Long non‑coding RNAs (lncRNAs) are common in the human body. Misregulated lncRNA expression can cause a variety of diseases in the human body. The present study aimed to investigate the effect of lncRNA differentiation antagonizing non‑protein‑coding RNA (DANCR) on glioma proliferation and autophagy through the microRNA (miR)‑33b/distal‑less homeobox 6 (DLX6)/autophagy‑related 7 (ATG7) axis. Reverse transcription‑quantitative PCR was used to detect DANCR and miR‑33b expression. Cell Counting Kit‑8 assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Transmission electron microscopy was used to determine the autophagy level by observing intracellular autophagosomes. A western blot assay was used to detect protein expression levels and determine the level of autophagy in different cells. The binding sites of miR‑33b and DANCR or DLX6 were detected using a dual‑luciferase reporter assay. A chromatin immunoprecipitation assay confirmed DLX6 as a transcript of ATG7. In vivo tumorigenesis of glioma cells was validated in nude mice. DANCR and DLX6 were highly expressed in glioma cells, while miR‑33b showed low expression in glioma cells. DANCR reduced the targeted binding of miR‑33b to DLX6 by sponging miR‑33b. The result verified that DANCR could promote ATG7 protein expression through miR‑33b/DLX6, promote intracellular autophagy and proliferation and reduce apoptosis. The present study identified the role of the DANCR/miR‑33b/DLX6/ATG7 axis in regulating autophagy, proliferation, and apoptosis in glioma cells, providing new ideas for glioma treatment.

Hemifacial microsomia (HM) is a craniofacial congenital defect involving the first and second branchial arch, mainly characterized by ocular, ear, maxilla-zygoma complex, mandible, and facial nerve malformation. HM follows autosomal dominant inheritance. Whole-exome sequencing of a family revealed a missense mutation in a highly conserved domain of ITPR1. ITPR1 is a calcium ion channel. By studying ITPR1\'s expression pattern, we found that ITPR1 participated in craniofacial development, especially the organs that corresponded to the phenotype of HM. In zebrafish, itpr1b, which is homologous to human ITPR1, is closely related to craniofacial bone formation. The knocking down of itpr1b in zebrafish could lead to a remarkable decrease in craniofacial skeleton formation. qRT-PCR suggested that knockdown of itpr1b could increase the expression of plcb4 while decreasing the mRNA level of Dlx5/6. Our findings highlighted ITPR1\'s role in craniofacial formation for the first time and suggested that ITPR1 mutation contributes to human HM.

Endometrial cancer features abnormal growth of cells of the inner lining of the uterus with the potential to invade to other organs. Accumulating evidence suggests that aberrant expression of long non-coding RNA (lncRNA) may facilitate cancer progression. The aim of the present study was to identify the molecular mechanisms of the lncRNA known as DLX6 antisense RNA 1 (DLX6-AS1) in endometrial cancer. Microarray-based analysis was utilized to predict expression profile and possible function pattern of DLX6-AS1 and DLX6 in endometrial cancer, and their expression was quantified in 78 clinically obtained endometrial cancer tissues and also in cell lines. We next assessed the effects of DLX6-AS1 and DLX6 on proliferation, invasion and apoptosis of endometrial cancer cells. A mouse xenograft model was established to confirm DLX6-AS1 functions and explore its underlying regulatory mechanisms in vivo. DLX6-AS1 and DLX6 were highly expressed in endometrial cancer tissues and cells, and their silencing weakened the proliferative and invasive abilities of endometrial cancer cells and tumours, while promoting apoptosis. Mechanistic investigations indicated that DLX6-AS1 formed a triplex structure with DLX6 via interaction with p300/E2F1 acetyltransferase. Thus, we find that functional up-regulation of DLX6-AS1 can promote endometrial cancer progression via a novel triplex mechanism that may prove to be great clinical significance for future treatments of endometrial cancer.

BACKGROUND: Lung adenocarcinoma (LAC), the primary histological type of non-small cell lung cancer (NSCLC), has displayed an increasing incidence and mortality worldwide. However, therapeutic approaches were limited. Dysregulation of some lncRNAs has been shown in various types of cancers including LAC. The aim of the present study was to vertify lncRNA DLX6-AS1 expression in LAC.
METHODS: Microarray assay revealed expression profile of lncRNAs in LAC. qRT-PCR ( quantitative reverse transcription PCR) was performed to identify lncRNA DLX6-AS1 expression level in 72 paired LAC and adjacent normal lung tissues. qRT-PCR and Western blotting were used to verify that down-regulation lncRNA DLX6-AS1 decreased DLX6 (distal-less homeobox 6) mRNA and protein expression.
RESULTS: Microarray analysis identified up-regulation of 272 lncRNAs and down-regulation of 635 lncRNAs in LAC tissues. The expression level of lncRNA DLX6-AS1 in LAC tissues was significantly higher compared to paired adjacent normal lung tissues (P< 0.05). In addition, its expression level was closed correlated with both histological differentiation (P = 0.004) and TNM stage (P = 0.033). qRT-PCR and Western blotting analysis showed that DLX6 mRNA and protein levels were lower in si-LncRNA group than in the NC (negative control) and Blank groups.
CONCLUSIONS: Microarray analysis identified that lncRNA DLX6-AS1 was up-regulated in LAC tissues. High DLX6-AS1 expression levels were significantly associated with both histological differentiation and TNM stage. Down-regulation of lncRNA DLX6-AS1 expression decreased the DLX6 mRNA and protein levels.