Abstract: Objective : To explore the putative roles of JNK, p-JNK and PPARγ expression in the carcinogenesis ofesophageal squamous cell carcinoma. Methods : We used immunohistochemistry to detect the expression ofJNK, p-JNK and PPAR γ in 15 normal esophageal epithelium tissue samples, 85 tissue samples ofesophageal intraepithelial neoplasia (EIN) and 60 tissue samples of esophageal squamous cell carcinoma(ESCC). Results : The positive expression rate of JNK was 20.0% in normal esophageal tissue, 37.6% in EIN tissue, and 55.0% in ESCC tissue. The positive expression rate of p-JNK was 33.3% in normal esophageal tis-sue, 55.3% in EIN tissue and 73.3% in ESCC tissue. The positive expression rates of JNK and p-JNK weresignificantly higher in ESCC than in normal esophageal epithelial tissue and EIN lesions (P<0.05). The posi-tive expression rates of JNK and p-JNK were significantly higher in high grade EIN than in normal esophagealtissue and low-grade EIN tissue (P<0.05). The positive expression rate of PPAR γ was 73.3% in normalesophageal tissue, 45.9% in EIN and 45.0% in ESCC, significantly lower than that in normal esophageal tis-sue (P<0.05). Among the ESCC cases, the rate of positive expression of JNK, p-JNK and PPARγ was closelyrelated to the degree of differentiation. The positive expression rates of JNK, p-JNK and PPARγ decreased asthe pathological grade increased (P<0.05). There was no significant correlation between the positive expres-sion rate of JNK, p-JNK or PPARγ and other clinicopathologic features including age, gender, tumor location,tumor size, depth of cancer invasion or lymph node metastasis (P>0.05). Conclusion : As the pathologicalgrade of esophageal epithelial malignancy increases, the positive expression rate of JNK and p-JNK increas-es while PPARγ expression decreases. JNK, p-JNK and PPARγ are involved in the carcinogenesis and pro-gression of ESCC.