Roles and Mechanisms of the Long Noncoding RNAs in Cervical Cancer

Abstract

Cervical cancer (CC) continues to be one of the leading causes of death for women across the world. Although it has been determined that papillomavirus infection is one of the main causes of the etiology of the disease, genetic and epigenetic factors are also required for its progression. Among the epigenetic factors are included the long noncoding RNAs (lncRNAs), transcripts of more than 200 nucleotides (nt) that generally do not code for proteins and have been associated with diverse functions such as the regulation of transcription, translation, RNA metabolism, as well as stem cell maintenance and differentiation, cell autophagy and apoptosis. Recently, studies have begun to characterize the aberrant regulation of lncRNAs in CC cells and tissues, including Homeobox transcript antisense RNA (HOTAIR), H19, Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), Cervical Carcinoma High-Expressed 1 (CCHE1), Antisense noncoding RNA in the inhibitors of cyclin-dependent kinase 4 (ANRIL), Growth arrest special 5 (GAS5) and Plasmacytoma variant translocation 1 (PVT1). They have been associated with several disease-related processes such as cell growth, cell proliferation, cell survival, metastasis and invasion as well as therapeutic resistance, and are novel potential biomarkers for diagnosis and prognosis in CC. In this review, we summarize the current literature regarding the knowledge we have about the roles and mechanisms of the lncRNAs in cervical neoplasia.

Bioinformatic identification of genomic instability-associated lncRNAs signatures for improving the clinical outcome of cervical cancer by a prognostic model

“…We further compared the prediction performance of the LncSig with two recently published lncRNA signatures: 3-lncRNAs (H19, MALAT1, and CCHE1) signature derived from Cáceres’ study (hereinafter referred to as CácereslncSig) 15 and 2-lncRNAs (HOTAIR and SNHG1) signature derived from Aalijahan’s study (hereinafter referred to as AalijahanlncSig) 16 using the same TCGA patient cohort. As shown in Fig.…”

E2F4 may be a core transcription factor in the lncRNA‐TF regulatory network in cervical cancer

“…EBIC may act as an oncogenic lncRNA through cooperation with EZH2 and may promote the migration of cervical cancer cells 20 . CCHE1 binds to PCNA mRNA and promotes its expression, thereby increasing cervical cancer cell proliferation 21 . HOTAIR not only promotes the proliferation and invasion of cervical cancer cells, but is also related to the recurrence of cervical cancer.…”

“… 20 CCHE1 binds to PCNA mRNA and promotes its expression, thereby increasing cervical cancer cell proliferation. 21 HOTAIR not only promotes the proliferation and invasion of cervical cancer cells, but is also related to the recurrence of cervical cancer. In addition, MALAT1, PVT1, H19, and XIST can promote cancer cell proliferation, invasion, and migration and play a role in the progression of cervical cancer.…”

The Regulatory Functions and the Mechanisms of Long Non-Coding RNAs in Cervical Cancer

“…Aberrant expression of lncRNAs has been previously and extensively reported in cervical cancer [ 35 ]. However, current studies (since March 2021) provide more progress about the importance of lncRNA dysregulation in promoting cervical cancer development, invasion, and metastasis through their interactions with several signaling pathways.…”

“…Accumulated evidence demonstrates that LncRNAs play an essential role in the development and progression of a variety of cancers via the Wnt signaling pathway. For example, in cervical cancer, several lncRNAs, including RP11-480112.5 , ASB16-AS1 , HOTAIR , CASC11 , CALML3-AS1 , and DANCER , are involved in modulating Wnt Signaling pathways [ 35 ]. More recently, several additional lncRNAs, including SNHG6 [ 37 ], EGFR-AS1 [ 38 ], SPINT1-AS1 [ 39 ], HNRNPU-AS1 [ 40 ], and LINC00665 [ 41 ] have been identified that contribute to the proliferation, migration, invasion, and EMT in cervical cancer via the Wnt signaling pathway ( Table 1 , Figure 1 ).…”