Accumulating researches have confirmed that circRNA abnormal expression plays a prominent role in the progression of colorectal cancer (CRC). The role of circ_0000218 in CRC and its potential mechanism are not clear. In this study, real-time polymerase chain reaction (RT-PCR) was employed to measure the circ_0000218, miR-139-3p and RAB1A mRNA expression in CRC tissues and cells. Immunohistochemistry and western blot were conducted to determine the RAB1A expression in CRC tissues and cells, respectively. Colony formation assay and BrdU method were employed to monitor the effect of circ_0000218 on cell proliferation. Transwell assay was adopted to detect cell migration and invasion. Dual luciferase reporter assay and RNA immunoprecipitation assay were adopted to confirm the targeting relationship between circ_0000218 and miR-139-3p, miR-139-3p and RAB1A. We demonstrated that circ_0000218 was notably upregulated in CRC tissues and cell lines, and its high expression level was markedly linked to the increase of T staging and local lymph node metastasis. Circ_0000218 overexpression enhanced the proliferation and metastasis of CRC cells while knocking down circ_0000218 caused the opposite effects. We also observed that miR-139-3p was negatively regulated by circ_0000218, while RAB1A was positively regulated by it. Collectively, this study suggested that circ_0000218 upregulated RAB1A and promoted CRC proliferation and metastasis via sponging miR-139-3p.

Colorectal cancer (CRC) is one of the most lethal tumor types worldwide. Circular RNAs (circRNAs), which are covalent closed loops of RNA, perform vital roles for the proliferation and metastasis of a variety of tumor types. In the present study, the expression, function and molecular mechanisms of action of a novel circRNA, circRNA_101951, were examined in CRC. The expression levels of circRNA_101951 in CRC tissue and cell lines were examined using reverse transcription-quantitative (RT-qPCR). Cell proliferation, the clone formation ability, cell apoptosis, the cell cycle and the cell migratory and invasive abilities were examined using MTT assays, colony formation assays, flow cytometric assays, and cell migration and invasion assays, respectively. The effects of circRNA_101951 on Kinesin II family member 3A (KIF3A) related gene expression were examined using RT-qPCR and western blot assays. The results indicated that circRNA_101951 was increased in CRC tissues and cell lines. The downregulation of circRNA_101951 inhibited cell proliferation and colony formation as well as cell migration and invasion of CRC cell lines. In addition, the downregulation of circRNA_101951 blocked the KIF3A-mediated epithelial-mesenchymal transition (EMT) pathway, which was detected by examining the expression levels of KIF3A and EMT related proteins. In conclusion, the current data revealed that circRNA_101951 may act as a potential biomarker for patients with CRC, and provided a novel insight demonstrating that the suppression of circRNA_101951 may be a potential therapeutic strategy for CRC.

Dysregulated microRNA-329 (miR-329) serves an important role in the progression of certain types of tumor. However, the exact function and mechanisms of miR-329 in papillary thyroid cancer (PTC) remain unknown. The present study investigated the function and mechanisms of miR-329 in regulating PTC cell progression. The results revealed that the expression of miR-329 was significantly downregulated in PTC tissues and cell lines compared with adjacent normal tissues and a human immortalized follicular cell line. miR-329 mimics notably decreased PTC cell proliferation, colony formation and WNT1 expression in vitro, as well as suppressing PTC tumor growth in vivo. In addition, luciferase assays determined that miR-329 was able to directly bind with the 3′untranslated region of WNT1. Furthermore, short interfering RNA-WNT1-induced downregulation of WNT1, which demonstrated similar effects to miR-329 overexpression. WNT1 overexpression rescued the tumor suppressive effects of miR-329 in PTC cells. The present study provided new insights into the role of miR-329 in PTC progression and suggests the potential application of miR-329 as a therapy for PTC.