LINC00472 suppresses oral squamous cell carcinoma growth by targeting miR-455-3p/ELF3 axis

Abstract

LINC00472 is reported to play a role in suppressing tumors in cancers such as lung cancer and hepatocellular carcinoma, among others. We made investigations into the effects of LINC00472 in oral squamous cell carcinoma (OSCC) progression to explore the underlying molecular mechanisms. By qRT-PCR, we assessed the LINC00472 expression in OSCC tissues and cells and performed functional analysis to investigate how LINC00472/miR-455-3p/ELF3 impacts OSCC cell proliferation, apoptosis, and cell cycle. The role that LINC00472 plays in OSCC tumor growth was examined by establishing a xenograft model. Down-regulation of LINC00472 occurred in tissues and cells of an OSCC tumor. LINC00472 overexpression caused OSCC cell proliferation to be inhibited, cell apoptosis to be promoted, and cell cycle arrest to be induced. As a competing endogenous RNA (ceRNA), LINC00472 can block miR-455-3p function and further promote ELF3 expression. The overexpression of miR-455-3p or ELF3 knockdown was shown to be capable of reversing the anti-tumor effects of LINC00472 in OSCC. In vivo experiments confirmed the tumor-suppressing role of LINC00472 in the progression of OSCC. In short, we found that the novel LINC00472 inhibits OSCC growth via the miR-455-3p/ELF3 axis. LINC00472 and its targeted miR-455-3p/ELF3 axis may represent valuable targets for treating OSCC.

Novel genome-wide DNA methylation profiling reveals distinct epigenetic landscape, prognostic model and cellular composition of early-stage lung adenocarcinoma

“…They may function as cis-regulatory elements such as enhancers and silencers, or as transcribed non-coding RNA to exert regulatory functions [ 34 – 36 ]. For example, MIR647, MIR99AHG, and LINC00472, identified in our differentially methylated analysis, could regulate the progression of oral squamous cell carcinoma, prostate cancer, and lung adenocarcinoma by promoting cell proliferation, migration, epithelial-mesenchymal transition, and other processes [ 37 – 40 ]. Although some genes annotated by EM-seq DMRs currently have no research revealing their biological functions, it does not seem to affect their potential as candidate biomarkers for tumor diagnosis because base sequences have been detected.…”

LINC00847 drives pancreatic cancer progression by targeting the miR-455-3p/HDAC4 axis

“…It has been demonstrated that MiR-455-3p has varying impacts on the development of various malignancies. For instance, miR-455-3p expression was elevated in oral squamous cell carcinoma, and overexpression of miR-455-3p prevented the anticancer effects of LINC00472 [ 13 ]. In contrast, miR-455-3p prevented the progression of prostate cancer cells in vitro and in vivo [ 20 ].…”

“…MiR-455-3p can interact with lncRNA to take part in the development of many tumors. By way of illustration, miR-455-3p sponged by LINC00472 could worsen the progression of oral squamous cell carcinoma [ 13 ]. Oppositely, miR-455-3p interacted with LINC00319 to suppress osteosarcoma progression [ 14 ].…”

Luteolin impacts deoxyribonucleic acid repair by modulating the mitogen-activated protein kinase pathway in colorectal cancer

“…Briefly, HCT-116 and HT-29 cells were incubated with luteolin (0, 10, 20, and 40 μM) in the presence or absence of 5 μM of cisplatin for 48 h. Subsequently, cells were cultivated with 10 μL of Annexin V in the dark for 15 min, followed by the addition of 10 µL of propidium iodide (PI) to the cell suspension. Finally, the apoptosis rate of the cells was detected using a FACScan flow cytometer (BD Biosciences, CA, USA) [ 28 , 29 ].…”

“…Subsequently, after rinsing with PBS, the cells were re-suspended in 500 μL of buffer containing 10 μL of RNAse (Sigma) and 25 µL of PI (BD Biosciences) and incubated at room temperature for 30 min in the dark. The percentage of cells in different phases (G1, S, and G2) of the cell cycle was detected by flow cytometry (BD Biosciences, Franklin, NJ, USA) [ 28 , 30 ].…”