BackgroundAccumulating evidences indicate that non-coding RNAs (ncRNAs) including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) acting as crucial regulators in osteosarcoma (OS). Previously, we reported that Rho associated coiled-coil containing protein kinase 1 (ROCK1), a metastatic-related gene was negatively regulated by microRNA-335-5p (miR-335-5p) and work as an oncogene in osteosarcoma. Whether any long non-coding RNAs participate in the upstream of miR-335-5p/ROCK1 axial remains unclear.MethodsExpression of differentiation antagonizing non-protein coding RNA (DANCR) and miR-335-5p/miR-1972 in osteosarcoma tissues were determined by a qRT-PCR assay and an ISH assay. Osteosarcoma cells’ proliferation and migration/invasion ability changes were measured by a CCK-8/EDU assay and a transwell assay respectively. ROCK1 expression changes were checked by a qRT-PCR assay and a western blot assay. Targeted binding effects between miR-335-5p/miR-1972 and ROCK1 or DANCR were verified by a dual luciferase reporter assay and a RIP assay. In vivo experiments including a nude formation assay as well as a CT scan were applied to detect tumor growth and metastasis changes in animal level.ResultsIn the present study, an elevated DNACR was found in osteosarcoma tissue specimens and in osteosarcoma cell lines, and the elevated DNACR was closely correlated with poor prognosis in clinical patients. Functional experiments illustrated that a depression of DANCR suppressed ROCK1-mediated proliferation and metastasis in osteosarcoma cells. The results of western blot assays and qRT-PCR assays revealed that DANCR regulated ROCK1 via crosstalk with miR-335-5p and miR-1972. Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972. Finally, the outcomes of in vivo animal models showed that DANCR promoted tumor growth and lung metastasis of osteosarcoma.ConclusionsLncRNA DANCR work as an oncogene and promoted ROCK1-mediated proliferation and metastasis through acting as a competing endogenous RNA (ceRNA) in osteosarcoma.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0837-6) contains supplementary material, which is available to authorized users.

Long non-coding RNAs (lncRNAs) play key roles in various malignant tumors, including colorectal cancer (CRC). Long non-coding RNA differentiation antagonizing non-protein coding RNA (DANCR) is overexpressed in CRC patients, but whether it affects CRC proliferation and metastasis via regulation of heat shock protein 27 (HSP27) remains unclear. In the present study, we found that DANCR was highly expressed and correlated with proliferation and metastasis in CRC. In addition, we demonstrated that DANCR and HSP27 were both targets of microRNA-577 (miR-577) and shared the same binding site. Furthermore, we revealed that DANCR promoted HSP27 expression and its mediation of proliferation/metastasis via miR-577 sponging. Finally, using an in vivo study, we confirmed that overexpression of DANCR promoted CRC tumor growth and liver metastasis. The present study demonstrated the function of DANCR in CRC and might provide a new target in the treatment of CRC.

Long non‐coding RNA (lncRNA) are extensively involved in various malignant tumors, including ovarian cancer (OC). In the present study, we focused on the expression and function of nuclear enriched abundant transcript 1 (NEAT1) in OC cells’ metastasis. We demonstrated that NEAT1 was upregulated in OC tissue specimens and cell lines. In addition, we revealed that depression of NEAT1 inhibited OC cells’ metastasis and the expression of Rho associated coiled‐coil containing protein kinase 1 (ROCK1), which is a metastasis‐related gene. Using online predictive software and a series of luciferase assays, we demonstrated that both NEAT1 and ROCK1 were the targets of microRNA‐382‐3p (miR‐382‐3p) and share similar microRNA responding elements (MRE). Furthermore, we illustrated that NEAT1 and miR‐382‐3p inhibited each other in a reciprocal manner. Finally, through antisense experiments we demonstrated that NEAT1 promoted ROCK1‐mediated metastasis by functioning as a ceRNA of miR‐382‐3p. In summary, the findings of this study revealed that NEAT1 promoted OC cells’ metastasis through regulating the miR‐382‐3p/ROCK1 axial. The present study might provide a new target for treating OC.

Signal transducers and activators of transcription (STAT) is a family of transcription factors which regulate cell proliferation, differentiation, apoptosis, metastasis, immune and inflammatory responses, and angiogenesis. STAT3 is a latent cytoplasmic transcription factor that belongs to STATs. STAT3 has been reported be regulates genes involved with cellular growth, proliferation and metastasis. Worldwide, colon cancer is one of the leading causes of cancer-related deaths. Cumulative evidence has established that STAT3 is essential for colon cancer progression to advanced malignancy. In our study, we showed that microRNA-1299 (miR-1299) was closely related to the TNM stage of colon cancer, and that the expression of miR-1299 was negatively correlated with the expression of STAT3 in colon cancer which means that miR-1299 can be a negative regulator of STAT3 in colon cancer. A total of 60 cases of different grades of colon samples were used to detect the expression of miR-1299. Results showed that miR-1299 was significantly lower in high-grade colons both in mRNA and protein levels. Furthermore, Overall survival (OS) in patients with low miR-1299 is shorter than 25.6 months, as compared with an OS of 28.4 months in patients with high level of miR-1299. We also confirmed that the overexpression of miR-1299 can not only downregulate the STAT3 pathway, but also inhibited colon cancer cell growth. Our findings could provide new insights into the molecular therapeutic of colon cancer.

MicroRNAs (miRNAs) have been reported as key regulators in numerous diseases including osteosarcoma. The function of microRNA-141-3p (miR-141-3p) and whether this function is achieved by regulation of GLI family zinc finger 2 (GLI2) in osteosarcoma remain unclear. In the present study, we found decreased expression of miR-141-3p, but increased expression of GLI2 in osteosarcoma tissues and cell lines. In addition, we demonstrated a negative correlation between miR-141-3p and GLI2. Furthermore, we revealed that elevation of miR-141-3p resulted in a marked inhibition of proliferation and promotion of apoptosis as well as an obviously decrease in GLI2 in osteosarcoma cell lines. Furthermore, we determined that GLI2 is a target of miR-141-3p by a constructed luciferase assay. In addition, we showed that miR-141-3p could negatively regulate GLI2 and its downstream parathyroid hormone-related protein 1 (PTHRP1). Finally, through a series of antisense experiments we confirmed that the effect of miR-141-3p on proliferation and apoptosis was achieved through the GLI2 pathway in osteosarcoma cells. The findings of the present study may provide a new target for treating osteosarcoma.