Rabbit Anti-Human KLF12 (a.a. 301-402) Polyclonal antibody

Background: The role of miR-200a-3p in gastric cancer (GC) remain unclear. Materials and methods: miR-200a-3p expression in 65 paired GC and adjacent tissues (AT) were evaluated by quantitative real-time PCR (qRT-PCR) and Western blot. Cell proliferation, cell cycle, and cell migration were assessed by cell growth counting assay, cell cycle analysis, and transwell assay, respectively. The target of miR-200a-3p was analyzed by dual-luciferase reporter assay. Results: miR-200a-3p in GC tissues was significantly reduced compared with AT. miR-200a-3p expression was closely associated with clinicopathological features (P < .05). SGC-7901 cell line demonstrated the lowest level of miR-200a-3p. Cell proliferation and colony formation was significantly inhibited by miR-200a-3p overexpression, but increased by miR-200a-3p knockdown (P < .05). miR-200a-3p upregulation increased the G1/S cell ratio. The 3'-UTR of KLF12 directly interacted with miR-200a-3p. Furthermore, increased levels of KLF12 expression was detected in GC tissues. A correlation analysis suggested a negatively correlation between miR-200a-3p and KLF12 mRNA expressions. Conclusion: miR-200a-3p was down-regulated in GC tissues and was correlated with clinicopathological features. miR-200a-3p overexpression inhibits GC cell proliferation, cell cycle, and cell migration. Furthermore, miR-200a-3p might act as a tumor suppressor in GC by targeting KLF12.

Long non-coding RNAs (lncRNAs) have been wildly verified to modulate multiple tumorigeneses, especially nasopharyngeal carcinoma (NPC). In present study, we aim to investigate the role of LINC00319 in the NPC carcinogenesis. It was indicated that LINC00319 was markedly increased in NPC tissues and cells in comparison to their corresponding controls. Moreover, the aberrant overexpression of LINC00319 indicated the poor prognosis of NPC patients. Silence of LINC00319 was able to suppress NPC cell growth in vitro while overexpression of LINC00319 inversed this process. Moreover, in vivo tumor xenografts were established using CNE-1/SUNE-1 cells to investigate the function of LINC00319 in NSCLC tumorigenesis. Rescue assay was performed to further confirm that LINC00319 contributed to NPC progression by regulating miR-1207-5p/KLF12 signal pathway. Taken together, our study discovered the oncogenic role of LINC00319 in clinical specimens and cellular experiments, showing the potential LINC00319/miR-1207-5p/KLF12 pathway. This results and findings provide a novel insight for NPC tumorigenesis.