<p>Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells</p>

Abstract

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer and its incidence continues to rise yearly. Photodynamic therapy (PDT) is a noninvasive form of cancer therapy, which utilizes the combined action of a photosensitizer, light, and oxygen molecules to selectively cause cellular damage to tumor cells. Vitamin K3 (VitK3) has been shown to induce apoptosis and inhibit the growth of tumor cells in humans. The purpose of this study was to determine the effect of VitK3 and ultraviolet radiation B (UVB) on oxidative damage, proliferation and apoptosis of A431 cells. Methods: CCK-8 assay was used to detect cell proliferation; Hoechst staining, TUNEL assay and flow cytometry analysis were used to detect apoptosis. Western Blot was perfomed to measure the expression of apoptosis-related proteins. Flow cytometry analysis was employed to detect the reactive oxygen species (ROS) levels and mitochondrial membrane potential. Finally, the role of VitK3 in combination with UVB on the proliferation and apoptosis of A431 cells was investigated using mice xenograft models. Results: We found that the co-treatment of VitK3 combined with UVB more significantly inhibited the growth and proliferation of A431 cells than either VitK3 or UVB alone. Hoechst 33258 staining and flow cytometry analysis revealed that apoptosis was more pronounced in the VitK3-UVB group compared to the VitK3 and UVB groups. Moreover, flow cytometry analysis showed that ROS and the depolarization of the mitochondrial membrane potential were higher in all the co-treatment groups compared to the control, VitK3, and UVB groups. The VitK3-UVB group exhibited a significantly lower tumor growth rate in mouse xenograft models. Conclusion: This study reveals that VitK3 combined with UVB inhibits the growth and induces apoptosis of A431 cells in vitro and suppresses tumor growth and promotes apoptosis of cSCC in vivo.

Preliminary Study on the Role and Mechanism of KIRREL3 in the Development of Esophageal Squamous Cell Carcinoma (ESCC)

“…The cell cycle and cellular evasion of apoptosis are closely related to cell proliferation. An imbalance in their control mechanisms can change cell growth and promote uncontrolled abnormal proliferation of tumor cells [32][33] . Our results suggest that KIRREL3 knockdown blocked cell cycle progression and promoted apoptosis.…”

Targeted Knockdown of Macrophage Migration Inhibitory Factor Enhances UVB Irradiation-Induced Apoptosis Via Increasing ROS Generation in Oral Squamous Cell Carcinoma

“…8 Shi et al found that vitamin K3 plus UVB treatment not only inhibited skin squamous cell proliferation but also induced apoptosis in vitro, while it inhibited tumor growth and promoted apoptosis in vivo . 11 Recently, with the emergence of photosensitizers and UV sensitizers, which confer advantages of high specific selectivity to tumor tissues and low toxicity, photodynamic therapy has become an effective method for tumor diagnosis and treatment and has been successfully applied to treat early-stage cancers of the oral cavity, pharynx, and larynx. 12 However, the effect of UVB irradiation on OSCC has not been studied.…”