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Review
. 2021 Nov 28;13(23):5987.
doi: 10.3390/cancers13235987.

The Emerging Role of Non-Coding RNAs in Pituitary Gland Tumors and Meningioma

Soudeh Ghafouri-Fard  1 , Atefe Abak  2 , Bashdar Mahmud Hussen  3 , Mohammad Taheri  4 , Guive Sharifi  5
Affiliations
Review

The Emerging Role of Non-Coding RNAs in Pituitary Gland Tumors and Meningioma

Soudeh Ghafouri-Fard et al. Cancers (Basel). .

Abstract

Long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) are non-coding transcripts which are involved in the pathogenesis of pituitary gland tumors. LncRNAs that participate in the pathogenesis of pituitary gland tumors mainly serve as sponges for miRNAs. CLRN1-AS1/miR-217, XIST/miR-424-5p, H19/miR-93a, LINC00473/miR-502-3p, SNHG7/miR-449a, MEG8/miR-454-3p, MEG3/miR-23b-3p, MEG3/miR-376B-3P, SNHG6/miR-944, PCAT6/miR-139-3p, lncRNA-m433s1/miR-433, TUG1/miR-187-3p, SNHG1/miR-187-3p, SNHG1/miR-302, SNHG1/miR-372, SNHG1/miR-373, and SNHG1/miR-520 are identified lncRNA/miRNA pairs that are involved in this process. Hsa_circ_0001368 and circOMA1 are two examples of circRNAs that contribute to the pathogenesis of pituitary gland tumors. Meanwhile, SNHG1, LINC00702, LINC00460, and MEG3 have been found to partake in the pathogenesis of meningioma. In the current review, we describe the role of non-coding RNAs in two types of brain tumors, i.e., pituitary tumors and meningioma.

Keywords: circRNA; lncRNA; meningioma; miRNA; pituitary gland cancer.

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Conflict of interest statement

The authors declare they have no conflicts of interests.

Figures

Figure 1
Figure 1
A schematic representation of the role of several non-coding RNAs in regulating the MAPK/ERK, PI3K/AKT, Wnt/β-Catenin, and BMP signaling pathways in pituitary gland tumors and meningiomas. The figure represents the potential crosstalk between various signaling cascades modulated via several ncRNAs in triggering the development of tumor cells. WNT-signaling is a crucial part of the crosstalk between key oncogenic cascades involved in pituitary gland tumors. Elements of the WNT cascades both could be regulated through diverse pathways, including MAPK/ERK, PI3K/AKT, and BMP, as well as transcriptional regulators containing p53 and MITF [32]. In addition, an accumulation of β-catenin in the cytoplasm could, in turn, lead to its translocation to the nucleus, where it could create a complex with TCF/LEF to trigger the transcription of RUNX2, Cyclin D1, and PIT1/2. Additionally, RUNX2 could modulate the transcription of various targets, including OCN, OSX, OPN, MMP13, and ALP [33]. Furthermore, BMP receptors could phosphorylate receptor-SMADs upon ligand binding. TCF12 and TWIST1 are basic helix-loop-helix transcription factors that could play an effective role in heterodimerization and suppressing transcription downstream of the BMP cascade [34]. According to the current report, lncRNA AFAP1-AS1 could enhance growth and inhibit apoptosis in pituitary adenomas through promoting PTEN expression and suppressing the expression levels of PI3K and AKT in tumor cells [29]. Moreover, another research has denoted that LINC00460 could elevate meningioma progression and metastasis through promoting the expression levels of MMP-2, MMP-9, and ZEB1 by sponging miR-539 and thereby acting as an oncogenic RNA in the meningioma malignancy [35]. Moreover, based on recent study, lncRNA SNHG1 via targeting miR-556-5p could elevate TCF12 expression, thereby promoting tumorigenesis of meningioma through the Wnt signaling cascade. In fact, TCF12 expression was positively modulated via SNHG1, and TCF12 could, in turn, enhance transcription of SNHG1 through binding with the promoter region of SNHG1 [36]. Green arrows indicate the upregulation of target genes modulated via ncRNAs (miRNAs and lncRNAs); red arrows depict inhibition regulated by them. All the information regarding the role of these ncRNAs in modulating pituitary gland tumors can be seen in Table 1, Table 2, Table 3, Table 4 and Table 5.
Figure 2
Figure 2
A schematic diagram of the role of various ncRNAs in modulating the TGF-β/SMAD signaling pathway in pituitary gland tumors. According to this cascade, it could be triggered through the binding of active TGF-β with TβRII and forming the TβRI-TβRII heteromeric complex, resulting in phosphorylation of Smad2/3, oligomerization with Smad4, and consequent nuclear translocation to modulate the transcription of ECM genes. Furthermore, Smad7 could play a remarkable role as a negative modulator of the TGF-β cascade. In addition, TGF-β has a significant part in triggering the activation of downstream signaling pathways containing MAPK, modulated by the Ras-Raf-MEK-ERK cascade, and TAK1, regulated by the TAB1 pathway. This could also lead to mediating the activation of MKK4-JNK and MKK3-p38 cascades and upregulation of AP-1 and ATF-2, respectively, and the overexpression of NF- κB to modulate profibrotic responses [61]. Previous studies have authenticated that several ncRNAs could have a significant part in regulating the TGF-β/SMAD cascade in pituitary gland tumors. As an illustration, recent literature has detected that overexpression of lnc-SNHG1 could considerably elevate the expression level of TβRII through activating TβRII/SMAD3 in invasive pituitary tumor cells via sponging miR-302/372/373/520 [31]. Furthermore, other research has indicated that upregulation of miR-93-5p could downregulate the expression level of Smad7, thereby activating the TGF-β1/Smad3 signaling-mediated fibrosis of prolactinoma cells [51]. Green arrows indicate the upregulation of target genes modulated via ncRNAs (miRNAs and lncRNAs); red arrows depict inhibition regulated by them.
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