مشخصات پژوهش

Background: Bladder cancer (BC) is among the top ten most common cancer types in the world [1]. The heterogeneity of BC calls for substantial research with more in-depth molecular characterization, with the hope of identifying new diagnostic and treatment options [2]. DNA methylation is an epigenetic mechanism involving the transfer of a methyl group. DNA methylation regulates gene expression by recruiting different proteins or by inhibiting the binding of transcription factors to DNA. Methylation can alter gene expression and regulate different signaling pathways such as autophagy [3]. Autophagy has a conserved mechanism whose main role is to recycle cellular components and maintain homeostasis through the removal of undesirable proteins [4]. ATG12 is one of the most important genes involved in autophagy pathways [5]. Aim: This study aimed to explore the function of the ATG12 gene in the autophagy pathway involved in BC based on bioinformatic databases. Methods: Clinical information and promotor methylation level of ATG12 in patients with BC was obtained from The Cancer Genome Atlas (TCGA) based on the following selection criteria including basic clinical information of sample types (normal and primary tumor), gender, age, stage, and nodal metastasis. All requirements were conducted on a large sample size (>400). Datasets were then compared to obtain the significant p-value. Results: Our results indicate that the promotor methylation level of ATG12 is decreased in BC compared with normal tissue. This decrease was observed in different BC stages (1-4), different age groups (21-40, 41-60, 61-80, and 81-100 ys), gender, and nodal metastasis status of BC. There were no significant differences in gender and nodal metastasis (N0, N1, N2, and N3) groups. Conclusion: Our study revealed that ATG12 can be considered an important factor in BC progress with diagnostic and prognostic values.