Colorectal cancer (CRC) is one of the most common human cancer types and a leading cause of cancer-related death. Accumulating evidence has confirmed that long non-coding RNAs have crucial roles in CRC progression. In the present study, the biological roles of LINC01535 were investigated and the interaction between long intergenic non-coding RNA (LINC)01535 and microRNA (miR)-761 in CRC was explored. LINC01535 expression was observed to be upregulated in CRC tissues and cell lines. A functional study suggested that LINC01535 silencing inhibited CRC cell proliferation and invasion but enhanced cisplatin sensitivity of CRC cells, while co-transfection with a miR-761 inhibitor reversed these biological effects. A luciferase reporter assay demonstrated that LINC01535 regulated miR-761 directly and RNA-binding protein immunoprecipitation further confirmed that the suppression of LINC01535 by miR-761 was via an RNA-induced silencing complex. Finally, knockdown of LINC01535 inhibited the growth of CRC cells in vivo. Collectively, the results suggested that LINC01535 exerts oncogenic functions in CRC by sponging miR-761. In conclusion, the present study indicated that LINC01535 promoted CRC progression through sponging miR-761, and may serve as a potential diagnostic biomarker and therapeutic target for CRC.

Doxorubicin (DOX), as a chemotherapy agent with marked therapeutic effect, can be used to treat certain types of cancer such as leukemia, lymphoma and breast cancer. However, the toxic effects of DOX on cardiomyocytes limit its clinical application. Oxidative stress has been documented to serve a pivotal role in DOX-induced cardiomyopathy. Previous studies have reported that 1,25(OH)2D3 has antioxidant and anti-inflammatory effects and can inhibit the renin-angiotensin system. However, the effects of 1,25(OH)2D3 on the pathophysiological processes of DOX-induced cardiomyopathy and its mechanisms remain poorly understood. To investigate these potential effects, C57BL/6J mice were used to construct a DOX-induced cardiomyopathy model and treated with 1,25(OH)2D3. At 4 weeks after the first injection of DOX, cardiac function and myocardial injury were evaluated by echocardiograph and ELISA. Masson's trichrome staining and RT-qPCR were used to assess myocardial fibrosis, and immunohistochemistry and western blotting were performed to analyze expression levels of inflammation and oxidative stress, and the NLRP3 inflammasome pathway. ChIP assay was used to assess the effects of 1,25(OH)2D3 on histone modification in the NLRP3 and Nrf2 promoters. The results showed that 1,25(OH)2D3 treatment increased LVEF and LVFS, reduced serum levels of BNP and cTnT, inhibited the collagen deposition and profibrotic molecular expression, and downregulated the levels of inflammatory cytokines in DOX-induced cardiomyopathy. ROS and antioxidant indices were also ameliorated after 1,25(OH)2D3 treatment. In addition, 1,25(OH)2D3 was found to inhibit the NLRP3 inflammasome and KEAP-Nrf2 pathways through regulation of the levels of H3K4me3, H3K27me3 and H2AK119Ub in the NLRP3 and Nrf2 promoters. In conclusion, the present study demonstrated that 1,25(OH)2D3 regulated histone modification in the NLRP3 and Nrf2 promoters, which in turn inhibits the activation of NLRP3 inflammasome and oxidative stress in cardiomyocytes, alleviating DOX-induced cardiomyopathy. Therefore, 1,25(OH)2D3 may be a potential drug candidate for the treatment of DOX-induced cardiomyopathy.

Volumetric measurement of polyacrylamide hydrogel (PAHG) is useful for surgical planning. It is not only a significant factor in the preoperative evaluation of breast augmentation, but may also directly affect the postoperative shape of the breast. The objective of the present study was to evaluate whether magnetic resonance imaging (MRI) is able to provide precise calculations of injected PAHG volumes. MRI scans of ten randomly selected patients were imported to Mimics software. The volumes of PAHG were obtained following the reconstruction of the injected PAHG. In order to assess the precision and observer independency of the technique, the volumes of PAHG were estimated by three plastic surgeons using this method. No significant differences were identified among the PAHG injection volumes calculated by the three observers (P=0.173). The intra-observer correlation coefficient was 0.964, which indicates the precision and feasibility of this method for calculating the volume of PAHG. The use of MRI in combination with Mimics software to calculate PAHG volumes is likely to be of significant clinical benefit in preoperative surgical planning.

