Anti-RUNX3 (internal region) polyclonal antibody

Non-small cell lung cancer (NSCLC) is still an unresolved source of tumor-related death internationally. Current studies have discovered that microRNAs (miRNAs) are associated with diverse cancers development, including NSCLC. Our paper focused on the functional character of miR-4286 in NSCLC. miR-4286 level in 68 cases of NSCLC tissues, matched neighboring nontumor tissues and different cancer cell lines were inspected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The connection concerning miR-4286 expression and clinicopathological features of patients with NSCLC were further determined. After knockdown or overexpression of miR-4286, cell viability, cell cycle, and/or apoptotic cells were examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assay, respectively. Moreover, the cell cycle- and apoptosis-related proteins were estimated by qRT-PCR and Western blot. In comparison with the matched nontumor tissues, miR-4286 was significantly enhanced in lung malignancy tissues and different cell lines. miR-4286 expression was related with the tumor-node-metastasis stage, lymphatic metastasis, and distant metastasis. Cell viability was ominously weakened by suppression of miR-4286 in A549 cells, whereas was statistically upregulated by overexpression of miR-4286 in NCI-H1299 cells. Additionally, we detected that suppression of miR-4286 tempted cell cycle arrest in G1 stage and fortified apoptosis in A549 cells. Runx3 was recognized as one target gene of miR-4286, and the impacts of suppression of miR-4286 on cell viability and apoptosis were through regulation of Runt-related transcription factor 3. Our study suggests that miR-4286 overexpression represents a tumor promoter role in NSCLC cells.

Colorectal cancer (CRC) is the third most common type of cancer. MicroRNAs have been reported to participate in the progression of various cancers. In previous studies, miR-301a-3p expression was shown to be upregulated in CRC tissues. However, the underlying mechanism of miR-301a-3p in CRC has not yet been elucidated. Herein, the level of miR-301a-3p was found to be significantly upregulated in CRC clinical tissues and cell lines (HT29 and SW620). In addition, overexpression of miR-301a-3p obviously promoted cell proliferation, migration and invasion, and inhibited cell apoptosis in CRC cells. Meanwhile, upregulated miR-301a-3p expression also enhanced the expressions of Bax, caspase-3, caspase-9, matrix metalloproteinase (MMP)-2, and MMP-9, while the expression of Bax-2 was decreased. Furthermore, deleted in liver cancer-1 (DLC-1) and runt-related transcription factor 3 (RUNX3) were verified to be direct target genes of miR-301a-3p. Furthermore, overexpression of DLC-1 and RUNX3 revealed antitumor effects in CRC cell lines with the inhibition of cell proliferation, migration and invasion, and the induction of cell apoptosis. In addition, the expressions of Bax, caspase-3, caspase-3, MMP-2, and MMP-9 could be decreased after upregulating the expressions of DLC-1 and RUNX3, along with the upregulation of Bax-2. Moreover, overexpression of miR-301a-3p could promote the growth of xenograft tumors and liver metastasis in vivo, along with reducing the expressions of DLC-1 and RUNX3. Overall, miR-301a-3p might act as a tumor inducer in CRC cells through negatively regulating DLC-1 and RUNX3.