PNU-74654 Suppresses TNFR1/IKB Alpha/p65 Signaling and Induces Cell Death in Testicular Cancer.
Wen-Jung ChenWen-Wei SungChia-Ying YuYu-Ze LuanYa-Chuan ChangSung-Lang ChenTsung-Hsien LeePublished in: Current issues in molecular biology (2022)
Testicular cancer (TC) is a rare malignancy worldwide and is the most common malignancy in males aged 15-44 years. The Wnt/β-catenin signaling pathway mediates numerous essential cellular functions and has potentially important effects on tumorigenesis and cancer progression. The search for drugs to inhibit this pathway has identified a small molecule, PNU-74654, as an inhibitor of the β-catenin/TCF4 interaction. We evaluated the therapeutic role of PNU-74654 in two TC cell lines, NCCIT and NTERA2, by measuring cell viability, cell cycle transition and cell death. Potential pathways were evaluated by protein arrays and Western blots. PNU-74654 decreased cell viability and induced apoptosis of TC cells, with significant increases in the sub G1, Hoechst-stained, Annexin V-PI-positive rates. PNU-74654 treatment of both TC cell lines inhibited the TNFR1/IKB alpha/p65 pathway and the execution phase of apoptosis. Our findings demonstrate that PNU-74654 can induce apoptosis in TC cells through mechanisms involving the execution phase of apoptosis and inhibition of TNFR1/IKB alpha/p65 signaling. Therefore, small molecules such as PNU-74654 may identify potential new treatment strategies for TC.
Keyphrases
- cell cycle arrest
- induced apoptosis
- cell death
- endoplasmic reticulum stress
- oxidative stress
- cell cycle
- papillary thyroid
- pi k akt
- signaling pathway
- small molecule
- cell proliferation
- squamous cell
- stem cells
- squamous cell carcinoma
- lymph node metastasis
- risk assessment
- germ cell
- climate change
- combination therapy
- high density