ObjectiveTo study the expression of insulin-like growth factor Ⅱ mRNA-binding protein 3 ( IMP3 ) and its clinicopathological significance in breast cancer.MethodsThe Maxvision immunohistochemistry was used to detect the expression of IMP3 protein in 103 cases of breast cancer and the adjacent normal breast tissues.Stem-loop real-time RT-PCR was used to detect the expression level of IMP3 mRNA in 30 cases of breast cancer and the matched non-tumor adjacent tissues.The relationship between the expression of IMP3 and the clinicopathological features of breast cancer was analyzed.Results62 cases were infiltrative ductal carcinoma,3cases were invasive lobular carcinoma,9 cases were microinfiltrative intraductal carcinoma,and 29 cases were special type of carcinoma.The difference of IMP3 expression between breast cancer group and normal breast tissue group had statistical significance( t =19.630,P =0.000)by t test.For infiltrative ductal carcinoma patients,IMP3 expression had no significant relation with age,tumor size,lymph node metastasis,histological grade,pTNM stage,ER,PR,or HER-2 ( P ＞ 0.05 ).IMP3 mRNA expression level of was significantly higher in tumor tissues than in the adjacent normal tissues (P ＜ 0.05 ).No significant association was found between the expression of IMP3 and the histological grade,tumor size,lymph node metastasis ( P ＞ 0.05 ).ConclusionIt is possible that IMP3 plays an important role in the generation,progression,invasion and metastasis of breast cancer.

Purpose: Drug resistance is one of the main causes of chemotherapy failure in patients with small cell lung cancer (SCLC), and extensive biological studies into chemotherapy drug resistance are required. Materials and Methods: In this study, we performed lncRNA microarray, in vitro functional assays, in vivo models and cDNA microarray to evaluate the impact of lncRNA in SCLC chemoresistance. Results: The results showed that KCNQ1OT1 expression was upregulated in SCLC tissues and was a poor prognostic factor for patients with SCLC. Knockdown of KCNQ1OT1 inhibited cell proliferation, migration, chemoresistance and promoted apoptosis of SCLC cells. Mechanistic investigation showed that KCNQ1OT1 can activate transforming growth factor-β1 mediated epithelial-to-mesenchymal transition in SCLC cells. Conclusion Taken together, our study revealed the role of KCNQ1OT1 in the progression and chemoresistance of SCLC, and suggested KCNQ1OT1 as a potential diagnostic and prognostic biomarker in SCLC clinical management.