To improve the bio-solubility and sustained-release properties of a carbon nanotube (CNT)-drug complex, the present study used a hydrophilic polymer, polyethylene glycol (PEG), and β-estradiol (E2), which targets the estrogen receptor in human breast cancer cells (HBCCs), to modify CNTs carrying lobaplatin (LBP) to form E2-PEG-CNT-LBP. The in vitro inhibitory effects against HBCCs and the in vivo pharmacological effect of the complex on heart, liver and kidney tissues were also evaluated. The results indicated that the inhibitory effects of this complex against HBCCs reached 80.44% within 72 h. A blood biochemical test of normal mice indicated that this complex reduced platelet counts, while aspartate aminotransferase levels were increased compared with those in the control group. Histopathological analysis revealed no obvious adverse effects on the heart, liver and kidneys. The in vivo results indicated that the novel E2-PEG-CNT-LBP complex had no obvious toxic effects while exhibiting sustained-release properties. The clearance of E2-PEG-CNT-LBP by non-specific uptake systems was delayed and its clearance was increased compared with LBP alone.

The role of caspase-6 in heart disease is not well understood, particularly with respect to cardiac arrhythmia. Also, the function of syndecan-1 in the stimulation of inflammation or a regenerative response after cardiac injury is unclear. Leptin receptor-deficient (C57BL/KS-leprdb/leprdb) mice were used in the present study. In addition to developing type 2 diabetes, they also develop initial- and end-stage cardiac arrhythmia after 5 and 8 months, respectively. The initial and end-stage arrhythmias were confirmed through progressive variations in the PP intervals observable in electrocardiograms. Histopathological images of the cardiac tissue exhibited scattered and loosened cardiac cells at the initial stage of cardiac arrhythmia, whereas tissue hardness and extensive structural changes in cardiomyocytes were evident at the end stage. At the molecular level, the progressive upregulation of caspase-6 was observed as the cardiac arrhythmia progressed. In the initial stage of arrhythmia, immunohistochemistry revealed that caspase-6 was expressed at the surface of cardiac cells, suggesting that caspase-6 targeted the extracellular matrix, leading to a loosening of the cardiac tissue structure. In the end stage of cardiac arrhythmia, caspase-6 expression was abundant in the cytoplasm, as well as at the cell surface, suggesting that caspase-6 may have cleaved intermediate filaments, paving the way for cellular morphological changes and apoptosis. Notably, syndecan-1 was upregulated 5.8-fold in the initial stage of cardiac arrhythmia, but downregulated at the end stage. Syndecan-1 may restrict the expression of caspase-6 in the initial stage of cardiac arrhythmia, while its downregulation at the end stage may allow destructive changes via caspase-6 overexpression. Furthermore, the knockdown of syndecan-1 using small interfering RNA enhanced the expression of caspase-6 in the cardiac tissue by factors of 1.8 and 1.2 at the initial and end stages of cardiac arrhythmia, respectively, compared with that in non-silenced cardiac tissue. Therefore, it may be concluded that syndecan-1 plays a major role in the regulation of caspase-6 during the pathological stages of cardiac arrhythmia.

The aim of this study was to investigate the expression of decorin (DCN) in the intestinal tissues of mice with inflammatory bowel disease (IBD) and its correlation with autophagy. The IBD mouse model was created by intrarectal injection of trinitrobenzene sulfonic acid. The pathology of colon tissues of the mice was examined using hematoxylin and eosin staining. Expression of DCN and the proteins associated with autophagy was detected using immunohistochemistry. Normal human colon mucosal epithelial cells (NCM460 cells) were transfected with DCN expression plasmid and the expression of DCN and autophagy-associated proteins was detected by western blot analysis. Cell apoptosis was studied using an Annexin V apoptosis detection assay and intracellular autophagosomes were observed using electron microscopy. The IBD mouse model was successfully established. Thickening, edema and inflammatory cell infiltration of the intestinal wall were observed in the IBD mice. The expression of DCN as well as the autophagy-associated proteins beclin 1 and LC3B, was increased in the intestinal tissues of the IBD mice. Furthermore, in the NCM460 cells transfected with DCN, the expression of beclin 1 and LC3B was upregulated, while p62 expression was downregulated. Intracellular autophagosomes were increased and apoptosis was decreased in the cells with DCN overexpression. Inhibition of autophagy reversed the effects of DCN on apoptosis. Therefore, DCN is able to induce autophagy and protect intestinal cells during the occurrence and development of IBD.

