Porphyromonas gingivalis lipopolysaccharide regulates cell proliferation, apoptosis, autophagy in esophageal squamous cell carcinoma via TLR4/MYD88/JNK pathway.
J Clin Biochem Nutr
; 74(3): 213-220, 2024 May.
Article
em En
| MEDLINE
| ID: mdl-38799145
ABSTRACT
The study aimed to explore the impact and potential mechanism of Porphyromonas gingivalis lipopolysaccharide (LPS-PG) on esophageal squamous cell carcinoma (ESCC) cell behavior. ESCC cells from the Shanghai Cell Bank were used, and TLR4, MYD88, and JNK interference vectors were constructed using adenovirus. The cells were divided into six groups Control, Model, Modelâ
+â
radiotherapyâ
+â
LPS-PG, Modelâ
+â
radiotherapyâ
+â
3-MA, Modelâ
+â
radiotherapyâ
+â
LPS-PGâ
+â
3-MA, and Modelâ
+â
radiotherapy. Various radiation doses were applied to determine the optimal dose, and a radioresistant ESCC cell model was established and verified. CCK8 assay measured cell proliferation, flow cytometry and Hoechst 33258 assay assessed apoptosis, and acridine orange fluorescence staining tested autophagy. Western blot analyzed the expression of LC3II, ATG7, P62, and p-ULK1. Initially, CCK8 and acridine orange fluorescence staining identified optimal LPS-PG intervention conditions. Results revealed that 10â
ng/ml LPS-PG for 12â
h was optimal. LPS-PG increased autophagy activity, while 3-MA decreased it. LPS-PGâ
+â
3-MA group exhibited reduced autophagy. LPS-PG promoted proliferation and autophagy, inhibiting apoptosis in radioresistant ESCCs. LPS-PG regulated TLR4/MYD88/JNK pathway, enhancing ESCC autophagy, proliferation, and radioresistance. In conclusion, LPS-PG, through the TLR4/MYD88/JNK pathway, promotes ESCC proliferation, inhibits apoptosis, and enhances radioresistance by inducing autophagy.
Texto completo:
1
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article