Tankyrase expression in lung bronchiolo-alveolar adenocarcinoma and its relationship with the WNT pathway
10.11958/20150339
- VernacularTitle:肺泡样肺腺癌中端锚聚合酶的表达及其与WNT信号通路的关系
- Author:
Chong LI
;
Xu ZHENG
;
Yanyan HAN
;
Yan LYU
;
Fu LAN
;
Jie ZHAO
- Publication Type:Journal Article
- Keywords:
adenocarcinoma,bronchiolo-alveolar;
tankyrase;
WNT signal way;
β-catenin;
lung adenocarcinoma;
c-myc
- From:
Tianjin Medical Journal
2016;44(6):733-735,652
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the expression of tankyrase (TNKS) and its relationship with WNT/β-catenin signal?ing pathway in lung acinar adenocarcinoma. Methods Seventy-two samples of single subtype alveolar like lung adenocarci?noma (lung adenocarcinoma group) and 67 specimens of normal lung tissue adjacent to carcinoma (adjacent to carcinoma group) were collected. Immunohistochemical method was used to detect expressions of TNKS, beta-catenin (β-catenin) and c-myc protein. The correlation of each protein expression in lung adenocarcinoma tissues was analyzed. The differential ex?pression of TNKS was detected by Western blot assay in two groups. Results Tankyrase protein was mainly expressed in cy?toplasm. The expression ofβ-catenin protein was mainly in cytoplasm and nuclear of lung adenocarcinoma. The expression ofβ-catenin was mainly in cytoplasm, and a small amount was in nuclear of the adjacent group. The c-myc protein was ex?pressed mainly in the nucleus. The positive expression rates of TNKS,β-catenin and c-myc protein were significantly high?er in lung adenocarcinoma group than those of adjacent to carcinoma group (P<0.05). The expression ofβ-catenin in cyto?plasm and nucleus was positively correlated with the expression of TNKS and c-myc (P<0.05). Western blot analysis showed that the relative expression level of TNKS was significantly higher in lung adenocarcinoma group than that of adja?cent to carcinoma group (0.497 ± 0.021 vs. 0.237 ± 0.015, t=13.00, P<0.01). Conclusion Abnormally high expression of TNKS in lung adenocarcinoma may promote the occurrence of lung cancer by regulating the WNT signaling pathways. Inhib?iting TNKS expression may become a new target to treat lung adenocarcinoma.
