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Bladder cancer (BC) is the second most common urological disease worldwide. Previous studies have reported that microRNA (miR)-16-5p is associated with the development of BC, but whether miR-16-5p regulates BC cell autophagy remains unknown. Thus, the aim of the present study was to investigate this issue. miR-16-5p expression in BC cells was assessed by reverse transcription-quantitative PCR. Cell viability and apoptosis were detected via Cell Counting Kit-8 and flow cytometry assays, respectively. For cell autophagy detection, autophagic flux was detected using a mCherry-green fluorescent protein-microtubule-associated proteins 1A/1B light chain 3B (LC3) puncta formation assay, followed by determination of autophagy-related protein markers. The targeting relationship between miR-16-5p and caspase recruitment domain family member 10 (BIMP1) was confirmed using a dual-luciferase reporter assay, followed by detection of the BIMP1/NF-κB signaling pathway. The results showed that miR-16-5p overexpression inhibited cell viability, whereas miR-16-5p knockdown promoted cell viability in BC. Furthermore, miR-16-5p overexpression induced autophagy, which was accompanied by increased autophagic flux and expression of the autophagy-related proteins LC3-II and beclin 1, as well as decreased p62 expression, whereas miR-16-5p silencing led to an inhibition of autophagy in BC cells. Moreover, autophagy inhibitor 3-methyladenine treatment inhibited cell autophagy and apoptosis in miR-16-5p-overexpressing cells. Mechanistic studies demonstrated that miR-16-5p could inhibit the BIMP1/NF-κB signaling pathway and this inhibition was achieved by directly targeting BIMP1. Furthermore, it was found that blockade of the BIMP1/NF-κB signaling pathway inversed the inhibitory effects of miR-16-5p knockdown on autophagy in BC cells. In vivo experiments further verified the tumor-suppressive effect on BC of the miR-16-5p/BIMP1/NF-κB axis. Therefore, the results of the present study indicated that miR-16-5p promotes autophagy of BC cells via the BIMP1/NF-κB signaling pathway, and an improved understanding of miR-16-5p function may provide therapeutic targets for clinical intervention in this disease.

Kidney cancer is among the most important causes of cancer-associated mortality worldwide. The present study aimed to evaluate protein kinase C α (PKCα) expression in kidney cancer tissues and cell lines, and its significance in apoptosis and migration. Expression of PKCα was analyzed using quantitative polymerase chain reaction and western blotting. In addition, the inhibitor of PKCα (calphostin C and GO6976) was used to treat kidney cancer cells. The ACHN cell line was generated with PKCα-small-interfering RNA (siRNA) and a stable expression of PKCα, in order to facilitate the analysis of apoptosis and migration of PKCα during knockdown and inactivation. Flow cytometry was used to determine the rates of apoptosis. Immunohistochemical staining was used to identify the localization of PKCα in renal clear cell carcinoma and normal sections. PKCα expression in normal tissues was found to be greater than in cancerous tissues. Furthermore, apoptosis was not promoted with PKCα inhibitors or PKCα-siRNA treatment, and a decrease of the migration ability was observed following transfection with PKCα-dominant negative. The results indicated that inhibition of PKCα might not contribute to apoptosis progression in kidney carcinoma.

Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine that is reported to regulate cellular motility and invasive capability during tumor progression. Fascin1, an actin-bundling protein, increases cell motility, migration and adhesion. To investigate the function of TGF-β1 and test whether fascin1 is an important mediator of the tumor response to TGF-β1 in bladder carcinoma cells, real-time RT-PCR and western blot analysis were used to test changes in fascin1 expression after TGF-β1 (10 ng/ml) treatment in T24 and BIU87 cells. Small interfering RNA (siRNA) technique was performed to silence fascin1. Cell viability and biological behavior changes were evaluated by cell growth (MTT), wound-healing and Matrigel invasion assays. In the present study, we found that the mRNA and protein levels of fascin1 in the T24 and BIU87 cells were significantly increased after 10 ng/ml TGF-β1 treatment (p

