Abstract:Objective: To investigate the expression of GATA-6 and Dickkopf-1 in pituitary adenomas and its clinical significance. Methods: 138 patients with pituitary adenomas were selected. The expressions of GATA-6 and Dickkopf-1 in pituitary adenomas and normal pituitary tissues were detected by real-time fluorescence reverse transcription and immunohistochemistry. The expression of GATA-6 and Dickkopf-1 in pituitary adenomas patients with different clinical features and the prognosis of pituitary adenomas with different levels of GATA-6 and Dickkopf-1 were analyzed. Results: The expression of Dickkopf-1 mRNA in pituitary adenoma group was lower than that in normal pituitary, and the expression of GATA-6 mRNA was higher than that in normal pituitary (P<0.01). The expression of Dickkopf-1 protein in pituitary adenoma group was lower than that in normal pituitary, and the expression of GATA-6 protein was higher than that in normal pituitary (P<0.01). The positive rate of Dickkopf-1 protein pituitary adenoma group was lower than that in normal pituitary gland, and the positive rate of GATA-6 protein pituitary adenoma group was higher than that in normal pituitary gland (P<0.01). The expression of Dickkopf-1 and GATA-6 protein was not significantly correlated with age (P>0.05). The expression of Dickkopf-1 and GATA-6 protein were significantly correlated with TNM stage, pathological grade, recurrence, depth of invasion, infiltration of vascular space, tumor maximum diameter and metastasis, and the higher TNM stage, pathological grade. The higher the credit stage, recurrence, depth of invasion, infiltration of vascular space, tumor diameter (>2cm), the lower the positive expression rate of Dickkopf-1 protein and the higher the positive expression rate of GATA-6 protein (P<0.01). The 3-year survival rate and survival time of Dickkopf-1 positive group were significantly higher than those of Dickkopf-1 negative group, and the 3-year survival rate and survival time of GATA-6 negative group were significantly higher than those of GATA-6 positive group (P<0.01). Conclusion: The expression of GATA-6 in pituitary adenomas is higher and the expression of Dickkopf-1 in pituitary adenomas is lower. GATA-6 play a promoting role in the course of occurrence and development of pituitary adenomas and Dickkopf-1 play a inhibiting role. The pituitary adenomas patients with high expression of Dickkopf-1 or low expression of GATA-6 can get better prognosis
[1] 王松林,李丹.脑垂体瘤的手术治疗方式及应用意义评价[J].中国现代药物应用,2017,11(4):76~77. [2] Casanueva FF, Barkan AL, Buchfelder M, et al. Criteria for the definition of pituitary tumor centers of excellence (PTCOE): a pituitary society statement[J]. Pituitary, 2017, 20(5):489~491. [3] Zhang J, Hou W, Tian L, et al. Anesthesia for the endoscopic nasal pituitary tumor resection:a comparison of two anesthetic techniques[J]. Chinese Journal of Neurosurgical Disease Research, 2017,5(9):78~79. [4] Shi ZD, Lee K, Yang D, et al. Genome editing in hPSCs reveals GATA6 haploinsufficiency and a genetic interaction with GATA4 in human pancreatic development[J].Stem Cell, 2017, 20(5):675~678. [5] Liu T, Zhang L, Wang Y, et al. Dickkopf-1 inhibits Wnt3a-induced migration and epithelial-mesenchymal transition of human lens epithelial cells[J]. Experimental Eye Research, 2017, 161(3):43~51. [6] Liu JT, Guo WB, Sun JY. Serum Dickkopf-1 acts as a new biomarker in human breast cancer[J]. Minerva Medica, 2017,8(2):334~340. [7] Jang J, Jung Y, Kim Y, et al. LPS-induced inflammatory response is suppressed by Wnt inhibitors, Dickkopf-1 and LGK974[J]. Scientific Reports, 2017, 7(2):612~615. [8] Xuan S, Sussel L. GATA4 and GATA6 regulate pancreatic endoderm identity through inhibition of hedgehog signaling[J]. Development, 2016, 143(5):780~781. [9] Martinelli P, Carrillode SPE, Cox T, et al. GATA6 regulates EMT and tumour dissemination, and is a marker of response to adjuvant chemotherapy in pancreatic cancer[J]. Gut, 2016, 66(9): 1665~1676. [10] Tian F, Chen J, Zheng S, et al. miR-124 targets GATA6 to suppress cholangiocarcinoma cell invasion and metastasis[J]. BMC Cancer, 2017, 17(1):175~177.