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Self-Esteem along with Excessive Ingesting between Teenage Children: The function involving Physique Disinvestment.
A ROC analysis suggested LIFR-AS1 expression could be reliably used to differentiate between normal and GC tumor tissue. In addition, elevated LIFR-AS1 expression was positively correlated with more advanced and aggressive GC features, such as larger tumor size, lymphatic metastasis, and more advanced TNM stage. Survival analyses revealed that elevated LIFR-AS1 expression was correlated with worse overall survival and disease-free survival. Multivariate analysis further confirmed the relevance of LIFR-AS1 as an independent predictor of GC patient outcomes. Conclusions In summary, these results indicate that the lncRNA LIFR-AS1 is a promising prognostic indicator in GC patients.Objective Visfatin is significantly upregulated in colorectal cancer (CRC). However, its exact role in CRC progression and the regulatory mechanism involved in this process have not been fully illuminated. The aim of this study was to investigate the roles of visfatin in CRC progression and the potential molecular mechanism. Materials and methods In vitro, two CRC cell lines (DLD-1 and SW480) were transfected with visfatin, si-visfatin, and their control vectors. Some cells were transfected with miR-140-3p mimics or miRNA negative control. Cell Counting Kit-8 and transwell invasive assays were used to detect cell proliferation and invasion ability. Luciferase reporter assays were performed to confirm whether CXC motif chemokine receptor 4 (CXCR4) directly targets miR-140-3p. Western blotting and qRT-PCR analyses were respectively conducted to evaluate the protein and mRNA levels of stromal cell-derived factor-1 (SDF-1) and CXCR4. In vivo, DLD-1 cells transfected with visfatin construct or vector control were inoculated into nude mice. After 5 weeks, the mice were sacrificed, and the tumor nodules were weighed. The expression of visfatin, SDF-1, and CXCR4 in tumor tissues was detected via immunohistochemistry analysis. Results In vitro, the transfection of visfatin promoted the proliferation and invasion of CRC cells, as well as upregulated the expression of SDF-1/CXCR4. MiR-140-3p directly targets the 3'untranslated region of CXCR4. MiR-140-3p expression was downregulated by treatment with visfatin, and miR-140-3p exerted similar effects to those of visfatin knockdown on the proliferation and invasion of CRC cells. In vivo, visfatin stimulated CRC tumor growth and downregulated miR-140-3p expression, whereas it upregulated SDF-1/CXCR4 expression. Conclusions Visfatin promotes CRC progression by downregulating the SDF-1/CXCR4-mediated expression of miR-140-3p both in vitro and in vivo.Objective Colorectal cancer (CRC) remains one of the most ordinary cancers worldwide. Recently, researches have suggested the important role of long noncoding RNAs (lncRNAs) in the progression of tumorigenesis. This study aims to identify how lncRNA OR3A4 functions in the development of CRC. Patients and methods OR3A4 expressions in 54 paired CRC tissues and CRC cell lines were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the in vitro functions of OR3A4 in CRC cells were identified by performing proliferation assay, wound healing assay, and transwell assay. Besides, the underlying mechanism of OR3A4 in CRC development was explored through Western blot and RT-qPCR. Interleukins inhibitor Results OR3A4 expression was significantly higher in CRC tissues than adjacent normal ones. Cell proliferation, migration, and CRC were inhibited after OR3A4 was knocked down in vitro, which were promoted after upregulation of OR3A4. Moreover, OR3A4 could activate the Wnt/β-catenin pathway, thus influencing phenotypes of CRC cells. Conclusions OR3A4 enhances CRC cell proliferation and migration by activating the Wnt/β-catenin signaling pathway.Objective To explore the expression and biological functions of linc00337 in colorectal cancer (CRC), as well as its underlying mechanism. Patients and methods The relative expression of linc00337 in 47 cases of CRC tissues and cells was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The si-linc00337 interference sequences were designed and transiently transfected into CRC cells. The interference efficiency was detected via qRT-PCR. Regulatory effect of linc00337 on proliferation of CRC cells was detected via colony formation assay. Cell cycle distribution and apoptosis rate after interference in linc00337 expression were determined using flow cytometry. Moreover, the effects of linc00337 knockdown on cell migration and invasion were detected using transwell assay. At last, the effect of si-linc00337 on the MEK/ERK signaling pathway was detected using Western blotting. Results The results of qRT-PCR showed that among the 47 cases of CRC tissues, the expression of linc00337 was up-regulated in 40 cases. Similarly, it was highly expressed in CRC cell lines. The results of colony formation assay manifested that cell proliferation declined after interference in linc00337 expression. The results of flow cytometry and transwell assay showed that interference in linc00337 expression arrested the cell cycle in G1/G0 phase, increased the apoptosis rate, and inhibited the invasion and migration of CRC cells. According to the results of Western blotting, expressions of molecular markers in the MEK/ERK pathway after interference in linc00337 expression were significantly changed. Conclusions Linc00337 is up-regulated in CRC tissues and cells. Interference in linc00337 expression can inhibit cell proliferation, migration, and invasion and promote apoptosis through the MEK/ERK pathway.Objective To investigate the expression and function of LINC00463 in pancreatic cancer (PC), and to demonstrate the relationship between LINC00473 expression and clinical pathological characteristics and prognosis of PC. Patients and methods Expressions of LINC00473 in PC tissues and cell lines were detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00473 siRNA was synthesized to knock down the LINC00473 expression in PANC-1 cells. Proliferation, invasion, and migration abilities of experimental cells were analyzed using cell counting kit-8 (CCK-8) assay and transwell assay, respectively. cAMP activity was detected and protein expression of β-catenin was measured to explain the underlying mechanism of LINC00473 in PC. The prognosis and clinical pathological features of PC patients were illustrated. Results LINC00473 was highly expressed in PC tissues and cells. Higher level of LINC00473 was relative with larger tumor size, worse tumor node metastasis (TNM) stage, worse tumor differentiation, higher rates of perineural invasion, and lymphatic invasion.
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