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Cancer stem cells (CSCs) are essentially responsible for tumor initiation, growth, progression, metastasis and recurrence, and cigarette smoke (CS) is closely involved in the occurrence and development of kidney cancer. However, the effect of CS on renal CSCs has not been elucidated yet. In the present study, tumorsphere formation assay was used to enrich renal CSCs from 786-O and ACHN cells. We illustrated that CS effectively promoted renal CSCs stemness by enhancing tumorsphere formation, increasing the expression of renal CSCs markers (CD133, CD44, ALDHA1, Oct4, and Nanog) and elevating CD133+ cell population. Moreover, our results showed that CS triggered the activation of Sonic Hedgehog (SHH) pathway, while inhibition of SHH pathway dampened the promotive effects of CS on renal CSCs. Finally, higher levels of renal CSCs markers and SHH pathway-related proteins were observed in kidney cancer tissues from smokers than non-smoking cancer tissues. Taken together, these results demonstrated the important role of SHH pathway in regulating CS-induced renal CSCs stemness augment. Findings from this study could provide new insight into the molecular mechanisms of CS-elicited stemness of renal CSCs.

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Oxidative stress and inflammation are critically implicated in ambient fine particulate matter (mean diameter < 2.5 μm; PM )-induced lung injury. Autophagy, playing a crucial role in various physiopathological conditions, modulates cellular homeostasis and stress adaptation. Resveratrol is a phytoalexin that exerts potent antioxidant effects on cardiopulmonary diseases. To date, the mechanisms by which resveratrol protects against PM remain to be elucidated. In the present study, we investigated the effect of resveratrol on PM -induced oxidative injury. The potential role of nuclear factor erythroid-2-related factor 2 and autophagy in this progress was explored. Human bronchial epithelial cells were treated with PM and the cytotoxicity and oxidative stress markers were determined. The results showed that PM decreased cell viability and elevated the level of lactate dehydrogenase. The levels of malondialdehyde and reactive oxygen species were increased by PM exposure. PM also induced a significant increase of the inflammatory cytokines including interleukin (IL)-6, IL-8, IL-1β and tumor necrosis factor α. Meanwhile, PM triggered autophagy formation and alteration of the nuclear factor erythroid-2-related factor 2 pathway. Furthermore, human bronchial epithelial cells were co-treated with PM and resveratrol in the presence or absence of 3-methylamphetamine, an inhibitor of autophagic formation. It was revealed that resveratrol intervention abolished PM -induced oxidative injury partially through the suppression of autophagy deregulation. Findings from this study could provide new insights into the molecular mechanisms of pulmonary intervention during PM exposure.

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