The results indicated that miR‑30a‑3p suppressed metastasis and enhanced the radiosensitivity of EC cells via downregulation IGF‑1R, suggesting that miR‑30a‑3p may be a potential therapeutic target in the treatment of EC.
A higher molar difference between IGFBP3 and IGF1, which estimates the free form of IGFBP3, was associated with a decreased risk of esophageal carcinoma (<i>P</i> = 0.0146), and people in the highest tertile had the lowest risk (OR = 0.107, 95%CI: 0.017-0.669).
The positive expression rates of IGF-1 and IGF-1R in EC were significantly higher than those in adjacent normal tissues (both P < 0.001), and the rate of IGFBP-3 in EC was significantly lower than that in adjacent normal tissues (P < 0.05).
Further subgroup analysis by gene type indicated that common polymorphisms in the IGF1/2, IGF-1R, and IGFBP-3/5 genes may be the main determinants for lung cancer risk, while IGF-1, IGF-1R, and IGFBP-1 genetic polymorphisms may increase the risk of esophageal cancer.
These results indicate that the IGF-1 axis has a key role in malignant progression of esophageal cancer, and represents a plausible mechanism through which visceral obesity impacts on esophageal adenocarcinoma risk and tumor biology.
Therefore, up-regulation of IGF-1 and survivin would seem to be responsible for 5-Fu chemoresistance in esophageal cancer patients and these factors may be the valuable predictors of 5-Fu chemoresistance in esophageal carcinoma.
IGF-1R expression and clinicopathological correlations were analyzed with a tissue microarray containing 234 esophageal cancer specimens (133 adenocarcinomas and 101 squamous cell carcinomas).