Bladder cancer frequently shows mutational activation of the oncogene Ras, which is associated with bladder carcinogenesis. However, the signaling pathway downstream of Ras remains to be fully elucidated. N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) is able to induce bladder cancer by driving the clonal expansion of initiated cells carrying the activated form of Ras. Phospholipase Cε (PLCε) is the main target of BBN, while the tumor promoting role of PLCε remains controversial. The present study examined the role of PLCε in BBN‑induced bladder carcinogenesis of mice with genetically inactivated PLCε. Using light and electron microscopy, the present study demonstrated that PLCε(‑/‑) mice were resistant to BBN‑induced bladder carcinogenesis. Furthermore, it was demonstrated that cyclooxygenase 2 and vascular endothelial growth factor‑A were affected by the PLCε background of the mice, suggesting that the role of PLCε in tumor promotion may be ascribed to augmentation of inflammatory responses and angiogenesis. These results indicated that PLCε is crucial for BBN‑induced bladder carcinogenesis as well as signaling downstream of Ras, and that PLCε is a candidate molecular target for the development of anti-cancer drugs.

RNA‑binding motif 3 (RBM3) is a cold‑shock protein that has been previously shown to attenuate cancer stem cell‑like features in prostate cancer (PCa) cells. However, the mechanism underlying RBM3 regulation in PCa cells is largely unknown. The present study investigated the impact of RBM3 expression on the whole transcriptome of PCa cells using high‑throughput RNA sequencing (RNA‑seq). Differentially expressed genes (DEGs) that were identified through RNA‑seq were applied to Gene Ontology (GO), pathway analysis, pathway‑action networks and protein‑protein interaction network analysis. GO and pathway ananlyses showed that RBM3 expression was associated with several metabolism pathways. Combining GO analysis and pathway analysis, certain DEGs, including phospholipase A2 group IIA (PLA2G2A), PLA2G2F, PLA2G4C, endothelin 1, cytochrome P450 family 2 subfamily B member 6, G protein subunit γ5, nitric oxide synthase 3 and CD38 molecule, were shown to be closely associated with RBM3 regulation in PCa cells. Furthermore, the changes in expression of selected genes upon RBM3‑knockdown in RNA‑seq were confirmed by separate reverse transcription‑quantitative‑polymerase chain reaction, validating the results of RNA‑seq. Thus, the present study provides a series of valuable reference genes and pathways for the future study of the pathogenic role of RBM3 in the development of PCa.

Aberrant expression of long noncoding RNAs (lncRNAs) is associated with cancer tumorigenesis and progression. It has been suggested that lncRNAs may be potential clinical diagnostic and prognostic biomarkers, and therapeutic targets. In the present study, the expression levels of small nucleolar RNA host gene 15 (SNHG15) were significantly upregulated in renal cell carcinoma (RCC) tissues and cell lines compared with in adjacent tissues and a proximal tubule epithelial cell line, as determined by reverse transcription‑quantitative polymerase chain reaction. Subsequently, knockdown of SNHG15 expression with small interfering RNA inhibited RCC proliferation, invasion and migration, was determined by western blotting and Transwell assays. Furthermore, the present study suggested that SNHG15 may be involved in the nuclear factor‑κB signaling pathway, induce the epithelial‑mesenchymal transition process, and promote RCC invasion and migration.

Bladder cancer (BCa) is the most common urological cancer, and more and more evidence suggests that microRNAs (miRNAs) play an important role in BCa pathogenesis. Aberrant miR-130b expression has been reported in several types of cancers. The aim of the present study was to elucidate the effects of miR-130b on BCa progression. miR‑130b expression in BCa cell lines and tissues was detected using real-time PCR (RT-PCR), and vestigial-like protein 4 (VGLL4) expression in tissue specimens and BCa cells that had been transfected with miR-130b mimics and inhibitors was detected using western blotting. Dual-luciferase reporter assay was performed to confirm whether the VGLL4 gene is a direct target of miR-130b, and in vitro cell function testing, Cell Counting Kit-8 (CCK-8) assay, colony formation assay, wound healing and Transwell assays were performed to examine BCa cell proliferation, migration and invasion ability after the cells were transfected with miR-130b mimics and inhibitors and VGLL4 siRNA. miR-130b was found to be upregulated in BCa cells and tissues. miR-130b overexpression promoted BCa cell proliferation, migration and invasion, whereas miR-130b inhibition had the opposite effects. Dual-luciferase reporter assay confirmed that the VGLL4 gene was a direct target of miR-130b and that VGLL4 suppression was crucial for miR‑130b-induced BCa cell proliferation, migration and invasion. The present study showed that miR-130b was significantly upregulated in BCa and may play an oncogenic role in BCa occurrence and development by targeting VGLL4. miR-130b may be a potential therapeutic target in the treatment of BCa.