Table 9.

Impact of resveratrol on the expression of genes in the context of lung cancer

Type of cancer	Dose range	Cell line	Target	Pathway	Function	Refs.
In vivo studies
Non-Small Cell Lung Cancer (NSCLC)	30 mg/kg 0–100 μM	H460, H1650, HCC827	HK2, Caspase-3, PARP,	AKT, ERK1/2, EGFR	RVT via suppressing the PI3K/AKT-HK2 pathway could play a role in the clinical prevention and treatment of NSCLC	[47]
In vitro studies
NSCLC	25–200 μM	H1703, H1975	XRCC1	AKT, ERK1/2	RVT via downregulating ERK1/2 and AKT-mediated XRCC1 could enhance the chemosensitivity to etoposide in NSCLC cells	[82]
NSCLC	200 μM	A549, H1299	Beclin-1, LC3 II/I, SIRT1, P62, p70S6K	AKT/mTOR, p38-MAPK	RVT by activating p38-MAPK and inhibiting the AKT/mTOR pathway could induce protective autophagy in NSCLC	[83]
NSCLC	0–50 μM	A549, HCC-15	LC3-II, P62, p53, Bax, Bcl-2, Bcl-xl, Caspase-3/8, PUMA, Cytochrome-c	AKT, NF-κB	RVT via suppressing the AKT/NF-κB pathway could sensitize lung cancer cells to TRAIL	[84]
Small Cell Lung Cancer (SCLC)	40 μg/mL	H446	c-Myc, AIF, Bcl-2, Bax, Bcl-xL, Cytochrome-c	PI3K/AKT	RVT via the PI3K/AKT/c-Myc pathway could inhibit viability in SCLC H446 cells	[85]