Title:Schisandrin B Inhibits Cell Viability and Malignant Progression of Melanoma Cells
via Wnt/β-catenin Signaling Pathway
Volume: 23
Issue: 15
Author(s): Jiayi Chen, Lingzhao Zhang, Yihuan Pu, Yangmei Chen, Yuxin Li, Xingyu Pan and Jin Chen*
Affiliation:
- Department of Dermatology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China
Keywords:
Melanoma, schisandrin B, anti-tumor, Wnt/β-catenin, traditional Chinese medicine, signaling pathway.
Abstract:
Background: Melanoma is of great interest due to its aggressive behavior and less favorable prognosis. The
need for the development of novel drugs for the treatment of melanoma is urgent. Considerable evidence indicated that
Schisandrin B (Sch B), a bioactive compound extracted from Schisandra chinensis, has numerous anti-tumor properties
in multiple malignant tumors. A few studies have reported the effect of Sch B on melanogenesis in the melanoma
B16F10 cell line; however, the specific anti-tumor effects and mechanisms need to be further explored.
Objective: This study aimed to investigate the effects of Sch B on the cell viability, migration, invasion, and cell cycleblocking
of melanoma cells and explore its potential anti-tumor mechanism in vitro and in vivo.
Methods: Melanoma cells (A375 and B16) were treated with different concentrations of Sch B (0, 20, 40, 60, or 80
μM), with dimethyl sulfoxide (DMSO) as control. The inhibitory effect of Sch B on A375 and B16 melanoma cells
was verified by crystal violet assay and CCK8 assay. The flow cytometry was performed to observe cell cycle blocking.
The effect of Sch B on the migration and invasion of melanoma cells was detected by wound healing assay and
transwell assay, respectively. Western blot analysis was used to determine protein expression levels. The growth of the
A375 melanoma xenograft-treated groups and immunohistochemical staining were conducted to assess the anti-tumor
effect of Sch B in vivo.
Results: The crystal violet assay and CCK8 assay showed that Sch B significantly inhibited melanoma cell viability in
a dose-dependent manner. Meanwhile, the flow cytometry analysis revealed that Sch B induced melanoma cell cycleblocking
at the G1/S phase. In addition, the wound healing assay and transwell assay showed that Sch B inhibited the
migration and invasion of melanoma cells. Furthermore, by establishing an animal model, we found that Sch B significantly
inhibited the growth of melanoma in vivo. The potential mechanism could be that Sch B inhibited the activity of
the Wnt/β-catenin signaling pathway.
Conclusion: These findings indicated that Sch B inhibits the cell viability and malignant progression of melanoma
cells via the Wnt/β-catenin pathway and induces cell cycle arrest. Our study suggests that Sch B has potential as a
bioactive compound for the development of new drugs for melanoma.
