Anticancer and apoptotic effect of alogliptin on A549 cancer cell line.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
The American Type Culture Collection's (ATCC) normal HBL100 cells and human lung A549 cells were used in the investigation.
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
Alo has caused cancer cell death through a variety of mechanisms, such as DPP4 inhibition, apoptotic pathway activation, and oxidative stress enhancement based on DPP-4, BAX, caspase-3, and MDA measurements.
[OBJECTIVE] Aim: To evaluate the anticancer, apoptotic, and antioxidant effects of Alo on A549 cells, both alone and in combination with CP, and to elucidate the molecular mechanisms underlying the de
- p-value P < 0.05
- p-value P < 0.0001
APA
Abbas SHR, Bairam AF (2026). Anticancer and apoptotic effect of alogliptin on A549 cancer cell line.. Wiadomosci lekarskie (Warsaw, Poland : 1960), 79(2), 346-354. https://doi.org/10.36740/WLek/217851
MLA
Abbas SHR, et al.. "Anticancer and apoptotic effect of alogliptin on A549 cancer cell line.." Wiadomosci lekarskie (Warsaw, Poland : 1960), vol. 79, no. 2, 2026, pp. 346-354.
PMID
41955594 ↗
Abstract 한글 요약
[OBJECTIVE] Aim: To evaluate the anticancer, apoptotic, and antioxidant effects of Alo on A549 cells, both alone and in combination with CP, and to elucidate the molecular mechanisms underlying the death of cancer cells.
[PATIENTS AND METHODS] Materials and Methods: The American Type Culture Collection's (ATCC) normal HBL100 cells and human lung A549 cells were used in the investigation. The cells were split into four groups. Following a 72-hour incubation period, ELISA assays were used to quantify the levels of the DPP-4 enzyme, apoptotic regulators (Bax and caspase-3), and oxidative stress marker (malondialdehyde) in lung cancer cell and normal cell lines. One-way ANOVA with significance set at P < 0.05 were used in the statistical analysis.
[RESULTS] Results: The findings showed that Alo reduced the activity of the DPP-4 enzyme in both cell lines (P < 0.0001). Molecular analysis showed a considerable increase in pro-apoptotic markers (BAX, Caspase-3). Higher amounts of malondialdehyde were indicative of increased oxidative stress in both monotherapy and combination. But in HBL 100 cells, Alo decreased BAX, caspase-3, and MDA levels.
[CONCLUSION] ConclusionS: Alo has caused cancer cell death through a variety of mechanisms, such as DPP4 inhibition, apoptotic pathway activation, and oxidative stress enhancement based on DPP-4, BAX, caspase-3, and MDA measurements.
[PATIENTS AND METHODS] Materials and Methods: The American Type Culture Collection's (ATCC) normal HBL100 cells and human lung A549 cells were used in the investigation. The cells were split into four groups. Following a 72-hour incubation period, ELISA assays were used to quantify the levels of the DPP-4 enzyme, apoptotic regulators (Bax and caspase-3), and oxidative stress marker (malondialdehyde) in lung cancer cell and normal cell lines. One-way ANOVA with significance set at P < 0.05 were used in the statistical analysis.
[RESULTS] Results: The findings showed that Alo reduced the activity of the DPP-4 enzyme in both cell lines (P < 0.0001). Molecular analysis showed a considerable increase in pro-apoptotic markers (BAX, Caspase-3). Higher amounts of malondialdehyde were indicative of increased oxidative stress in both monotherapy and combination. But in HBL 100 cells, Alo decreased BAX, caspase-3, and MDA levels.
[CONCLUSION] ConclusionS: Alo has caused cancer cell death through a variety of mechanisms, such as DPP4 inhibition, apoptotic pathway activation, and oxidative stress enhancement based on DPP-4, BAX, caspase-3, and MDA measurements.
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🏷️ 같은 키워드 · 무료전문 — 이 논문 MeSH/keyword 기반
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