Upregulation of long noncoding RNA linc02544 and its association with overall survival rate and the influence on cell proliferation and migration in lung squamous cell carcinoma

Abstract

Background Long noncoding RNAs (lncRNAs) exert crucial biological functions by regulating miRNAs, which are implicated in cancer progression and tumorigenesis. A previous study has indicated that lncRNA linc02544 expression is upregulated in lung adenocarcinoma, whereas, the role of linc02544 in LUSC is elusive. Methods The differential linc02544 expression in LUSC tissues and adjacent non-tumor tissues were evaluated with RT-qPCR. Kaplan-Meier curve was conducted to evaluate the clinical prognostic significance of linc02544. Then cellular experiments were performed to assess the influence of linc02544 in LUSC proliferation, invasion, and migration, and a western blot assay was used to measure the metastasis-related protein levels. The downstream miRNAs were verified using the LncBase Experimental v.2 database and dual-luciferase reporter assay. Results Linc02544 was overexpressed in LUSC tissues from positive lymph node metastasis-positive and TNM high-stage patients. Low linc02544 expression was associated with a longer survival rate. Downregulation of linc02544 by si-linc02544 restrained cell growth capacities, migration, and invasion abilities. Expression of MMP-2, MMP-9, and vimentin was decreased while E-cadherin was increased in si-linc02544 cells compared with that in untreated cells. Mechanistically, we identified that linc02544 acted as a sponge of miR-138-5p, which expression had a negative correlation. E2F3 was a potential target of miR-138-5p, Conclusions Notably, high linc02544 expression was associated with severe clinical parameters and was a putative prognostic predictor for patients with LUSC. Downregulation of linc02544 may weaken the LUSC cell proliferation, migration, and invasion by regulating miR-138-5p/E2F3, which maybe serve as a biomarker for the prognosis and target treatment of LUSC.

Identification of lncRNAs Deregulated in Epithelial Ovarian Cancer Based on a Gene Expression Profiling Meta-Analysis

“…Previous data about the influence of these lncRNAs in invasion or metastasis and unfavorable prognosis can be found in other cancers and reinforce our findings. LINC02544 is overexpressed in lung squamous cell carcinoma patients with lymph node metastasis, and it promotes proliferation, migration, and invasion in vitro by sponging miR-138-5p—a potential target of E2F3 [ 91 ]; increased expression of LINC02544 has also been related to in vitro invasion and unfavorable prognosis in breast cancer [ 92 ]. LINC01235 is upregulated in gastric cancer patients versus healthy individuals and metastatic versus non-metastatic gastric cancer patients, promoting migration, invasion, and EMT, as well as negatively affecting prognosis [ 93 , 94 ].…”

IncRNA VIM-AS1 expression is positively correlated with the prognosis and immune infiltration in lung adenocarcinoma

“…Multiple projects have shown that lncRNAs are associated with the prognosis and the growth of cancer cells [12][13][14][15] . Glioma tissues and cells showed signi cant downregulation of p53 expression and a signi cant increase in lncRNA PVT1 expression.…”

Involvement of transcribed lncRNA uc.291 in hyperproliferative skin disorders

“…NcRNAs represent a subclass of RNAs that are transcribed but not translated with different lengths, structures, and functions. Interestingly, their interactions with other cellular RNAs and/ or proteins contribute to the creation of an intricate network capable of shaping cellular phenotypes through the regulation of both cellular transcription and translation, so that ncRNAs act as epigenetic regulators [21] which impact on cell proliferation, differentiation, cell death and metabolism, especially in cancer [22][23][24][25]. Long Non-Coding RNA (lncRNAs), a group of ncRNA longer than 200 nucleotides, are already known to play important roles in skin homeostasis, such as for example the Anti-Differentiation ncRNA (ANCR) and the Terminal-Differentiation Induced ncRNA (TINCR), which can regulate epidermal proliferation and differentiation, respectively [26,27].…”