Long Intergenic Non-Coding RNA LINC00885 Promotes Tumorigenesis of Cervical Cancer by Upregulating MACC1 Expression Through Serving as a Competitive Endogenous RNA for microRNA-432-5p

Abstract

Purpose Long intergenic non-protein coding RNA 885 (LINC00885) has been well studied in breast cancer; however, its contribution in cervical cancer remains unclear. In this study, we aimed to determine the detailed functions of LINC00885 in cervical cancer and elucidate the underlying molecular regulation mechanism. Methods The expression status of LINC00885 in cervical cancer was determined using reverse transcription-quantitative polymerase chain reaction and by searching The Cancer Genome Atlas database. The detailed functions of LINC00885 in cervical cancer cells were confirmed using Cell Counting Kit 8 assay, flow cytometry analysis, Transwell cell migration and invasion assays, and tumor xenograft assay. Mechanistic experiments included bioinformatics prediction, RNA immunoprecipitation, luciferase reporter assay, and rescue experiments. Results LINC00885 was clearly overexpressed in cervical cancer, which was linked with unfavorable clinical outcomes. Functionally, LINC00885 deficiency suppressed cervical cancer cell proliferation, migration, and invasion but stimulated cell apoptosis in vitro. Furthermore, loss of LINC00885 restricted the growth of cervical cancer cells in vivo. Mechanistically, LINC00885 functioned as a competitive endogenous RNA for microRNA-432-5p (miR-432-5p) in cervical cancer. Furthermore, metastasis-associated colon cancer 1 (MACC1) was confirmed as the direct target of miR-432-5p, and LINC00885 could enhance MACC1 expression by sequestering miR-432-5p. Rescue experiments revealed that silencing of miR-432-5p or upregulation of MACC1 expression could effectively counteract the restrained aggressive properties of cervical cancer cells induced by LINC00885 deficiency. Conclusion LINC00885 upregulated MACC1 expression in cervical cancer cells by sponging miR-432-5p, thereby promoting cancer progression. The LINC00885/miR-432-5p/MACC1 pathway may help in the identification of potential prognostic biomarkers and therapeutic targets in cervical cancer.

The E6 Oncoprotein of HPV16 AA-c Variant Regulates Cell Migration through the MINCR/miR-28-5p/RAP1B Axis

“…The role of MINCR has been studied in some types of cancer, where it has been found to inhibit the activity of some miRNAs through the ceRNA function [ 24 , 28 , 29 , 30 ]. For example, in bladder cancer cells, MINCR regulates the expression of EZH2 through miR-26a-5p, while silencing MINCR decreases cell proliferation and invasion and increases apoptosis [ 31 ].…”

LINC00885 promotes cervical cancer progression through sponging miR-3150b-3p and upregulating BAZ2A

“…Besides, bioinformatics analysis and experimental results showed that LINC00885 positively regulated BAZ2A expression and miR-3150b-3p negatively regulated BAZ2A expression, indicating that BAZ2A was regulated by LINC00885/miR-3150b-3p axis. Based on a recent study, LINC00885 could facilitate CC tumorigenesis by sponging miR-432-5p to up-regulate MACC1 [ 34 ]. Results of current rescue assays indicated that LINC00885 regulated CC cell proliferation and apoptosis through miR-3150b-3p/BAZ2A axis.…”

Construction of miRNA‐lncRNA‐mRNA co‐expression network affecting EMT‐mediated cisplatin resistance in ovarian cancer

“…Overexpression of this lncRNA is closely associated with a lower survival rate and poor prognosis in breast and cervical cancer patients. 127 , 128 Lu et al 129 demonstrated that high expression of PAX8‐AS1 is associated with poor relapse‐free survival in thyroid cancer patients. However, a recent study reported the tumour suppressor role of PAX8‐AS1.…”

“…Abba et al reported the molecular effects of LINC00885 as a new oncogenic lncRNA associated with early breast cancer progression. Overexpression of this lncRNA is closely associated with a lower survival rate and poor prognosis in breast and cervical cancer patients 127,128 . Lu et al 129 demonstrated that high expression of PAX8‐AS1 is associated with poor relapse‐free survival in thyroid cancer patients.…”