Abstract
Aims: A growing number of studies have unveiled that long non-coding RNA (lncRNA) is conductive to cervical cancer (CC) development. However, the effect of LIPE-AS1 is remained to be studied in CC.Main Methods: Reverse transcription-polymerase chain reaction (RT-PCR) was employed to measure LIPE-AS1 expression in CC tissues and the adjacent normal tissues. Additionally, we conducted gain- and loss-of functional experiments of LIPE-AS1 and adopted CCK8 assay, BrdU assay, and in vivo tumor formation experiment to test the proliferation of CC cells (HCC94 and HeLa). Besides, the apoptosis, invasion, and epithelial-mesenchymal transformation (EMT) of CC cells were estimated using flow cytometry, transwell assay, and western blot, respectively. Further, LIPE-AS1 downstream targets were analyzed through bioinformatics, and the binding relationships between LIPE-AS1 and miR-195-5p were verified via dual-luciferase activity experiment and RNA Protein Immunoprecipitation (RIP) assay. Moreover, rescue experiments were conducted to confirm the effects of LIPE-AS1 and miR-195-5p in regulating CC development and the expressions of MAPK signaling pathway related proteins were detected by RT-PCR, western blot, and immunofluorescence.Key Findings: LIPE-AS1 was over-expressed in CC tissues (compared to normal adjacent tissues) and was notably related to tumor volume, distant metastasis. Overexpressing LIPE-AS1 accelerated CC cell proliferation, migration and EMT, inhibited apoptosis; while LIPE-AS1 knockdown had the opposite effects. The mechanism studies confirmed that LIPE-AS1 sponges miR-195-5p as a competitive endogenous RNA (ceRNA), which targets the 3′-untranslated region (3′-UTR) of MAP3K8. LIPE-AS1 promoted the expression of MAP3K8 and enhanced ERK1/2 phosphorylation, which were reversed by miR-195-5p.Significance: LIPE-AS1 regulates CC progression through the miR-195-5p/MAPK signaling pathway, providing new hope for CC diagnosis and treatment.
Highlights
Cervical cancer (CC), as one prevailing gynecological malignant tumor, ranks second among female malignancies following breast cancer, and even ranks first in some developing countries [1]
Rescue experiments were conducted to confirm the effects of LIPE-AS1 and miR-195-5p in regulating CC development and the expressions of MAPK signaling pathway related proteins were detected by Reverse transcription-polymerase chain reaction (RT-PCR), western blot, and immunofluorescence
The results showed that LIPE-AS1 was remarkably up-regulated in CC tissues (Figure 1A)
Summary
Cervical cancer (CC), as one prevailing gynecological malignant tumor, ranks second among female malignancies following breast cancer, and even ranks first in some developing countries [1]. LncRNA MIR210HG was found to be elevated in CC tissues and related to FIGO staging, metastasis and worse survival of CC patients. It promoted CC proliferation, invasion, and epithelial-mesenchymal transformation (EMT) by regulating the miR-503-5p/TRAF4 axis [4]. Li et al reported that lncRNA CCAT1 was over-expressed in CC tissues, and CCAT1 knockout restrained CC development via inhibiting cell proliferation, migration, invasion, EMT, and accelerating cell apoptosis [5]. Some lncRNAs, such as lncRNA PTENP1, were reported to inhibit cervical cancer development [6]. We first determined the LIPE-AS1 level in CC tissues and cells and studied the relationship of LIPE-AS1 level with the clinic pathological characteristics of CC patients
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