TABLE 3.
In vitro effects of nicotine on lung cancer under nonphysiologic conditions and/or with nonpharmacological concentrations of nicotine
| Lung Cancer Cell Line | Nicotine | Duration of Treatment | Serum Concentration | Cellular Response (Assay) | Result (Relative to Control) | Reference |
|---|---|---|---|---|---|---|
| H460, H157 | 0.01– | 7 days | 10% | Viability (MTT) | H460: 5% increase (10, 100 μM), 5% decrease (1 mM) | Chen et al. (2002) |
| 1 mM | H157: 5% decrease (10 μM), 5% increase (0.1–1 mM) | |||||
| 201T | 10 μM | 48 h | 10% | Viability (MTS) | No effect | Carlisle et al. (2007) |
| H460 | 10 nM, 0.01–1 mM | 5 days | 10% | Viability (Cell Titer-Glo) | 12.5%–50% increase | Zheng et al. (2007) |
| (10 nM, 10–100 μM),* no effect (1 mM) | ||||||
| A549, H1299 | 1 nM to 10 mM | 72 h | Not indicated | Viability (MTT) | A549: 5%–18% increase (1 nM to 10 μM), no effect (100 μM), 5%–40% decrease (1–10 mM)† | Puliyappadamba et al. (2010) |
| H1299: 10%–30% increase (1–100 nM), no effect (1–100 μM), | ||||||
| 40%–80% decrease (1–10 mM)† | ||||||
| H446 | 2.5–15 μM | 12–72 h | 10% | Viability (MTT) | 0%–85% decrease† | Zeng et al. (2012) |
| A549 | 0.01, 10 μM | 24 h | 10% | Viability (MTS) | No effect (0.01 μM), | Gao et al. (2016) |
| 75% decrease (10 μM)* | ||||||
| A549, H1975 | 10 nM to 100 μM | 48 h | 0% for 72 h, then treated | Viability (MTS) | A549: 12.5% increase (50 nM to 100 μM),* H1975: no effect | Mucchietto et al. (2017) |
| Proliferation (cell counting) | A549: 33%–66% increase,* H1975: no effect | |||||
| A549 | 0.5–10 μM | 72 h | 0% | Growth (BrdU) | 0%–9% increase | Jarzynka et al. (2006) |
| Line1 | 1 μM | 18 h | 0% for 72 h, then treated | Growth (BrdU) | 180% increase† | Davis et al. (2009) |
| LKR | 1 μM | 24 h | 0.2% for 24 h, then treated | Growth ([3H]-thymidine) | 200% increase† | Nishioka et al. (2010) |
| A549, H1299 | 1 nM to 100 μM | 24 h | Not indicated | Growth ([3H]-thymidine) | 5%–20% increase (1 nM to 1 μM),† | Puliyappadamba et al. (2010) |
| 5%–20% decrease (10–100 μM)† | ||||||
| A549 | 1 μM | 18 h | 0% for 36 h, then treated | Growth (BrdU) | 150% increase* | Dasgupta et al. (2011) |
| A549, H1650 | 1 μM | 18 h | 0% for 24 h, then treated | Growth (BrdU) | 175%–180% increase† | Pillai et al. (2011) |
| 24 h | Invasion (Boyden) | 90%–100% increase† | ||||
| A549, H1650 | 1 μM | 18 h | 0% for 24 h, then treated | Growth (BrdU) | 75%, 100% increase† | Nair et al. (2014) |
| 24 h | Invasion (Boyden) | 75%, 150% increase† | ||||
| LLC | 1 pM to 100 μM | Not indicated | 0.1% | Proliferation (cell counting) | No effect | Heeschen et al. (2001) |
| H157, H1703 | 100 nM | 3 daysa | 0.1% | Proliferation (cell counting) | 50%–95% increase* | Tsurutani et al. (2005) |
| H1299 | 10 nM | Previously treated for 72 h, then seeded | Not indicated | Proliferation (colony formation) | 150% increase† | Puliyappadamba et al. (2010) |
| A549 | 0.01–10 μM | 18 h | 0% (before and during treatment) | Invasion (Boyden) | 10% decrease (10 nM), 50%–160% increase (0.1–1 μM), 90% increase (10 μM)† | Dasgupta et al. (2009) |
| 24 h | 0% (during treatment) | Migration (wound healing) | 10%–100% increase (0.01–1 μM), 25% increase (10 μM)† | |||
| N417 | 500 μM | Previously treated for 7 days, then seeded | 10% | Proliferation (colony formation) | 130% increase* | Martínez-García et al. (2010) |
| 0.5% | Migration (Transwell) | 55% increase* | ||||
| A549, H1299 | 0.1–1 μM | 36 h | 0% for 24 h, treated, then seeded | Proliferation (cell counting) | 50%–200% increase* | Liu et al. (2015) |
| Migration (wound healing) | 30% increase* | |||||
| Invasion (Transwell) | 20% increase* | |||||
| A549, H1650, H1975, H23, H358 | 1 μM | 24 h | 0% for 36 h, then treated | Invasion (Boyden) | 120%–430% increase* | Pillai et al. (2015) |
| A549, H1299 | 1 μM, | 48 h | 0% for 12 h, then treated | Viability (CCK-8) | 25%, 40% increase* | Gong et al. (2014) |
| 10 nM | 48 h | Invasion (Transwell) | 75% increase* | |||
| 48 h | Migration (wound healing) | 25%, 30% increase* | ||||
| 72 h | ||||||
| A549, H460, LLC, T1 | 5, 10 μM | 24 h | 10% | Viability (MTS, MTT) | No effect | Kyte et al. (2018) |
| A549, H460 | 1 μM | 48–96 h | 0%–5% | Viability (MTS, MTT) | A549: no effect, H460: 25% increase with 0% serum at 96 h* | |
| A549 | 5 μM | 48 h | 10% | Invasion (QCM) | 950% increase* | Zhang et al. (2007) |
| 5, 10 μM | 16 h | Angiogenesis (HIF-1α) | 1000%, 1100% increase* | |||
| 5, 10 μM | 16 h | Angiogenesis (VEGF) | 130%, 170% increase* | |||
| A549, H1299, H1975 | 10, 50 μM | 24 h | 10% | Viability (MTT) | A549: 40% increase (10 μM),* no effect (50 μM) | Ma et al. (2014) |
| H1299: 13%, 14% increase, H1975: 65% increase (10 μM),* 40% increase (50 μM) | ||||||
| A549 | 5 μM | 16 h | Angiogenesis (HIF-1α) | 25% increase | ||
| A549 | 5 μM | 16 h | Angiogenesis (VEGF) | 150% increase | ||
| A549 | 5 μM | 36 h | 10% | Invasion (Transwell) | 230% increase* | Shi et al. (2015) |
| 16 h | Angiogenesis (VEGF protein, mRNA) | 25% increase,* 700% increase* | ||||
| 16 h | Angiogenesis (HIF-1α mRNA) | 100% increase* |
BrdU, bromodeoxyuridine; CCK-8, cell counting kit-8; 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; QCM, QCM (TM) collagen-based cell invasion assay; T1, primary human lung carcinoma; VEGF, vascular endothelial growth factor.
a
Nicotine was replaced every 24 h.
*
Statistically significant.
†
Statistical significance not indicated.