Deciphering miRNAs associated with cellular stress response and apoptosis mechanisms regulated by p53 activity in patients with lower lip cancer
Bozgeyik, Ibrahim, Koparal, Mehtap, Ege, Bilal, Bozgeyik, Esra, Kurt, Muhammed Yusuf, Ceylan, Onur
Cancers of the lips and oral cavity are a leading cause of death worldwide. Although they account for only 2% of the global cancer burden, they significantly affect the comfort of patients and eventually lead to a person's death. Also, defects in the cellular stress response and apoptosis mechanisms regulated by p53 activity is an important hallmark of cancer cells. Here, we aimed to decipher miRNAs associated with cellular stress response and apoptosis mechanisms regulated by p53 activity in patient with lower lip cancer and reveal the association of these miRNAs with the clinical course of the disease. The present research included a total of 40 eligible individuals with pathologically confirmed lower lip cancer diagnosis. Formalin-fixed, paraffin-embedded (FFPE) tissue samples of patients were obtained, and miRNAs expressions were analyzed by qPCR. Immunohisto-chemistry was used to determine p53 and Ki67 expression status. While three of these miRNAs (miR-130a,-375, and-128a) were found to be elevated in tumor cells compared to normal tissues of lower lip cancer patients, five were downregulated (let-7a,-7b,-7c, and miR-138,-23a), but only three were significantly altered. Particularly, we identified three miRNA signatures in which miR-128a was significantly upregulated and miR-23a and let-7c were significantly downregulated in patients with lower lip cancer. Remarkably, let-7c identified to be a promising prognostic factor for lip cancer. Our findings demonstrate that these miRNAs play important regulatory roles in lower lip cancer pathobiology, highlighting their potential relevance in diagnosis and prognosis of these patients. Moreover, these miRNAs can be targeted in future therapeutic interventions against lower lip cancer.
- Journal
- PATHOLOGY RESEARCH AND PRACTICE
- Year
- 2022
- Volume
- 236
- ISSN
- 0344-0338
- eISSN
- 1618-0631
- DOI
- 10.1016/j.prp.2022.153952
- WoS UID
- WOS:000834021400002