[Modified Shenqi Dihuang Decoction acts on hormone-sensitive prostate cancer by inhibiting glycolysis through the PI3K/Akt /mTOR signaling pathway].
Zhonghua Nan Ke Xue
; 28(1): 48-55, 2022 Jan.
Article
em Zh
| MEDLINE
| ID: mdl-37459078
ABSTRACT
Objective:
To evaluate the effect of Modified Shenqi Dihuang Decoction (MSDD) on human hormone-sensitive LNCaP prostate cancer cells and its action mechanism.METHODS:
LNCaP prostate cancer cells were treated with MSDD, followed by detection of the proliferation and apoptosis of the cells by MTT assay and flow cytometry respectively and measurement of glucose uptake and lactate production by glucose uptake assay and colorimetry respectively. The expressions of the apoptosis-related proteins Bcl-2, Bax and cleaved-caspase-3, glycolysis-related proteins HK2, GLUT1, PKM2 and LDHA, and PI3K/AKT/mTOR pathway-related proteins in the LNCaP cells were determined by Western blot. The effect of MSDD on the LNCaP cells was observed with the glycolysis inducer oligomycin and the PI3K activator 740 Y-P.RESULTS:
MSDD inhibited the proliferation, induced the apoptosis, increased the levels of Bax and cleaved-caspase 3 and decreased the level of Bcl-2 in the LNCaP cells in a dose-dependent manner. After MSDD intervention, the glucose uptake and lactate production in the LNCaP cells were significantly reduced, the expressions of HK2, GLUT1, PKM2 and LDHA and the phosphorylation levels of Akt, PI3K and mTOR were markedly suppressed. Oligomycin and 740 Y-P reversed the inhibitory effect of MSDD on the proliferation of the LNCaP cells, and 740 Y-P reversed that on glucose uptake, lactic acid production and the expressions of the glycolysis-related proteins HK2, GLUT1, PKM2 and LDHA in the LNCaP cells.CONCLUSIONS:
Modified Shenqi Dihuang Decoction inhibits the proliferation of LNCaP prostate cancer cells by suppressing glycolysis and the PI3K/Akt/mTOR signaling pathway.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Tipo de estudo:
Diagnostic_studies
Idioma:
Zh
Ano de publicação:
2022
Tipo de documento:
Article