In this early experience, EMD appears to be a feasible and minimally invasive treatment for some patients with upper-GI SETs originating from the muscularis propria. Although there is a higher risk of perforation than with ESD, this will improve with extended practice, and perforations have become manageable endoscopically.
Background: Colorectal cancer (CRC) is a common malignant tumor in digestive system. Circular RNA (circRNA) circ_0007142 has been identified as an oncogene in CRC. However, the mechanism of circ_0007142 in CRC was rarely reported. Materials and Methods: The levels of circ_0007142, dedicator of cytokinesis 1 (DOCK1), microRNA-122-5p (miR-122-5p), and cell division cycle 25A (CDC25A) in CRC tissues (n=31) and cells were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability and colony-forming ability were evaluated via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and colony-formation assay, respectively. The migrated and invaded abilities were monitored by Transwell assay. The dual-luciferase reporter assay was performed to validate the interactions between miR-122-5p and circ_0007142 or CDC25A. The protein level of CDC25A was detected via Western blot assay. The biological role of circ_0007142 was examined by xenograft tumor model in vivo. Results: The levels of circ_0007142 and CDC25A were enhanced and the level of miR-122-5p was declined in CRC tissues and cells, while the level of DOCK1 had no fluctuation. Circ_0007142 sponged miR-122-5p and CDC25A was a target of miR-122-5p. Circ_0007142 knockdown impeded cell proliferation, colony formation, migration, and invasion in CRC cells by regulating miR-122-5p. Besides, miR-122-5p inhibitor promoted cell proliferation, colony formation, migration, and invasion in CRC cells by modulating CDC25A. Circ_0007142 regulated CDC25A expression in CRC cells by sponging miR-122-5p. Moreover, circ_0007142 knockdown blocked CRC tumor growth in vivo. Conclusion: Circ_0007142 modulated CDC25A expression to promote CRC progression by sponging miR-122-5p.
Long non-coding RNAs (lncRNAs) exert regulatory functions on various biological processes in cancer cells, including proliferation, apoptosis and mobility. Prostate cancer-associated transcript 1 (PCAT-1) is a novel lncRNA that promotes cell proliferation in prostate cancer, however, the effect of PCAT‑1 in hepatocellular carcinoma (HCC) remains to be elucidated. The present study hypothesized that PCAT‑1 also exerts an important effect in HCC. The current study investigated PCAT-1 expression levels in HCC tissue samples and HepG2 and Bel‑7402 cell lines using the reverse transcription-quantitative polymerase chain reaction. The results demonstrated that PCAT-1 was upregulated in HCC tissue samples and cell lines compared with adjacent non‑cancerous tissues and the L02 normal liver epithelial cell line. PCAT‑1 suppression using PCAT‑1 small hairpin RNA in HepG2 and Bel‑7402 cells inhibited cell proliferation and migration, and induced apoptosis. Overexpression of PCAT‑1 induced synthetic plasmid vectors was demonstrated to increase cell proliferation and migration, and inhibit apoptosis. Results from the present study suggest that PCAT‑1 exerts an oncogenic effect in HCC and silencing PCAT-1 may be a potential novel therapeutic strategy for HCC.
Osteopontin (OPN) plays an important role in metastasis and relapse of human cancer. However, the whole story of OPN relating to cancer has been far from clear untill now. To investigate the expression of OPN in hepatocellular carcinoma (HCC) and its relationships with recurrence and metastasis of HCC, normal and malignant liver tissues from patients with HCC were analyzed using immunohistochemical staining. OPN expression was inhibited by small interfering RNA (siRNA) in HCC cells lines, and then colony formation and matrigel invasion were examined. The results showed that expression of OPN was associated with metastasis of HCC with a positive rate of OPN in the tissue of HCC (70.00%), which was highly more obvious than those in paracarcinoma tissue and normal liver tissue (P < 0.01). In HCC cell lines, OPN depletion could reduce formed colony and metastasizing numbers in vitro. In conclusion, Expression of OPN in the tissue of HCC is related to metastasis or metastases. Specific siRNA could decrease expressions of OPN at both mRNA and protein levels, and abates the invasiveness of hepatocellular carcinoma cells, suggesting that OPN might be a promising agent for treatment of metastasis and recurrence of HCC.
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