Cancer stem cells (CSCs) are considered to serve a key role in tumor progression, recurrence and metastasis. Tumorsphere culture is the most important method for enriching CSCs and is widely used in basic research and drug screening. However, the traditional suspension cell culture system has several disadvantages, including low efficiency, high cost and difficult procedure, making it difficult to produce tumorspheres on a large scale. In the present study, two biomaterials, methylcellulose (MC) and gellan gum (GG), were used to construct a novel culture system based on the traditional system. Subsequently, the characteristics of the novel three-dimensional (3D) culture system were evaluated, the design scheme was optimized, and the morphological and biological features of the tumorspheres cultured in this 3D system were compared with the traditional system. The results revealed that the tumorspheres cultured in the novel 3D system presented a higher seeding density and improved morphology, while maintaining stem-like properties. This evidence suggests that a simple, efficient and low-cost culture system that produces tumorspheres on a large scale was successfully constructed, which can be widely used in various aspects of stem cell research.

Although long non-coding (lnc)RNAs have been reported to be involved in the pathological development of bladder cancer, the functions of lncRNA prostate cancer-associated transcript 6 (PCAT6) and its underlying mechanism of action in bladder cancer remain unknown. The present study aimed to investigate the effect of PCAT6 in bladder cancer progression and explore its potential application as a novel treatment target. The expression of PCAT6 and miR-143-3p in bladder cancer tissues, adjacent normal tissues and cell lines was measured using reverse transcription-quantitative PCR. Fluorescence in situ hybridization assay was used to detect the subcellular localization of PCAT6. MTT, EdU, Transwell and wound healing assays were conducted to assess the biological function of PCAT6 on cell proliferation, migration and invasion. Putative binding sites between miR-143-3p and PCAT6 or PDIA6 were predicted using starBase, Lncbase and TargetScan analyzes. Dual-luciferase reporter assay was also used to confirm the potential binding between PCAT6 and miR-143-3p. RNA immunoprecipitation assay was performed to verify the possible interaction between PCAT6 and miR-143-3p. Western blotting was used to measure the expression of PDIA6. The results demonstrated that the expression levels of PCAT6 were upregulated in bladder cancer tissues relative to those in adjacent normal bladder tissues. Knockdown of PCAT6 served a role in suppressing the proliferation, migration and invasion of T24T and EJ bladder cancer cells. PCAT6 knockdown contributed to a reduction of PDIA6 expression at the mRNA and protein levels compared with that in negative control-transfected cells, whilst the miR-143-3p inhibitor partially mitigated this reduction effect. In addition, rescue experiments revealed that the miR-143-3p inhibitors reversed the effects of PCAT6 silencing on the malignant phenotypes of bladder cancer. Collectively, the results of the present study demonstrated that PCAT6 may serve an oncogenic role in bladder cancer via the miR-143-3p/PDIA6 axis. These results may provide a potential therapeutic target for the treatment of bladder cancer.

The aim of the present study was to determine the role of nucleolar and spindle-associated protein 1 (NuSAP1) in human liver cancer. NuSAP1 expression was determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blotting and immunohistochemistry in hepatocellular carcinoma (HCC) and adjacent tissues. The expression of NuSAP1 gene was detected by RT-qPCR in liver cancer cell lines. Expression information for NuSAP1 was determined using the UALCAN and Oncomine databases. The Kaplan-Meier plotter and The Cancer Genome Atlas databases were used to obtain overall survival data for liver cancer. Liver cancer cell lines HepG2 and Huh-7 were transfected with lentiviral particles to silence the endogenous NuSAP1 gene expression. RT-qPCR and western blotting were performed to confirm the silencing efficiency. Cell Counting Kit-8 was used to estimate the effects of NuSAP1 silencing on HepG2 and Huh-7 cell proliferation. Cell cycle and apoptosis analyses were performed using flow cytometry. Cell invasion was assessed using the Transwell assay with microscopy imaging. The results revealed that the NuSAP1 expression levels in HCC tissues were significantly increased compared with the adjacent tissues. The survival time of patients with HCC with a high NuSAP1 expression was markedly decreased compared with that of patients with HCC with a low expression level of NuSAP1. Functional studies revealed that NuSAP1 silencing significantly reduced HepG2 and Huh-7 cell proliferation and invasion. Increased apoptosis and cell cycle arrest at the G1 phase were observed following NuSAP1 knockdown. NuSAP1 silencing significantly inhibited the mRNA expression of DNA methyltransferase but not glioma-associated oncogene. NuSAP1 contributed to liver cancer development by reducing apoptosis and promoting cell cycle progression. The abnormal expression level of NuSAP1 may serve a role in promoting liver cancer progression.