
Nat Protoc. 2009;4(8):1184-91
pubmed: 19617889
Eur Rev Med Pharmacol Sci. 2015 Sep;19(17):3187-93
pubmed: 26400521
J Cell Biol. 2017 Aug 7;216(8):2295-2304
pubmed: 28630146
Cell Metab. 2016 Jan 12;23(1):27-47
pubmed: 26771115
Bioinformatics. 2014 Apr 1;30(7):923-30
pubmed: 24227677
Cells. 2020 Dec 08;9(12):
pubmed: 33302475
Cells. 2019 Mar 03;8(3):
pubmed: 30832409
Nat Rev Cancer. 2021 Oct;21(10):669-680
pubmed: 34272515
Exp Biol Med (Maywood). 2017 Jan;242(2):184-193
pubmed: 27633578
Genome Biol. 2014;15(12):550
pubmed: 25516281
Trends Genet. 2018 Sep;34(9):704-721
pubmed: 30017313
BMC Genomics. 2013 Jun 10;14:386
pubmed: 23758785
Front Oncol. 2020 Oct 06;10:555825
pubmed: 33123468
Oncol Lett. 2019 Mar;17(3):2795-2801
pubmed: 30854054
Int J Cancer. 2017 Dec 15;141(12):2379-2391
pubmed: 28631330
Biochim Biophys Acta Bioenerg. 2017 Aug;1858(8):641-654
pubmed: 28342810
Int J Mol Sci. 2020 Dec 21;21(24):
pubmed: 33371204
Analyst. 2010 Dec;135(12):3094-102
pubmed: 20978686
Iran J Pharm Res. 2012 Winter;11(1):235-40
pubmed: 24250445
Sci Rep. 2020 Oct 1;10(1):16343
pubmed: 33004973
Nucleic Acids Res. 2020 Jan 8;48(D1):D498-D503
pubmed: 31691815
BMC Cancer. 2017 Nov 3;17(1):711
pubmed: 29100507
Sci Rep. 2017 Mar 17;7:44541
pubmed: 28303926
Oncol Lett. 2019 Sep;18(3):2212-2219
pubmed: 31452722
Nature. 1965 Feb 13;205:698-9
pubmed: 14287410
Technol Cancer Res Treat. 2012 Aug;11(4):333-44
pubmed: 22712605
Biochim Biophys Acta. 2015 Jan;1853(1):111-25
pubmed: 25307522
Bioinformatics. 2013 Jan 1;29(1):15-21
pubmed: 23104886
Nat Methods. 2018 Jul;15(7):475-476
pubmed: 29967506
Appl Spectrosc. 2007 Feb;61(2):199-203
pubmed: 17331312
Atherosclerosis. 1993 Nov;103(2):181-93
pubmed: 8292094
Int J Mol Sci. 2020 Dec 31;22(1):
pubmed: 33396303
Proc Natl Acad Sci U S A. 1990 Oct;87(20):8140-4
pubmed: 2236027
Anal Biochem. 2005 Apr 1;339(1):36-40
pubmed: 15766707
Pathol Res Pract. 2011 Jun 15;207(6):377-82
pubmed: 21621926
Cancer Biol Ther. 2018 May 4;19(5):391-399
pubmed: 29336659
Nat Rev Cancer. 2020 Feb;20(2):74-88
pubmed: 31686003
Neoplasma. 2016;63(3):362-70
pubmed: 26925782
Cell Chem Biol. 2019 Jan 17;26(1):85-97.e4
pubmed: 30449675
Nat Cell Biol. 2019 May;21(5):542-551
pubmed: 31048766
Front Cell Dev Biol. 2021 Aug 23;9:688855
pubmed: 34497804
Aquat Toxicol. 2006 Apr 20;77(1):53-63
pubmed: 16325934
Methods Mol Biol. 2018;1706:91-110
pubmed: 29423795
Iran J Pharm Res. 2016 Winter;15(1):213-20
pubmed: 27610161