Table 4 NM-induced injuries that may contribute to cancer

TiO₂-NPs

5–6 nm

ICR mice

1.25, 2.5, and 5 mg/kg b.w., nasal exposure, 9 months

Caused pulmonary tumorigenesis

[82]

Lipid-NPs

150 nm

Kunming mice

16.5 mg/kg b.w., oral administration, 5, 10, 15, and 20 w

Enhanced the oncogenic effects of diethylnitrosamine and resulted in liver cancer in mice

[84]

SWCNTs

Width: 0.1–1 μm, length: 0.8–1.2 nm

BEAS-2B cells

In vitro: 0.02 μg/cm², 12 and 24 w; in vivo: 2 × 10⁶ B-SWCNTs and passage-control cells, subcutaneous injection, 12 and 14 d

Induced malignant transformation and tumorigenesis

[81]

SWCNTs

Width: 0.8 to 1.2 nm, length: 0.1 to 1 μm

BEAS-2B cells

0.1 μg/mL, 6 months

Triggered gene expression alterations related to oncogenic potential

[79]

SWCNT

Width: 0.1–1 μm, length: 0.8–1.2 nm

SAEC cells and BEAS-2B cells

In vivo: 2 × 10⁶ SWCNT-treated SAEC and BEAS-2B cells, subcutaneous; in vitro: 0.1 μg/mL, 6 months; injection, 21, 28, and 35 d

Induced the transformation of human lung epithelial cells to stem-like cells with malignant properties

[80]

Si-NPs

57.66 ± 7.30 nm

BALB/c nude mice, BEAS-2B cells

In vivo: 1 × 10⁷ Si-NP-treated cells, subcutaneous injection, 3–4 w; In vitro: 5 μg/mL, 18 w

Induced malignant transformation and tumorigenesis of human lung epithelial cells via P53 signaling

[83]