TABLE 2.
In vitro effects of nicotine on lung cancer
| Lung Cancer Cell Line | Nicotine (μM) | Duration of Treatment | Serum Concentration | Cellular Response (Assay) | Result (Relative to Control) | Reference |
|---|---|---|---|---|---|---|
| 14 SCLC and NSCLC lines | 0.1–1 | 5 days | 10% | Viability (MTT) | No effect | Maneckjee and Minna (1990) |
| H460, H157 | 0.1–1 | 7 days | 10% | Viability (MTT) | No effect | Chen et al. (2002) |
| 201T | 1 | 48 h | 10% | Viability (MTS) | No effect | Carlisle et al. (2007) |
| H460 | 0.1, 1 | 5 days | 10% | Viability (Cell Titer-Glo) | 20%, 25% increase* | Zheng et al. 2007) |
| A549 | 1 | 24 h | 10% | Viability (MTT) | 20% increase* | Zhang et al. (2009) |
| Growth ([3H]-thymidine) | 50% increase* | |||||
| A549, H1299 | 0.1, 1 | 72 h | Not indicated | Viability (MTT) | H1299: 20%, 5% increase† | Puliyappadamba et al. (2010) |
| A549: 10%, 15% increase† | ||||||
| 72 h | Growth ([3H]-thymidine) | H1299: 15%, 5% increase† | ||||
| A549: 20%, 10% increase† | ||||||
| Previously treated for 72 h, then seeded | Proliferation (colony formation) | A549: 175% increase (1 μM)† | ||||
| H441, H1299 | 1 | 30 min or 7 daya | 10% | Viability (MTT) | 100%, 75% increase (30 min),* | Al-Wadei et al. (2012) |
| 375%, 250% increase (7 days)* | ||||||
| H446 | 0.1–1 | 12–72 h | 10% | Viability (MTT) | 8, 5% increase at 12 h (0.1, 0.25 μM),† no effect at 24–48 h, | Zeng et al. (2012) |
| 8% decrease at 72 h (0.5, 1 μM)† | ||||||
| A549 | 1 | 3–5 days | 10% | Viability (MTT) | 40%–80% increase* | Wu et al. (2013) |
| 24 h | Invasion (Boyden) | 60% increase* | ||||
| A549 | 0.1, 1 | 24 h | 10% | Viability (MTS) | 40%, 55% decrease* | Gao et al. (2016) |
| LKR, H5800 | 1 | 2 wkb | 10% | Proliferation (colony formation) | 13%, 24% increase† | Nishioka et al. (2010) |
| SW900 | 1 | 24 h | Not indicated | Proliferation (cell counting) | 275% increase* | Chernyavsky et al. (2015) |
| A549 | 1 | 24 h | 10% | Invasion (Transwell) | 7% increase | Sun and Ma (2015) |
| 8 or 24 h | Migration (wound healing) | 10% increase (8 h), 28% increase (24 h)* | ||||
| A549, H460, LLC, T1 | 0.1–1 | 24 h | 10% | Viability (MTS, MTT) | No effect | Kyte et al. (2018) |
| A549, H460 | 1 | 48–96 h | Viability (MTS, MTT) | No effect | ||
| 1 | 48 h | Proliferation (cell counting) | No effect | |||
| 1 | 24 h | Proliferation (colony formation) | No effect | |||
| A549 | 0.5, 1 | 16 h | 10% | Angiogenesis (HIF-1α) | 350%, 750% increase* | Zhang et al. (2007) |
| Angiogenesis (VEGF) | 14% increase (0.5 μM), | |||||
| 43% increase (1 μM)* | ||||||
| A549, H1299, H1975 | 0.1, 1 | 24 h | 10% | Viability (MTT) | A549: 39, 52% increase* | Ma et al. (2014) |
| H1299: 13% increase (0.1 μM), | ||||||
| 20% increase (1 μM)* | ||||||
| H1975: 30% increase (0.1 μM), | ||||||
| 52% increase (1 μM)* | ||||||
| A549 | 0.1–1 | 16 h | Angiogenesis (HIF-1α) | 20%–40% increase (0.1, 0.5 μM), | ||
| 100% increase (1 μM)* | ||||||
| A549 | 0.1–1 | 16 h | Angiogenesis (VEGF) | 75%, 125% increase (0.1, 0.5 μM), | ||
| 175% increase (1 μM)* |
HIF-1α, hypoxia-inducible factor 1-α; LLC, Lewis lung carcinoma; MTS, (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium); MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; SCLC, small cell lung cancer; T1, primary human lung carcinoma; VEGF, vascular endothelial growth factor.
a
Nicotine was replaced every 24 h.
b
Nicotine was replenished every 4 days.
*
Statistically significant.
†
Statistical significance not indicated.