STAT3 Pathways Contribute to β-HCH Interference with Anticancer Tyrosine Kinase Inhibitors.
STAT3 Transcription Factor
/ metabolism
Humans
Protein Kinase Inhibitors
/ pharmacology
Signal Transduction
/ drug effects
Cell Line, Tumor
Hexachlorocyclohexane
/ pharmacology
Antineoplastic Agents
/ pharmacology
Neoplasms
/ drug therapy
Cell Proliferation
/ drug effects
Cell Survival
/ drug effects
Tyrosine Kinase Inhibitors
STAT3
chemoresistance
environmental pollutants
signaling transduction
β-hexachlorocyclohexane
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
04 Jun 2024
04 Jun 2024
Historique:
received:
30
04
2024
revised:
27
05
2024
accepted:
30
05
2024
medline:
19
6
2024
pubmed:
19
6
2024
entrez:
19
6
2024
Statut:
epublish
Résumé
Organochlorine pesticides (OCPs) are a class of environmentally persistent and bioaccumulative pollutants. Among these, β-hexachlorocyclohexane (β-HCH) is a byproduct of lindane synthesis, one of the most worldwide widespread pesticides. β-HCH cellular mechanisms inducing chemical carcinogenesis correspond to many of those inducing chemoresistance, in particular, by the activation of signal transducer and activator of transcription 3 (STAT3) signaling pathways. For this purpose, four cell lines, representative of breast, lung, prostate, and hepatocellular cancers, were treated with β-HCH, specific tyrosine kinase inhibitors (TKIs), and a STAT3 inhibitor. All cell samples were analyzed by a viability assay, immunoblotting analysis, a wound-healing assay, and a colony formation assay. The results show that β-HCH reduces the efficacy of TKIs. The STAT3 protein, in this context, plays a central role. In fact, by inhibiting its activity, the efficacy of the anticancer drug is restored. Furthermore, this manuscript aimed to draw the attention of the scientific and socio-healthcare community to the issue of prolonged exposure to contaminants and their impact on drug efficacy.
Identifiants
pubmed: 38892372
pii: ijms25116181
doi: 10.3390/ijms25116181
pii:
doi:
Substances chimiques
STAT3 Transcription Factor
0
Protein Kinase Inhibitors
0
STAT3 protein, human
0
Hexachlorocyclohexane
59NEE7PCAB
Antineoplastic Agents
0
beta-hexachlorocyclohexane
YM80ODM9PD
Tyrosine Kinase Inhibitors
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : SAPIENZA UNIVERSITY
ID : Numero protocollo: RP123188F3E745A7
Organisme : FONDAZIONE FEDERICO CALABRESI
ID : 2023