Recent studies show that Karyopherin alpha 2 (KPNA2) is up-regulated in quite a number of cancers and associated with poor prognosis. Here, we found that expression levels of KPNA2 and OCT4 are up-regulated in bladder cancer tissues and significantly associated with primary tumor stage and bladder cancer patients' poorer prognosis. Our data also showed decreased cell proliferation and migration rates of bladder cancer cell lines when the expression of KPNA2 and OCT4 was silenced. Meanwhile, cell apoptosis rate was increased. Furthermore, Co-IP and immunofluorescence assay showed the KPNA2 interacts with OCT4 and inhibits OCT4 nuclear transportation when KPNA2 was silenced. Thus, we confirmed that up-regulated KPNA2 and OCT4 expression is a common feature of bladder cancer that is correlated with increased aggressive tumor behavior. Also, we propose that KPNA2 regulates the process of OCT4 nuclear transportation in bladder cancer.
Background/Aims: Increasing evidence has shown that miR-216b plays an important role in human cancer progression. However, little is known about the function of miR-216b in renal cell carcinoma. Methods: The expression levels of miR-216b in renal cell carcinoma tissues and cell lines were examined by qRT-PCR. The biological role of miR-216b in renal cell carcinoma proliferation and/or metastasis was examined in vitro and in vivo. The target of miR-216b was identified by a dual-luciferase reporter assay. The expression level of KRAS protein was measured by western blotting. Results: The expression of miR-216b was downregulated in clear cell renal cell carcinoma (ccRCC) cell lines and specimens compared to the adjacent normal tissues. Furthermore, miR-216b can bind to the 3’untranslated region (UTR) of KRAS and inhibit the expression of KRAS through translational repression. The in vitro study revealed that miR-216b attenuated ccRCC cell proliferation and invasion. Furthermore, in vivo study also showed that miR-216b suppressed tumor growth. MiR-216b exerted its tumor suppressor function through inhibiting the KRAS-related MAPK/ERK and PI3K/AKT pathways. Conclusion: Our findings provide, for the first time, significant clues regarding the role of miR-216b as a tumor suppressor by targeting KRAS in ccRCC.
Background: To study the effects of long non-coding ribonucleic acid (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on the proliferation and apoptosis of malignant melanoma cells, and to explore its specific regulatory mechanism through the nuclear factor-κB (NF-κB) signaling pathway. Methods: LncRNA HOTAIR small-interfering RNAs (siRNAs) were designed and synthesized, and the effects of si-HOTAIR transfection on the proliferation and apoptosis of malignant melanoma cells were detected via cell counting kit-8 (CCK-8) assay, 4',6-diamidino-2-phenylindole (DAPI) staining assay and flow cytometry, respectively. The gene expressions were determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), the changes in NF-κB pathway-related proteins and apoptosis-associated proteins after interference in lncRNA HOTAIR were detected via Western blotting, and the level of NF-κB in each group was determined via ELISA. Results: The results of CCK-8 assay revealed that the cell proliferation rate significantly declined gradually in si-HOTAIR group compared with that in si-NC group and control group (P<0.05). The results of Western blotting and ELISA showed that the activity of NF-κB in si-HOTAIR group was weakened (P<0.05), suggesting that down-regulation of HOTAIR can suppress the activity of NF-κB. Compared with si-NC group and control group, si-HOTAIR group had remarkably increased gene and protein expressions of pro-apoptotic Bax, and remarkably decreased gene and protein expressions of anti-apoptotic Bcl-2 (P<0.05), demonstrating that down-regulation of HOTAIR can promote apoptosis. Conclusion: Down-regulation of lncRNA HOTAIR can inhibit the proliferation and promote the apoptosis of malignant melanoma cells and suppress the NF-κB pathway.
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