PDIA6 Contributes to Aerobic Glycolysis and Cancer Progression in Oral Squamous Cell Carcinoma

Abstract

Background/Objective: Accumulated evidence has demonstrated that aerobic glycolysis serves as a regulator of tumor cell growth, invasion and angiogenesis. Herein, we explored the role of protein disulfide isomerase family 6 (PDIA6) in the aerobic glycolysis and the progression of oral squamous cell carcinoma (OSCC). Methods: The expression pattern of PDIA6 in OSCC tissues was determined by qPCR and western blotting. Lentivirus and small interfering RNAs (siRNAs) were introduced into cells to upregulate and downregulate PDIA6 expression. CCK-8, flow cytometry, transwell and xenotransplantation models were applied to detect cell proliferation, apoptosis, migration, invasion and tumorigenesis, respectively. Results: A high expression pattern of PDIA6 was observed in OSCC tissues, which was closely associated with lower overall survival and malignant clinical features in OSCC. Compared with the control group, overexpression of PDIA6 induced significant enhancements in cell growth, migration, invasiveness and tumorigenesis and decreased cell apoptosis, while knockdown of PDIA6 caused opposite results. In addition, overexpression of PDIA6 increased glucose consumption, lactate production and ATP level in OSCC cells.Conclusion: This study demonstrated that PDIA6 expression was elevated in OSCC tissues, and overexpression of it promoted OSCC progression and aerobic glycolysis.

Long non‑coding RNA PCAT6 regulates bladder cancer progression via the microRNA‑143‑3p/PDIA6 axis

“…PDIA6 belongs to the protein disulfide isomerase (PDI) family and is widely expressed in various types of human cancer, including breast cancer (32) and ovarian cancer (33). Increasing evidence suggests that PDIA6 is associated with the progression of various types of cancer (34)(35). For example, Kim et al (36) reported that inhibition of PDIA6 may transduce EGFR signaling by activating and inducing A disintegrin and metalloprotease 17 during the migration and invasion of U87MG glioblastoma cells.…”