<p>lncRNA DLX6-AS1 Promotes Proliferation of Laryngeal Cancer Cells by Targeting the miR-26a/TRPC3 Pathway</p>

Abstract

Purpose: Laryngeal cancer is the most prevalent tumor type in head and neck cancers. Early diagnosis is considered as an important strategy for improving prognosis. The lncRNA DLX6-AS1 has been shown to modulate tumor phenotypes in several types of cancer, but the role of DLX6-AS1 in laryngeal cancer and its concrete mechanisms are not clear. Methods: Tissue samples from laryngeal cancer patients and corresponding clinical data were used for detailed analysis. The laryngeal cancer cell lines HEp-2 and Tu-177 were studied. Cell proliferation, ROS production, mitochondrial respiratory function, intracellular and mitochondrial calcium influx were assessed. Western blotting, quantitative RT-PCR and luciferase assays were used to analyze the interactions. A xenografted tumor model was established to analyze the effects of DLX6-AS1 on tumor growth in vivo. Results: lncRNA DLX6-AS1 had increased expression in tumor tissues compared with adjacent normal tissues and in higher clinical stages compared with lower stages, which was associated with poor prognosis. In detail, DLX6-AS1 knockdown decreased cell proliferation and affected key mitochondrial metabolic parameters in both HEp-2 and Tu-177 cells. Moreover, DLX6-AS1 knockdown suppressed TRPC3-mediated mitochondrial calcium uptake and ROS production. Furthermore, miR-26a functioned as a link between these two molecules, as it could be absorbed by DLX6-AS1 and thus regulated the levels of TRPC3. Finally, the DLX6-AS1/miR-26a/TRPC3 axis modulated laryngeal cancer proliferation both in vitro and in vivo. Conclusion: This study provides new evidence that a novel lncRNA, DLX6-AS1, regulates mitochondrial calcium homeostasis, respiration and tumor proliferation via modulating the miR-26a/TRPC3 axis in laryngeal cancer.

Silencing long non‐coding RNA DLX6‐AS1 or restoring microRNA‐193b‐3p enhances thyroid carcinoma cell autophagy and apoptosis via depressing HOXA1

“…For instance, in laryngeal cancer, DLX6‐AS1 expression trends towards an elevation in clinical cancer tissues and its depletion obstruct the proliferative activity of HEp‐2 and Tu‐177 cells. 27 Also, increased DLX6‐AS1 is presented in colorectal cancer tissues and depleting DLX6‐AS1 restricts metastasis of colorectal cancer cells and arrests cell phase progression. 28 Besides, oesophageal squamous cell carcinoma specimens express elevated DLX6‐AS1 and DLX6‐AS1 down‐regulation is attributed to depressed cell proliferation and metastasis.…”

“…Explored in other cancers, the inhibitory function of DLX6-AS1 has also echoed with the discoveries in this work. For instance, in laryngeal cancer, DLX6-AS1 expression trends towards an elevation in clinical cancer tissues and its depletion obstruct the proliferative activity of HEp-2 and Tu-177 cells 27.…”

LncRNA DUXAP8 promotes the progression of laryngeal cancer through targeting miR-384/ POU2F1 axis

“…For example, lncRNA SNHG1 promotes cell proliferation in laryngeal cancer through regulating Notch1 signaling pathway [28]. lncRNA DLX6-AS1 promotes the proliferation of laryngeal cancer cells via targeting the miR-26a/TRPC3 axis [29]. LncRNA TUG1 promotes cell proliferation and migration of laryngeal cancer cells [30].…”

DLX6-AS1: a putative lncRNA candidate in multiple human cancers

“…Liu et al . (Refs 2, 32, 50, 74) demonstrated that DLX6-AS1 had increased expression in tumour tissues compared with adjacent normal tissues and in higher clinical stages compared with lower stages (Ref. 50).…”

“…In addition, an in vivo study conducted by Liu et al . (Refs 2, 32, 50, 74) reported that DLX6-AS1 triggered the invasion, and migration of HCC via a mechanistic regulation among miR-513c, cullin 4A (Cul4A), and annexin A10 (ANXA10). Thus, the knockout of lncRNA DLX6-AS1 hindered miR-513c-mediated Cul4A suppression and eventually enhanced the ubiquitination-dependent degradation of ANXA10, thereby inhibiting the incidence and progress of HCC (Ref.…”