Growth Suppression of Cancer Spheroids With Mutated KRAS by Low-toxicity Compounds from Natural Products.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Aug 2021
Historique:
received: 22 05 2021
revised: 04 06 2021
accepted: 05 06 2021
entrez: 20 7 2021
pubmed: 21 7 2021
medline: 30 7 2021
Statut: ppublish

Résumé

Among compounds from natural products selectively suppressing the growth of cancer spheroids, which have mutant (mt) KRAS, NP910 was selected and its derivatives explored. The area of HKe3 spheroids expressing wild type (wt) KRAS (HKe3-wtKRAS) and mtKRAS (HKe3-mtKRAS) were measured in three-dimensional floating (3DF) cultures treated with 18 NP910 derivatives. The 50% cell growth inhibition (GI50) was determined by long-term 3DF (LT3DF) culture and nude mice assay. We selected NP882 (named STAR3) as the most effective inhibitor of growth of HKe3-mtKRAS spheroids with the least toxicity among NP910 derivatives. GI50s of STAR3 in LT3DF and nude mice assay were 6 μM and 30.75 mg/kg, respectively. However, growth suppression by STAR3 was observed in 50% of cell lines independent of KRAS mutation, suggesting that the target of STAR3 was not directly associated with KRAS mutation and KRAS-related signals. STAR3 is a low-toxicity compound that inhibits growth of certain tumour cells.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
Among compounds from natural products selectively suppressing the growth of cancer spheroids, which have mutant (mt) KRAS, NP910 was selected and its derivatives explored.
MATERIALS AND METHODS METHODS
The area of HKe3 spheroids expressing wild type (wt) KRAS (HKe3-wtKRAS) and mtKRAS (HKe3-mtKRAS) were measured in three-dimensional floating (3DF) cultures treated with 18 NP910 derivatives. The 50% cell growth inhibition (GI50) was determined by long-term 3DF (LT3DF) culture and nude mice assay.
RESULTS RESULTS
We selected NP882 (named STAR3) as the most effective inhibitor of growth of HKe3-mtKRAS spheroids with the least toxicity among NP910 derivatives. GI50s of STAR3 in LT3DF and nude mice assay were 6 μM and 30.75 mg/kg, respectively. However, growth suppression by STAR3 was observed in 50% of cell lines independent of KRAS mutation, suggesting that the target of STAR3 was not directly associated with KRAS mutation and KRAS-related signals.
CONCLUSION CONCLUSIONS
STAR3 is a low-toxicity compound that inhibits growth of certain tumour cells.

Identifiants

pubmed: 34281875
pii: 41/8/4061
doi: 10.21873/anticanres.15207
doi:

Substances chimiques

Antineoplastic Agents 0
Biological Products 0
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

4061-4070

Informations de copyright

Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Sayuri Hashimoto (S)

Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.

Masayoshi Nagai (M)

Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.

Kensuke Nishi (K)

Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Section of Otolaryngology, Department of Medicine, Fukuoka Dental College, Fukuoka, Japan.

Shuhei Ishikura (S)

Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Central Research Institute for Advanced Molecular Medicine, Fukuoka University, Fukuoka, Japan.

Kazuhiko Nakabayashi (K)

Department of Maternal-Fetal Biology, National Center for Child Health and Development, Tokyo, Japan.

Ryo Yazaki (R)

Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.

Takashi Ohshima (T)

Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.

Masahiko Suenaga (M)

Department of Chemistry, Graduate School of Science, Kyushu University, Fukuoka, Japan.

Senji Shirasawa (S)

Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Central Research Institute for Advanced Molecular Medicine, Fukuoka University, Fukuoka, Japan.

Toshiyuki Tsunoda (T)

Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan tsunoda@fukuoka-u.ac.jp.
Central Research Institute for Advanced Molecular Medicine, Fukuoka University, Fukuoka, Japan.

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Classifications MeSH