Long non‑coding RNA AFAP1‑AS1 facilitates the growth and invasiveness of oral squamous cell carcinoma by regulating the miR‑145/HOXA1 axis

Li, Minghe; Yu, Dongsheng; Li, Zhihong; Zhao, Cong; Su, Chang; Ning, Jun

doi:10.3892/or.2020.7908

Cited by 12 publications

(6 citation statements)

References 34 publications

(53 reference statements)

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“…The subcellular location of AFAP1-AS1 appears to vary in different tumor cell lines. 45 , 46 As AFAP1-AS1 has been reported to be mainly located in the cytoplasm of OSCC cells, 47 it could regulate CCNA2 expression through the ceRNA network. Candidate miRNAs predicted by bioinformatics analyses were miR-655-3p, miR-320a, and miR-145-5p.…”

Section: Discussionmentioning

confidence: 99%

Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

Li¹,

Liu²,

Li³

et al. 2021

CMAR

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Background: Evidence has indicated that dysregulation of long noncoding RNAs (lncRNA) is a critical factor in the occurrence of many diseases, including cancer. The lncRNA AFAP1-AS1 has been shown to participate in oncogenesis, metastasis, or drug resistance in many types of cancer. However, the potential role of AFAP1-AS1 in oral squamous cell carcinoma (OSCC) has not been fully elucidated. Methods: Bioinformatics analysis was performed to compare AFAP1-AS1 expression levels in OSCC cancer samples and in normal controls. The biological function of AFAP1-AS1 was studied through loss-of-function assays. To study the potential mechanisms, high-throughput sequencing was applied to OSCC cancer samples and a series of bioinformatics analyses were performed. The effects of AFAP1-AS1 on OSCC tumor growth was evaluated by in vivo xenograft tumor formation assays. Results: Bioinformatics analyses indicated that AFAP1-AS1 was upregulated in OSCC. Overexpression of AFAP1-AS1 was positively correlated with lymph node metastasis, tumor stage, and pathological grade. Down-regulation of AFAP1-AS1 in OSCC led to decreased proliferation in vitro and, notably, inhibition of tumor growth in vivo. Further research indicated that AFAP1-AS1 regulated OSCC cell proliferation by targeting CCNA2. Conclusion: AFAP1-AS1 promotes tumor proliferation and indicates a poor prognosis in OSCC, providing a potential therapeutic strategy.

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Section: Discussionmentioning

confidence: 99%

Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

Li¹,

Liu²,

Li³

et al. 2021

CMAR

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“…Re‐expression of microRNA‐145 in the SCC‐9 cell line inhibited cell proliferation, cell migration, cell invasion in vitro and reduced tumor growth in vivo by down‐regulating HOXA1 inactivating the ERK/MAPK signaling pathway. Another study by Li et al 61 reported that AFAP1‐AS1 targets miR‐145 thus positively upregulating the HOXA1 expression in oral cancer, promoting proliferation, invasion, and migration.…”

Section: Hox Centric Targeted Regulation In Oral Cancermentioning

confidence: 99%

In silico interaction of HOX cluster‐embedded microRNAs and long non‐coding RNAs in oral cancer

Padam

Basavarajappa

Shenoy

et al. 2021

J Oral Pathology Medicine

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HOX genes are members of the homeotic transcription factor family, organized into four paralogous clusters. HOX complexes are believed to have arisen by genome-wide duplications during evolution. In humans, there are about 200 homeobox genes of which 39 are HOX genes, which are segregated onto four chromosomes, HOXA -7p15, HOXB -17q21.2, HOXC -12q13, and HOXD -2q31 (Figure 1). 1,2 The protein product of the HOX gene is a transcription factor that contains a conserved homeodomain region. 2 The homeodomain consists of the helix-turn-helix protein motif responsible for sequence-specific DNA binding. HOX genes are the pivotal regulators of growth and development. They regulate events such as differentiation, metabolism, apoptosis, autophagy, and their deregulation leads to various disorders and diseases including cancer. 3

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“…The expression of lncRNA-PNUTS is elevated and correlates with the mRNA level of ZEB1. A number of lncRNAs have been identified as EMT modulators in oral cancer [ 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 ,…”

Section: Epithelial-to-mesenchymal Transition: Emtmentioning

confidence: 99%

Impact of Non-Coding RNAs on Chemotherapeutic Resistance in Oral Cancer

et al. 2022

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Drug resistance in oral cancer is one of the major problems in oral cancer therapy because therapeutic failure directly results in tumor recurrence and eventually in metastasis. Accumulating evidence has demonstrated the involvement of non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in processes related to the development of drug resistance. A number of studies have shown that ncRNAs modulate gene expression at the transcriptional or translational level and regulate biological processes, such as epithelial-to-mesenchymal transition, apoptosis, DNA repair and drug efflux, which are tightly associated with drug resistance acquisition in many types of cancer. Interestingly, these ncRNAs are commonly detected in extracellular vesicles (EVs) and are known to be delivered into surrounding cells. This intercellular communication via EVs is currently considered to be important for acquired drug resistance. Here, we review the recent advances in the study of drug resistance in oral cancer by mainly focusing on the function of ncRNAs, since an increasing number of studies have suggested that ncRNAs could be therapeutic targets as well as biomarkers for cancer diagnosis.

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Long non‑coding RNA AFAP1‑AS1 facilitates the growth and invasiveness of oral squamous cell carcinoma by regulating the miR‑145/HOXA1 axis

Cited by 12 publications

References 34 publications

Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

In silico interaction of HOX cluster‐embedded microRNAs and long non‐coding RNAs in oral cancer

Impact of Non-Coding RNAs on Chemotherapeutic Resistance in Oral Cancer

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