Pharmacological inhibition of BCL-2 with the FDA-approved drug venetoclax impairs longitudinal bone growth.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
17 05 2023
Historique:
received: 02 03 2023
accepted: 10 05 2023
medline: 19 5 2023
pubmed: 18 5 2023
entrez: 17 5 2023
Statut: epublish

Résumé

Treatment-related skeletal complications are common in childhood cancer patients and survivors. Venetoclax is a BCL-2 inhibitor that has shown efficacy in hematological malignancies in adults and is being investigated in pediatric cancer clinical trials as a promising therapeutic modality. Venetoclax triggers cell death in cancer cells, but whether it exerts similar effects in normal bone cells, is unknown. Chondrogenic ATDC5 cells, E20 fetal rat metatarsal bones, and human growth plate biopsies were treated with different concentrations of venetoclax. Female NMRI nu/nu mice were treated with venetoclax or vehicle for 15 days. Mice were X-rayed at baseline and at the end of the experiment to assess longitudinal bone growth and body weight was monitored throughout the study. Histomorphometric and immunohistochemical analyses were performed to evaluate treatment effects on the growth plate cartilage. Venetoclax decreased the viability of chondrocytes and impaired the growth of ex vivo cultured metatarsals while reducing the height of the resting/proliferative zone and the hypertrophic cell size. When tested in vivo, venetoclax suppressed bone growth and reduced growth plate height. Our experimental data suggest that venetoclax directly targets growth plate chondrocytes suppressing bone growth and we, therefore, encourage careful monitoring of longitudinal bone growth if treating growing children with venetoclax.

Identifiants

pubmed: 37198212
doi: 10.1038/s41598-023-34965-4
pii: 10.1038/s41598-023-34965-4
pmc: PMC10192431
doi:

Substances chimiques

Proto-Oncogene Proteins c-bcl-2 0
venetoclax N54AIC43PW

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

8054

Informations de copyright

© 2023. The Author(s).

Références

Toxicol Lett. 2014 Jan 13;224(2):196-200
pubmed: 24172751
J Bone Miner Res. 2008 May;23(5):621-32
pubmed: 18086008
Eur J Surg Oncol. 2003 Feb;29(1):49-58
pubmed: 12559077
Development. 2015 Mar 1;142(5):817-31
pubmed: 25715393
Nature. 2003 May 15;423(6937):332-6
pubmed: 12748651
Cancer Res. 2007 Oct 15;67(20):10078-86
pubmed: 17942942
Bone. 2007 Nov;41(5):842-50
pubmed: 17884747
Front Pharmacol. 2019 Jun 21;10:697
pubmed: 31293422
J Natl Cancer Inst. 2014 Mar;106(3):djt459
pubmed: 24586107
Cancer Res. 1995 Jan 15;55(2):354-9
pubmed: 7812968
N Engl J Med. 2016 Jan 28;374(4):311-22
pubmed: 26639348
BMC Cancer. 2016 Feb 13;16:97
pubmed: 26874859
Dev Cell. 2001 Nov;1(5):645-53
pubmed: 11709185
Nat Med. 2013 Feb;19(2):202-8
pubmed: 23291630
Pediatr Res. 2006 May;59(5):625-9
pubmed: 16627871
Pediatr Blood Cancer. 2015 Jan;62(1):45-51
pubmed: 25257751
Future Oncol. 2018 Sep;14(21):2115-2129
pubmed: 29595064
J Biol Chem. 2009 Dec 25;284(52):36659-36669
pubmed: 19846553
Nat Rev Cancer. 2014 Jan;14(1):61-70
pubmed: 24304873
Oncotarget. 2017 Sep 1;8(41):69295-69302
pubmed: 29050204
J Bone Miner Res. 2004 Nov;19(11):1805-12
pubmed: 15476580
Int J Cancer. 2021 Dec 1;149(11):1863-1876
pubmed: 34278568
Blood. 2016 Sep 8;128(10):1382-95
pubmed: 27343252
Trends Endocrinol Metab. 2013 May;24(5):222-8
pubmed: 23402768
Neuro Oncol. 2017 Oct 19;19(11):1542-1552
pubmed: 28605510
Cancers (Basel). 2021 Dec 29;14(1):
pubmed: 35008312
Aging (Albany NY). 2020 Jun 23;12(12):11185-11199
pubmed: 32575074
J Pediatr. 2007 Apr;150(4):370-5, 375.e1
pubmed: 17382112
Cell Res. 2014 Oct;24(10):1266-9
pubmed: 25145361
Cell Death Dis. 2020 Aug 24;11(8):701
pubmed: 32839432
FASEB J. 2019 Apr;33(4):4962-4974
pubmed: 30657335
Nat Methods. 2012 Jul;9(7):671-5
pubmed: 22930834
Ann Oncol. 2019 Jun 1;30(6):908-920
pubmed: 31111878
Blood Rev. 2018 Jan;32(1):8-28
pubmed: 28802908
Cell Death Differ. 2018 Jan;25(1):37-45
pubmed: 29099482
PLoS One. 2014 Jan 20;9(1):e86629
pubmed: 24466179

Auteurs

Lilly Velentza (L)

Division of Pediatric Endocrinology, Department of Women's and Children's Health, Karolinska Institutet, Visionsgatan 4, BioClinicum J9:30, SE-171 64, Stockholm, Sweden. lilly.velentza@ki.se.

Malin Wickström (M)

Childhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.

Per Kogner (P)

Childhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.

Claes Ohlsson (C)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Farasat Zaman (F)

Division of Pediatric Endocrinology, Department of Women's and Children's Health, Karolinska Institutet, Visionsgatan 4, BioClinicum J9:30, SE-171 64, Stockholm, Sweden.

Lars Sävendahl (L)

Division of Pediatric Endocrinology, Department of Women's and Children's Health, Karolinska Institutet, Visionsgatan 4, BioClinicum J9:30, SE-171 64, Stockholm, Sweden.
Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.

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Classifications MeSH