ABSTRACT
OBJECTIVE: To illustrate the role of LINC00641 in inducing the malignant progression of colorectal cancer (CRC) through the miRNA-424-5p/PLSCR4 feedback loop. PATIENTS AND METHODS: LINC00641 levels in paired CRC and non-tumoral tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Its prognostic potential in CRC was assessed by Kaplan-Meier method. Changes in proliferative and migratory abilities of HCT116 and SW620 cells transfected with si-LINC00641 were evaluated by 5-Ethynyl-2'- deoxyuridine (EdU), cell counting kit-8 (CCK-8) and transwell assay. The feedback loop LINC00641/miRNA-424-5p/PLSCR4 was identified through Dual-Luciferase reporter assay and its involvement in CRC progression was finally explored by rescue experiments. RESULTS: LINC00641 was upregulated in CRC tissues, which was an unfavorable factor to the overall survival of CRC. Proliferative and migratory abilities of HCT116 and SW620 cells were inhibited by knockdown of LINC00641. LINC00641 could competitively bind miRNA-424-5p, thereby abolishing its inhibitory effect on PLSCR4 expression. Knockdown of PLSCR4 could inhibit proliferative and migratory abilities of HCT116 and SW620 cells. CONCLUSIONS: LINC00641 stimulates proliferative and migratory abilities of CRC through the miRNA-424-5p/PLSCR4 feedback loop.
Subject(s)
Colorectal Neoplasms/metabolism , MicroRNAs/metabolism , Phospholipid Transfer Proteins/metabolism , RNA, Long Noncoding/metabolism , Cell Movement , Cell Proliferation , Cells, Cultured , Colorectal Neoplasms/pathology , Female , Humans , Male , MicroRNAs/genetics , Middle Aged , Phospholipid Transfer Proteins/genetics , RNA, Long Noncoding/geneticsABSTRACT
Curative therapy for diabetes mellitus mainly involves pancreas or islet transplantation to recruit insulin-producing cells. This approach is limited, however, because of both the shortage of donor organs and allograft rejection. Intra-bone marrow bone marrow transplantation (IBM-BMT) has recently been shown to be effective in inducing donor-specific tolerance in mice and rats without the use of immunosuppressants. After induction of diabetes in 15 C3H mice with streptozotocin, the mice received both allotransplants of bone marrow cells from C57BL/6 mice by IBM-BMT and injections via the portal vein of insulin-producing cells that were induced in vitro from stem cells derived from adult C57BL/6 bone marrow. We evaluated the expression of these cells by examining the expression of not only insulin but also the crucial transcription factors insulin I and insulin II. The diabetic mice were treated with IBM-BMT and precultured insulin-producing cells. Hyperglycemia was normalized by 5 days after the treatment and remained normal for more than 45 days. This strategy might be applicable to patients with type I diabetes mellitus.
