Abstract
Background/objectiveAccumulated 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).MethodsThe 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.ResultsA 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.ConclusionThis study demonstrated that PDIA6 expression was elevated in OSCC tissues, and overexpression of it promoted aerobic glycolysis and OSCC progression.
Highlights
Oral squamous cell carcinoma (OSCC), as a major type of head and neck cancer, ranks the sixth most common malignant tumor in the world and ranks eighth in cancer-related mortalities [1]
protein disulfide isomerase family 6 (PDIA6) was overexpressed in OSCC tissues To explore the role of PDIA6 in the progression of OSCC, we first assessed its expression profile in OSCC tissues
PDIA6 high expression predicted poor prognosis and malignant clinicopathologic features in OSCC we evaluated the clinical value of PDIA6 in OSCC
Summary
Oral squamous cell carcinoma (OSCC), as a major type of head and neck cancer, ranks the sixth most common malignant tumor in the world and ranks eighth in cancer-related mortalities [1]. Despite big Aerobic glycolysis, known as the Warburg effect, is one of the main features of cancer cells [6, 7]. Glucose uptake and lactate production are increased in tumor cells via the aerobic glycolysis pathway to meet the requirement of elevated bioenergetic and biosynthetic demand for growth, metastasis, and invasion, leading to lactate content increase and pH value decrease. Evidence has demonstrated that elevated lactate level is closely associated with tumor growth, invasion, and angiogenesis [9, 10]. Cai et al [11] reported that lactate dehydrogenase A (LDHA) was highly expressed in OSCC tissues and cell lines, and knockdown of it repressed cell proliferation, migration, invasion, and in vivo tumor formation through inhibiting glycolysis. Targeting aerobic glycolysis pathway is a promising method for cancer treatment [12]
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