RNA-seq and ATAC-seq analysis on MARK3-inducible cells

High-grade serous ovarian carcinoma (HGSOC) is the most aggressive gynecological malignancy, often found at late clinical stages due to the rapid dissemination and metastasis, which causes approximately 70% of deaths from ovarian cancer. Although it is essential to elucidate the etiology and the molecular mechanisms underlying HGSOC, it is still unclear how genetic dysregulations and biological processes promote HGSOC initiation and progression. Here, we conducted a functional analysis of the microtubule affinity-regulating kinase 3 (MARK3) to explore the possibility that this enzyme acts as a tumor suppressor in HGSOC. To gain insights into the molecular mechanism by which MARK3 activity repressed oncogenic signaling pathways, we conducted RNA-seq and ATAC-seq analyses using MARK3-inducible 293T and/or OVCAR3 cells. Overall design: RNA-seq of two groups (No doxycycline-treated and doxycycline-treated OVCAR3 cell line) each with 3 biological replicates. ATAC-seq of two groups (No doxycycline-treated and doxycycline-treated OVCAR3 and 293T cell lines) each with no replicate.