BackgroundThe present study aimed to investigate the clinicopathological significance and biological roles of RASSF6 in human bladder cancers.Materials and methodsImmunohistochemistry and Western blots were used to examine the protein expression of RASSF6 in bladder cancer tissues. Biological roles of RASSF6 were examined using MTT, colony formation assay, Matrigel invasion assay, cell cycle analysis, AnnexinV/PI staining and JC-1 staining. Western blot analysis was used to examine the potential mechanism.ResultsWe found that RASSF6 was downregulated in 73 of 138 bladder cancer specimens, which correlated with advanced stages. RASSF6 overexpression decreased the cell growth rate and inhibited invasion ability in T24 cell line. Downregulation of RASSF6 using siRNA increased the cell proliferation rate and promoted invasion in 5637 cell line. Cell cycle studies showed that RASSF6 overexpression suppressed the process of cell cycle progression. RASSF6 overexpression also increased the cellular response to doxorubicin (DOX) treatment. AnnexinV/PI staining showed that RASSF6 overexpression promoted DOX-induced apoptosis with increased cytochrome c and cleavage of caspase-3 and caspase-9. We also showed that RASSF6 overexpression downregulated the mitochondrial membrane potential, while RASSF6 depletion showed the opposite effect. Western blot analysis demonstrated that RASSF6 overexpression repressed p-Rb and Bcl-xL while upregulating p21 expression. In addition, we found that RASSF6 overexpression affected the Hippo signaling pathway by downregulating YAP. Depletion of YAP downregulated Bcl-xL expression and abolished the effect of RASSF6 on Bcl-xL. Depletion of YAP also upregulated the level of apoptosis and downregulated mitochondrial membrane potential. YAP siRNA abolished the effects of RASSF6 on DOX-induced apoptosis and loss of mitochondrial membrane potential.ConclusionTaken together, our results showed that RASSF6 was downregulated in bladder cancers. RASSF6 inhibited cell proliferation and invasion, as well as the progression of cancer, by regulating DOX sensitivity and mitochondrial membrane potential, possibly via the Hippo signaling pathway.
BackgroundWe analyzed the clinical and imaging characteristics of patients with breast ductal carcinoma in situ with microinvasion (DCISM) and breast ductal carcinoma in situ (DCIS).MethodsWe analyzed the records of 40 patients diagnosed with DCISM and 61 patients with DCIS who were hospitalized at Shengjing Hospital (Shenyang, China) from January 2009 to June 2016. The size, hardness, and degree of calcification of tumors were determined by mammography and ultrasonography.ResultsIn all, 37 DCISM patients and 45 DCIS patients showed clinical palpable masses (92.5% vs 73.77%, P = 0.018). Mammography showed that the mean size of tumor was larger in DCISM patients than that of DCIS patients (3.13 ± 1.51 vs 2.68 ± 1.77, P = 0.030). Ultrasound examination revealed calcification shadows in the solid tumor mass in 17 DCISM cases and 11 DCIS patients (42.5 vs 18.03%, P = 0.007). Furthermore, estrogen receptor positivity and progesterone receptor positivity were more common in DCIS patients (32.5% vs 54.10%, P = 0.033; 22.5% vs 45.90%, P = 0.017), and the percentage of menopausal patients were higher in DCISM patients than that of DCIS patients (70.00% vs 47.54%, P = 0.026).ConclusionClinically palpable and calcified tumor masses on sonography are more commonly encountered in DCISM lesions.
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