RTA‑408 induces p38‑dependent apoptosis and suppresses cell viability in hepatocellular carcinoma cells.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
추출되지 않음
I · Intervention 중재 / 시술
RTA-408 for 24 h
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
Inhibition of p38 partially restored cell viability and reduced apoptosis. [CONCLUSION] RTA-408 suppresses HCC cell survival through a p38-dependent stress response associated with NRF2 activation and LC3B/p62 accumulation.
[INTRODUCTION] Hepatocellular carcinoma (HCC) remains difficult to treat, highlighting the need for new therapeutic strategies.
APA
Chen WC, Chong YB, et al. (2026). RTA‑408 induces p38‑dependent apoptosis and suppresses cell viability in hepatocellular carcinoma cells.. Hepatic oncology, 13(1), 2659967. https://doi.org/10.1080/20450923.2026.2659967
MLA
Chen WC, et al.. "RTA‑408 induces p38‑dependent apoptosis and suppresses cell viability in hepatocellular carcinoma cells.." Hepatic oncology, vol. 13, no. 1, 2026, pp. 2659967.
PMID
42041104 ↗
Abstract 한글 요약
[INTRODUCTION] Hepatocellular carcinoma (HCC) remains difficult to treat, highlighting the need for new therapeutic strategies. RTA-408 (omaveloxolone), a synthetic oleanane triterpenoid and NRF2 pathway modulator, has reported anticancer activity, but its mechanisms in HCC are not fully understood.
[MATERIALS AND METHODS] HepG2 and PLC/PRF/5 (PP5) cells were treated with RTA-408 for 24 h. Cell viability, apoptosis, and signaling pathways were evaluated using MTT assay, Annexin V/7-AAD flow cytometry, and western blotting. The role of p38 signaling was examined using the p38 inhibitor SB203580.
[RESULTS] RTA-408 reduced cell viability in a concentration-dependent manner and increased apoptosis in both cell lines. At 600 nM, apoptosis increased to approximately 18.43% in HepG2 cells and 24.71% in PP5 cells. RTA-408 increased p38 phosphorylation and NRF2 expression and was accompanied by LC3B and p62 accumulation and elevated cleaved caspase-3. Inhibition of p38 partially restored cell viability and reduced apoptosis.
[CONCLUSION] RTA-408 suppresses HCC cell survival through a p38-dependent stress response associated with NRF2 activation and LC3B/p62 accumulation.
[MATERIALS AND METHODS] HepG2 and PLC/PRF/5 (PP5) cells were treated with RTA-408 for 24 h. Cell viability, apoptosis, and signaling pathways were evaluated using MTT assay, Annexin V/7-AAD flow cytometry, and western blotting. The role of p38 signaling was examined using the p38 inhibitor SB203580.
[RESULTS] RTA-408 reduced cell viability in a concentration-dependent manner and increased apoptosis in both cell lines. At 600 nM, apoptosis increased to approximately 18.43% in HepG2 cells and 24.71% in PP5 cells. RTA-408 increased p38 phosphorylation and NRF2 expression and was accompanied by LC3B and p62 accumulation and elevated cleaved caspase-3. Inhibition of p38 partially restored cell viability and reduced apoptosis.
[CONCLUSION] RTA-408 suppresses HCC cell survival through a p38-dependent stress response associated with NRF2 activation and LC3B/p62 accumulation.
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