Original Article
Abnormality of p16/p38MAPK/p53/Wipl pathway in papillary thyroid cancer
Abstract
Objective: To investigate the expression of the pl6/p38MAPK/p53/Wipl pathway in patients with papillary thyroid cancer (PTC) and its clinical significance.
Methods: The protein expressions of Wipl, p53, p38MAPK, and p16 in 70 cases of PTC tissues and 20 cases of normal thyroid tissues were detected by immunohistochemical staining. The correlations of Wipl protein high-expression with p53, p38MAPK, and pl6 protein expressions were analyzed.
Results: The high-expression rate of Wipl protein in the PTC tissue was 64.3% (45/70), which was significantly different than that in normal thyroid tissue (0/20) (P<0.01). There were no significant differences between the paired groups in terms of age, gender, tumor size, and lymph node metastasis (all P>0.05). The Wipl protein high-expression was negatively correlated with the expressions of p38MAPK, p53 and pl6 (r value was –0.620, 0.356 and 0.550, respectively, and all P<0.01).
Conclusions: The pl6/p38MAPK/p53/Wipl pathway is abnormal in PTC, and this abnormality may possibly be associated with the aberrantly up-regulated Wipl, which can induce inhibition of p38MAPK, p53 and p16.of p38MAPK, p53
and pl6 (r value was –0.620, 0.356 and 0.550, respectively, and all P<0.01).
Conclusions: The pl6/p38MAPK/p53/Wipl pathway is abnormal in PTC, and this abnormality may
possibly be associated with the aberrantly up-regulated Wipl, which can induce inhibition of p38MAPK, p53
and pi6.
Methods: The protein expressions of Wipl, p53, p38MAPK, and p16 in 70 cases of PTC tissues and 20 cases of normal thyroid tissues were detected by immunohistochemical staining. The correlations of Wipl protein high-expression with p53, p38MAPK, and pl6 protein expressions were analyzed.
Results: The high-expression rate of Wipl protein in the PTC tissue was 64.3% (45/70), which was significantly different than that in normal thyroid tissue (0/20) (P<0.01). There were no significant differences between the paired groups in terms of age, gender, tumor size, and lymph node metastasis (all P>0.05). The Wipl protein high-expression was negatively correlated with the expressions of p38MAPK, p53 and pl6 (r value was –0.620, 0.356 and 0.550, respectively, and all P<0.01).
Conclusions: The pl6/p38MAPK/p53/Wipl pathway is abnormal in PTC, and this abnormality may possibly be associated with the aberrantly up-regulated Wipl, which can induce inhibition of p38MAPK, p53 and p16.of p38MAPK, p53
and pl6 (r value was –0.620, 0.356 and 0.550, respectively, and all P<0.01).
Conclusions: The pl6/p38MAPK/p53/Wipl pathway is abnormal in PTC, and this abnormality may
possibly be associated with the aberrantly up-regulated Wipl, which can induce inhibition of p38MAPK, p53
and pi6.
