The potential roles of p53 signaling reactivation in pancreatic cancer therapy

Globally, pancreatic cancer (PC) is a common and highly malignant gastrointestinal tumor that is characterized by an insidious onset and ready metastasis and recurrence. Over recent decades, the incidence of PC has been increasing on an annual basis; however, the pathogenesis of this condition remains enigmatic. PC is not sensitive to radio- or chemotherapy, and except for early surgical resection, there is no curative treatment regime; consequently, the prognosis for patients with PC is extremely poor. Transcription factor p53 is known to play key roles in many important biological processes in vertebrates, including normal cell growth, differentiation, cell cycle progression, senescence, apoptosis, metabolism, and DNA damage repair. However, there is a significant paucity of basic and clinical studies to describe how p53 gene mutations or protein dysfunction facilitate the occurrence, progression, invasion, and resistance to therapy, of malignancies, including PC. Herein, we describe the involvement of p53 signaling reactivation in PC treatment as well as its underlying molecular mechanisms, thereby providing useful insights for targeting p53-related signal pathways in PC therapy.