Urquhartburks8240

These findings highlight for the first time the significance of tricellulin in colorectal cancer development and progression. Further study may validate tricellulin as a novel biomarker and target for colorectal cancer.Emerging studies have demonstrated that long non‑coding RNAs (lncRNAs) play essential roles in tumorigenesis. However, the role and function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) have not been completely elucidated. The present study explored the function of a novel lncRNA, RP11‑156L14.1, in HSCC. RP11‑156L14.1 was revealed to be highly expressed in HSCC tissues and cell lines. Knockdown of RP11‑156L14.1 inhibited proliferation, migration, and invasion in HSCC cells. Furthermore, RP11‑156L14.1 regulated epithelial‑mesenchymal transition (EMT) by controlling EMT‑related protein expression. Mechanistically, RP11‑156L14.1 exerted its function as a competing endogenous RNA (ceRNA) and directly interacted with miR‑548ao‑3p. The present study also demonstrated that miR‑548ao‑3p regulated signal sequence receptor subunit 1 (SSR1) expression by targeting SSR1 3'‑UTR. Moreover, the xenograft HSCC tumor model revealed that knockdown of RP11‑156L14.1 markedly suppressed HSCC tumor growth in vivo. In summary, these findings indicated that the lncRNA RP11‑156L14.1 functions as an oncogene in HSCC by competing with miR‑548ao‑3p in regulating SSR1 expression. The RP11‑156L14.1/miR‑548ao‑3p/SSR1 axis could be utilized as a potential novel biomarker and therapeutic target for HSCC.Pulmonary hypertension (PH) in newborns and adults is a disease that can lead to right heart failure and result in a shorter lifespan. PH was induced by maintaining pregnant rats in a hypoxic chamber for 4 h twice a day, from days 7‑21 of pregnancy. Hypoxia was confirmed by a decrease in the partial pressure of oxygen (PaO2) and the oxygen saturation (SaO2) of arterial blood in the aorta. The body weight of newborns from hypoxic rats was ~20% decreased compared with the control newborns of normoxic rats. The vascular wall thickness/vascular diameter values of hypoxia treated pubs were increased compared with that of control newborns 7 days after birth; however, it decreased to similar levels than in the control group after 3 months, and then further decreased to significantly lower levels than in the control group at 6 months after birth. At birth, the lung tissues of newborns from hypoxic rats exhibited an increase in the levels of mRNA and proteins associated with PH such as HIF‑1α, HIF‑2α, V2R, TGF‑β, TNF‑α, Ang‑2 and α‑SMA. At 3 and 6 months after birth, the levels of both V2R mRNA and protein in offspring from hypoxic rats were at least 2‑fold higher, whereas the expression of all other factors decreased compared with the control offspring. By contrast, HIF‑2α and Ang‑2 expression levels were significantly increased in the 6‑month‑old control offspring from normoxic rats. V2R overexpression in pups induced by hypoxia in maternal rats was sustained until their adulthood. V2R may be a marker for detecting PH.Early diagnosis and therapy in the first stages of a malignant disease is the most crucial factor for successful cancer treatment and recovery. Currently, there is a high demand for novel diagnostic tools that indicate neoplasms in the first or pre‑malignant stages. MicroRNAs (miRNA or miR) are small non‑coding RNAs that may act as oncogenes and downregulate tumor‑suppressor genes. The detection and mutual discrimination of the three common female malignant neoplasia types breast (BC), ovarian (OC) and endometrial cancer (EC) could be enabled by identification of tumor entity‑specific miRNA expression differences. In the present study, the relative expression levels of 25 BC, EC and OC‑related miRNAs were assessed by reverse transcription‑quantitative PCR and determined using the 2‑ΔΔCq method for normalization against the mean of four housekeeping genes. Expression levels of all miRNAs were analyzed by regression against cell line as a factor. An expression level‑based discrimination between BC and OC cell types was obtained for a subgroup of ten different miRNA types. miR‑30 family genes, as well as three other miRNAs, were found to be uniformly upregulated in OC cells compared with BC cells. BC and EC cells could be distinguished by the expression profiles of six specific miRNAs. In addition, four miRNAs were differentially expressed between EC and OC cells. In conclusion, miRNAs were identified as a potential novel tool to detect and mutually discriminate between BC, OC and EC. Based on a subset of 25 clinically relevant human miRNA types, the present study could significantly discriminate between these three female cancer types by means of their expression levels. For further verification and validation of miRNA‑based biomarker expression signatures that enable valuable tumor detection and characterization in routine screening or potential therapy monitoring, additional and extended in vitro analyses, followed by translational studies utilizing patients' tissue and liquid biopsy materials, are required.G protein‑coupled receptors (GPCRs) are the largest family of membrane receptors and activate several downstream signaling pathways involved in numerous physiological cellular processes. GPCRs are usually internalized and desensitized by intracellular signals. Numerous studies have shown that several GPCRs interact with sorting nexin 27 (SNX27), a cargo selector of the retromer complex, and are recycled from endosomes to the plasma membrane. Recycled GPCRs usually contain specific C‑terminal