همایش ملی بیوانفورماتیک ایران

صفحه اصلی / 4th international edition and 13th Iranian Conference on Bioinformatics

Reduced PINK1 Expression in Bladder Cancer: Insights into Autophagy Dysregulation and Therapeutic Potential

نویسندگان :

Shayan Jahangirzadeh¹ Mehdi Asghari Vostakolaei² Asadollah Asadi³ Masoumeh Valipour⁴

1- Department of Biology, Faculty of Basic Science, Azarbaijan Shahid Madani University, Tabriz, Iran 2- Cancer Immunology and Immunotherapy Research Center, Ardabil University of Medical Sciences, Ardabil, Iran 3- Department of Biology, Faculty of Science, University of Mohaghegh Ardabili, Ardabil, Iran 4- Department of Biology, Faculty of Basic Science, Azarbaijan Shahid Madani University, Tabriz, Iran

کلمات کلیدی :

Bladder Cancer،PINK1،TCGA،Bioinformatics،Autophagy

چکیده :

Background: Bladder cancer (BC) is one of the most common malignancies worldwide, characterized by high recurrence and progression rates, which pose significant challenges for patient management (Tran, Xiao et al. 2021). Understanding its molecular underpinnings is essential for developing more effective therapies (Mikhaleva, Pechnikova et al. 2021). Autophagy, a vital cellular process that degrades and recycles damaged organelles and proteins, plays a dual role in cancer, supporting cell survival under stress while potentially suppressing tumor initiation (Das, Shukla et al. 2021). The PTEN-induced kinase 1 (PINK1) gene, best known for its role in mitochondrial quality control, has emerged as a key regulator of autophagy. Aberrations in PINK1 expression disrupt autophagic pathways, contributing to cancer progression (Gan, Callegari et al. 2022). Investigating the relationship between PINK1 and autophagy in bladder cancer may reveal promising therapeutic targets. Methods: PINK1 expression levels in bladder cancer patients were retrieved from The Cancer Genome Atlas (TCGA) using specific selection criteria. These criteria included basic clinical data such as sample types (normal and primary tumor), histological subtypes, molecular subtypes, patient weight, and cancer stage. The analysis utilized a large sample size (>400), and the datasets were compared to identify statistically significant p-values. Results: Our findings reveal that PINK1 expression levels are reduced in bladder cancer tissues compared to normal tissues. This reduction was consistently observed across various BC stages (1–4), weight categories, histological subtypes, and molecular subtypes. Conclusion: Our study demonstrates a significant reduction in PINK1 expression levels in bladder cancer tissues compared to normal tissues, consistently observed across various clinical and molecular subgroups, including different stages, weight categories, and histological and molecular subtypes. These findings suggest that PINK1 dysregulation may play a crucial role in BC pathogenesis, potentially through its impact on autophagic pathways and mitochondrial quality control. The consistent downregulation of PINK1 across diverse patient subsets highlights its potential as a biomarker for BC progression and a candidate for targeted therapeutic intervention. Further research is warranted to elucidate the precise mechanisms linking PINK1 to bladder cancer biology and to explore its clinical utility in improving diagnosis, prognosis, and treatment strategies.

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