Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway

Abstract

Background

Oral cancer (OC) is one of the most common cancers around the world. Despite the progress in treatment, the prognosis of OC remains poor, especially for patients with advanced diseases. It urges the development of novel therapeutic options against OC. Lycopene (LYC) is an antioxidant with chemoprotective properties against cancer. However, little is known about the mechanisms underlying the protective role of LYC in OC tumorigenesis.

Methods

In this study, we investigated the anti-cancer effect of LYC on the progression of OC in vitro and in vivo and explored the underlying mechanisms involved in this process.

Results

LYC inhibited OC cell proliferation, migration, invasion, apoptosis, and xenograft tumor growth in a dose-dependent manner. Furthermore, we found that LYC might inhibit epithelial–mesenchymal transition and induce apoptosis in OC cells by deactivating the PI3K/AKT/m-TOR signaling through increasing the levels of E-cadherin and Bax and downregulating N-cadherin, p-PI3K, p-AKT, p-m-TOR, and bcl-2.

Conclusion

We reported for the first time that LYC exhibited anti-cancer effects on OC development both in vitro and in vivo via regulating EMT process and apoptosis. These findings provide support for the potential clinical use of LYC in OC treatment.

Keywords:

• oral cancer
• lycopene
• EMT
• apoptosis
• AKT

Disclosure

The authors report no conflicts of interest in this work.