Human endogenous retroviruses (HERVs) are retroviral sequences passed from parent to offspring in a Mendelian fashion. Due to relatively recent endogenization and correlation to human illness, interest in the HERV-K (HML-2) subclade has increased. Expression of HML-2---specific transcripts and proteins in melanoma cell lines was first discovered about a decade ago. Since there are at least 96 known HML-2 proviruses within the human genome, others have studied the HML-2 transcriptome in melanoma to identify the proviral sequences responsible for such expression. More recently, cDNA cloning frequency was used to detect HML-2 expression in melanoma cell lines and patient samples. Though they were able to detect the expression of several proviruses, cDNA cloning frequency is not as sensitive as RNA-sequencing and therefore they could have missed the expression of poorly expressed proviruses or the expression of rare proviruses. Furthermore, determining transcriptional mechanisms responsible for HML-2 expression in melanoma using cDNA cloning frequency data would be difficult while one could easily do this using a stranded library. Due to the potential role of expressed rare HML-2 proviruses in cancer etiology, and to understand transcriptional mechanisms responsible for HML-2 expression in melanoma, I submitted cellular RNA from five melanoma cell lines and three primary melanocyte populations for RNA-seq. I detected five proviruses that were uniquely expressed in melanoma compared to primary melanocytes. 7q22.2 was the highest expressing provirus followed by 3q12.3, which based on comparison to breast cancer and Tera-1s was only detected in cancerous cell lines. Most proviruses that were expressed in melanoma were young, human specific, and were mostly located in extragenic regions and driven by sense transcription. Two proviruses---7p22.1a and 7p22.1b---contain intact ORFs for Env, yet I was unable to detect the presence of Env in whole cell lysate. Furthermore, three proviruses were capable of LTR-driven transcription in some of my melanoma cell lines which appears to be partially driven by transcription factor binding to LTRs. In conclusion, this work expands upon the known HML-2 transcriptome in melanoma while offering a larger view on HML-2 expression in cancer. It also shows one potential cause of HML-2 expression in melanoma and identifies the potential proviruses responsible for previous HML-2 protein production. Future work should include analyzing the effect epigenetic regulation has on HML-2 expression in cancer. Furthermore, future work should focus on analyzing patient samples to identify unique proviruses expressed in cancer so HML-2 expression can be evaluated for potential therapeutic and diagnosis purposes.