postsynaptic density protein 95/Discs large protein/Zonula occludens 1 (PDZ) binding motifs, which are specifically recognized by SNX27, and return to the cell surface as functionally naïve receptors. Aberrant endosome‑to‑membrane recycling of GPCRs mediated by SNX27 may serve a critical role in cancer growth and development. Therefore, SNX27 may be a novel target for cancer therapies.Long non‑coding (lnc)RNAs have been found to play a crucial role in tumor progression. The present study aimed to investigate the association between lncRNA RASSF8‑AS1 and laryngeal squamous cell carcinoma (LSCC) and the underlying mechanisms. Reverse transcription‑quantitative PCR was used to measure the mRNA expression level of RASSF8‑AS1, microRNA(miR)‑664b‑3p and transducin‑like enhancer of split 1 (TLE1) in LSCC. The associations between RASSF8‑AS1 and miR‑664b‑3p, and between miR‑664b‑3p and TLE1 were investigated using a dual luciferase reporter assay, while the former was further verified using an RNA immunoprecipitation (RIP) assay. The association between RASSF8‑AS1 and miR‑664b‑3p on cell biological functions was investigated in vitro using MTS, colony formation and Transwell assays. The RASSF8‑AS1 mRNA expression level was decreased in LSCC cell lines and carcinoma tissues, while overexpression of RASSF8‑AS1 reduced the migration, invasion and proliferation abilities of LSCC cells. Furthermore, luciferase and RIP assays confirmed that RASSF8‑AS1 was a competitive endogenous (ce)RNA by sponging miR‑664b‑3p to activate TLE1. miR‑664b‑3p was negatively modulated by RASSF8‑AS1; however, TLE1 was positively regulated by RASSF8‑AS1. Functionally, RASSF8‑AS1 acted as a ceRNA to upregulate TLE1 by sponging miR‑664b‑3p. In conclusion, the RASSF8‑AS1/miR‑664b‑3p/TLE1 axis acts by suppressing LSCC progression and may provide a novel insight for the molecular mechanism of LSCC.Breast cancer (BC) has a poor prognosis and a high number of visceral metastases. Serine protease inhibitor, clade E member 1 (SERPINE1) is a molecule involved in several human malignancies. However, it remains unknown if SERPINE1 plays a role in the development of taxane resistance in TNBC cells. In the present study, the role and mechanism of SERPINE1 in the development of paclitaxel (PTX) resistance in TNBC cells were investigated. A bioinformatics analysis of gene expression profiles in PTX‑resistant cells indicated that SERPINE1 was significantly associated with PTX resistance. Oxaliplatin in vivo Furthermore, the levels of SERPINE1 mRNA and protein were higher in PTX‑resistant cells with respect to those in PTX‑sensitive parent cells. Knockdown of SERPINE1 significantly inhibited cell survival and induced cell apoptosis in vitro. In addition, SERPINE1 silencing led to downregulation of the key angiogenetic vascular endothelial growth factor A (VEGFA). Furthermore, suppression of SERPINE1 markedly attenuated tumor growth in vivo. Collectively, these findings indicated that SERPINE1 significantly contributed to the proliferation and apoptosis of TNBC cells by regulating VEGFA expression. The present study demonstrated SERPINE1 as an oncogene in PTX drug resistance of breast cancer, and revealed that it may serve as a possible target for treating BC.Hepatitis C virus (HCV) infection is a global public health problem. Cirrhosis and hepatocellular carcinoma are the main causes of death in patients with chronic hepatitis C (CHC) infection. Liver fibrosis is an important cause of cirrhosis and end‑stage liver disease after CHC infection. Along with the course of infection, liver fibrosis exhibits a progressive exacerbation. Hepatic stellate cells (HSCs) are involved in both physiological and pathological processes of the liver. During the chronic liver injury process, the activated HSCs transform into myofibroblasts, which are important cells in the development of liver fibrosis. At present, HCV infection still lacks specific markers for the accurate detection of the disease condition and progression. Therefore, the present review focused on HSCs, which are closely related to HCV‑infected liver fibrosis, and analyzed the changes in the HSCs, including their surface‑specific markers, cytokine production, activation, cell function and morphological structure. The present review aimed to propose novel diagnostic markers, at both the cellular and molecular level, which would be of great significance for the timely diagnosis of the disease. According to this aim, the characteristic changes of HSCs during HCV infection were reviewed in the present article.Bladder cancer (BC) is a serious malignancy worldwide due to its distant metastasis and high recurrence rates. Increasing evidence has indicated that dysregulated long non‑coding RNAs (lncRNAs) are involved in tumorigenesis and progression in multiple malignancies. However, their clinical significances, biological functions and molecular mechanisms in BC remain poorly understood. Hence, the present study investigated the expression profile of lncRNAs and mRNAs in five BC tissues and the corresponding adjacent normal specimens using high‑throughput RNA sequencing (RNA‑seq). A total of 103 differentially expressed (DE) lncRNAs were identified, including 35 upregulated and 68 downregulated ones in BC tissues. Similarly, a total of 2,756 DE‑mRNAs were detected, including 1,467 upregulated and 1,289 downregulated. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses, and lncRNA‑miRNA‑mRNA network analyses suggested that these dysregulated lncRNAs are potentially implicated in the onset and progression of BC.