Lentinan Exerts Antitumor Activity in Non-small Cell Lung Cancer through P53-mediated Cytochrome c Release and Caspase Activation: A Preclinical Study.

INTRODUCTION

Lentinula edodes is regarded as a functional food and dietary supplement due to its significant nutritional and medicinal value. Lentinan (LTN) was reported to enhance immune function and exhibit antitumor activity. Although numerous studies have confirmed the inhibitory effect of LTN on tumors in vitro, its underlying mechanisms remain unclear.

METHODS

The present study was designed to investigate the anticancer effects of LTN and the associated mechanisms in a non-small cell lung cancer (NSCLC) cell model.

RESULTS

Lentinan has been demonstrated to exert anti-proliferative effects on NSCLC cells. Furthermore, studies indicate that it effectively induces cell cycle arrest, promotes apoptosis, and suppresses the migration and invasion capabilities of NSCLC cells. Mechanistically, LTN has been observed to upregulate the expression of P53-related proteins and downregulate matrix metalloproteinases (MMPs). These findings strongly suggest that LTN induces apoptosis in NSCLC cells through caspase activation mediated by mitochondrial cytochrome c release. We also employed Magnetic Resonance Imaging (MRI) to monitor tumor growth in mice, with results demonstrating a significant reduction in tumor size in the treatment group. Additionally, Laser Speckle Contrast Imaging was utilized to assess blood perfusion in the axillary region of these mice.

DISCUSSION: This study indicates that LTN, as a natural compound, exhibits the potential for multi-target action in the treatment of NSCLC. By inducing the mitochondrial apoptosis pathway and modulating tumor cell behavior, LTN demonstrates significant antitumor effects. These findings provide a solid experimental foundation for the further clinical development of LTN.

CONCLUSION

These in vivo experiments further demonstrated that LTN exhibits a significant inhibitory effect on tumor growth in a lung cancer model.