Pehrson Chappell (storyteller46)

nse improved the predictive efficacy of 2-year PFS. It may be helpful to identify patients who are at high-risk of relapse and to guide early clinical intervention of these patients.Epidermal growth factor receptor (EGFR) expression is commonly upregulated in sporadic colorectal cancer (CRC) and its high expression is associated with poor prognosis in patients with CRC. CA-SSR1 is a dinucleotide CA repeat of the EGFR gene that can modulate EGFR transcription and is a potential target of the mismatch repair machinery in tumours with microsatellite instability (MSI). In the present study, 160 sporadic colon cancer samples were analysed for EGFR CA-SSR1 polymorphism and MSI status. Additionally, EGFR mRNA and protein expression levels in the tumour centre and in the invasive tumour front, compared with those in adjacent normal tissue samples, were evaluated in 80 tumour samples. An inverse association was identified between EGFR mRNA levels and the sum of repeats in both alleles of the CA-SSR1 polymorphism in normal tissues. Changes in CA-SSR1 were detected in the tumour centre as well as in the invasive tumour front and metastases in all MSI high (MSI-H) tumours. Analysis of EGFR expression at the mRNA and protein levels according to MSI status revealed lower EGFR mRNA and protein expression in MSI-H tumours than microsatellite-stable (MSS) tumours. Furthermore, higher EGFR levels in the invasive tumour front compared with in the tumour centre in MSS tumours were identified, suggesting a role of EGFR in tumour progression and higher invasive potential of MSS than MSI-H tumours.Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs/miRs) were reported to be associated with the development of ovarian cancer (OC). Increasing evidence demonstrated that lncRNA SNHG20 and miR-338-3p were involved in OC. However, the functional mechanism of lncRNA SNHG20 and miR-338-3p in OC development remains unknown. The expression of SNHG20, miR-338-3p and myeloid cell leukemia 1 (MCL1) was detected by reverse transcription-quantitative PCR. MTT assay, flow cytometry and transwell migration and invasion assays were used to assess cell proliferation, apoptosis, migration and invasion, respectively. The relative protein expression was detected by western blot analysis. The interaction between miR-338-3p and SNHG20 or MCL1 was predicted by starBase v3.0, and subsequently confirmed by dual-luciferase reporter assay. Besides, mouse xenograft assay was carried out to explore the effect of SNHG20 on tumor growth in vivo. The levels of SNHG20 and MCL1 were upregulated, while miR-338-3p level was downregulated in OC tissues and cells. SNHG20 knockdown repressed OC cell proliferation, migration, invasion and epithelial-mesenchymal transition, and induced apoptosis. Interestingly, SNHG20 targeted miR-338-3p to regulate MCL1 expression. miR-338-3p depletion or MCL1 overexpression could reverse the effects of SNHG20 knockdown on OC cells. Besides, SNHG20 knockdown impeded tumor growth in vivo. In conclusion, the present study demonstrated that SNHG20 regulates OC development via modulation of the miR-338-3p/MCL1 axis, providing the theoretical basis for the treatment of OC.The aim of the present study was to investigate the association of long non-coding RNA T cell factor 7 (lncRNA TCF7) with disease risk, prognosis and its cellular function in multiple myeloma (MM). A total of 132 de novo symptomatic patients with MM and 50 controls were enrolled. Plasma cells from patients with MM and controls were separated from bone marrow samples to detect lncRNA TCF7 expression using reverse transcription-quantitative PCR. In addition, treatment responses, event-free survival (EFS) and overall survival (OS) were measured. The effects of lncRNA TCF7 on proliferation, apoptosis and microRNA-200c (miR-200c) expression were assessed by gain- and loss-of-function experiments in RPMI-8226 and U-266 cells. The results d