Track

Abstract

Melanoma is a common skin cancer affecting millions globally, with treatments ranging from surgical excision and radiation to immunotherapy, particularly in metastatic cases. For melanomas harboring the BRAF V600 mutation, targeted therapies such as Vemurafenib, Dabrafenib, and Encorafenib have proven effective. Prior studies suggest that decreased PTEN expression is associated with increased Breslow’s depth, thereby elevating the risk of metastasis. Mutations in CDK4 have been linked to familial melanoma, making CDK4 inhibitors a promising therapeutic option. BFL-1, an anti-apoptotic protein from the BCL2 family, contributes to neutrophil survival and homeostasis and is regulated by the PI3K and JAK/STAT signaling pathways.

In vitro assays were conducted using CHL-1 (BRAF wild-type) and SK-MEL-5 (BRAF V600 mutant) melanoma cell lines. CHL-1 cells were cultured in DMEM, and SK-MEL-5 in EMEM, both supplemented with 10% FBS. Cell invasion and migration were assessed using Matrigel-coated invasion chambers and scratch wound healing assays. Western blot and qRT-PCR analyses were performed to measure gene and protein expression levels of PTEN, CDK4, and BFL-1.

In vitro, CHL-1 cells were found to be significantly more invasive than SK-MEL-5 cells. qRT-PCR results showed higher mRNA levels of PTEN and BCL2A1 in SK-MEL-5 cells, whereas CHL-1 cells exhibited higher protein expression of PTEN and CDK4.