Long Non-Coding RNAs in Diagnosis, Treatment, Prognosis, and Progression of Glioma: A State-of-the-Art Review
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Abstract:
Glioma is the most common malignant central nervous system tumor with significant mortality and morbidity. Despite considerable advances, the exact molecular pathways involved in tumor progression are not fully elucidated, and patients commonly face a poor prognosis. Long non-coding RNAs (lncRNAs) have recently drawn extra attention for their potential roles in different types of cancer as well as non-malignant diseases. More than 200 lncRNAs have been reported to be associated with glioma. We aimed to assess the roles of the most investigated lncRNAs in different stages of tumor progression and the mediating molecular pathways in addition to their clinical applications. lncRNAs are involved in different stages of tumor formation, invasion, and progression, including regulating the cell cycle, apoptosis, autophagy, epithelial-to-mesenchymal transition, tumor stemness, angiogenesis, the integrity of the blood-tumor-brain barrier, tumor metabolism, and immunological responses. The well-known oncogenic lncRNAs, which are upregulated in glioma, are H19 , HOTAIR , PVT1 , UCA1 , XIST , CRNDE , FOXD2-AS1 , ANRIL , HOXA11-AS , TP73-AS1 , and DANCR . On the other hand, MEG3 , GAS5 , CCASC2 , and TUSC7 are tumor suppressor lncRNAs, which are downregulated. While most studies reported oncogenic effects for MALAT1 , TUG1 , and NEAT1 , there are some controversies regarding these lncRNAs. Expression levels of lncRNAs can be associated with tumor grade, survival, treatment response (chemotherapy drugs or radiotherapy), and overall prognosis. Moreover, circulatory levels of lncRNAs, such as MALAT1, H19, HOTAIR, NEAT1, TUG1, GAS5, LINK-A , and TUSC7 , can provide non-invasive diagnostic and prognostic tools. Modulation of expression of lncRNAs using antisense oligonucleotides can lead to novel therapeutics. Notably, a profound understanding of the underlying molecular pathways involved in the function of lncRNAs is required to develop novel therapeutic targets. More investigations with large sample sizes and increased focus on in-vivo models are required to expand our understanding of the potential roles and application of lncRNAs in glioma.Keywords:
MALAT1
HOTAIR
GAS5
MEG3
Tumor progression
PVT1
XIST
Competing Endogenous RNA
HOTAIR
GAS5
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MALAT1
MEG3
GAS5
Macrophage polarization
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Glioma is the most common malignant central nervous system tumor with significant mortality and morbidity. Despite considerable advances, the exact molecular pathways involved in tumor progression are not fully elucidated, and patients commonly face a poor prognosis. Long non-coding RNAs (lncRNAs) have recently drawn extra attention for their potential roles in different types of cancer as well as non-malignant diseases. More than 200 lncRNAs have been reported to be associated with glioma. We aimed to assess the roles of the most investigated lncRNAs in different stages of tumor progression and the mediating molecular pathways in addition to their clinical applications. lncRNAs are involved in different stages of tumor formation, invasion, and progression, including regulating the cell cycle, apoptosis, autophagy, epithelial-to-mesenchymal transition, tumor stemness, angiogenesis, the integrity of the blood-tumor-brain barrier, tumor metabolism, and immunological responses. The well-known oncogenic lncRNAs, which are upregulated in glioma, are H19 , HOTAIR , PVT1 , UCA1 , XIST , CRNDE , FOXD2-AS1 , ANRIL , HOXA11-AS , TP73-AS1 , and DANCR . On the other hand, MEG3 , GAS5 , CCASC2 , and TUSC7 are tumor suppressor lncRNAs, which are downregulated. While most studies reported oncogenic effects for MALAT1 , TUG1 , and NEAT1 , there are some controversies regarding these lncRNAs. Expression levels of lncRNAs can be associated with tumor grade, survival, treatment response (chemotherapy drugs or radiotherapy), and overall prognosis. Moreover, circulatory levels of lncRNAs, such as MALAT1, H19, HOTAIR, NEAT1, TUG1, GAS5, LINK-A , and TUSC7 , can provide non-invasive diagnostic and prognostic tools. Modulation of expression of lncRNAs using antisense oligonucleotides can lead to novel therapeutics. Notably, a profound understanding of the underlying molecular pathways involved in the function of lncRNAs is required to develop novel therapeutic targets. More investigations with large sample sizes and increased focus on in-vivo models are required to expand our understanding of the potential roles and application of lncRNAs in glioma.
MALAT1
HOTAIR
GAS5
MEG3
Tumor progression
PVT1
XIST
Competing Endogenous RNA
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Citations (45)
Long noncoding RNAs (lncRNAs) have great impact on the carcinogenesis and progression of gastric cancer (GC). Recent studies show that the over-expression of H19, HOTAIR, TINCR and LINC00152 and the down-expression of MEG3, GAS5, LET and AA174084 are closely related to the occurrence, invasion, metastasis and prognosis of GC. lncRNAs provide an opportunity to develop new strategies for the diagnosis and treatment of GC.
Key words:
Stomach neoplasms; Tumor markers, biological; Diagnosis; Therapy
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Bisphosphonates (BPs) are inhibitors of osteoclast-mediated bone resorption used for the treatment of multiple myeloma (MM) patients with osteolytic lesions. Bisphosphonate-induced osteonecrosis of the jaw (BONJ) is an infrequent drug-caused adverse event of these agents. Long noncoding RNAs (lncRNAs) are a set of more than 200 base pairs, noncoding RNA molecules, which are critical posttranscriptional regulators of gene expression. Our study was aimed at evaluating 17 lncRNAs, whose targets were previously validated as key elements in MM, bone metabolism, and angiogenesis in MM subjects without BONJ (MM group), in MM subjects with BONJ (BONJ group), and a group of healthy controls (CTRL group). Our results demonstrated a different lncRNA profile in BONJ patients compared to MM patients and controls. Two lncRNAs (DANCR and MALAT1) were both downregulated compared to controls and MM, twelve (HOTAIR, MEG3, TP73-AS1, HOTTIP, HIF1A-AS2, MANTIS, CTD-2201E18, CTD1-2003C8, R-471B22, RP1-43E13, RP11-553L6.5, and RP1-286D6) were overexpressed in MM with BONJ, and one (H19) was upregulated compared with only MM. Two lncRNAs (JHDMD1 and MTMR9LP) had higher expression, but these differences were not statistically significant. The examined lncRNAs target several genes and metabolic pathways. An altered lncRNA signature could contribute to the onset of BONJ or have a protective action. Targeting these lncRNAs could offer a possibility for the prevention or therapy of BONJ.
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MEG3
Cathepsin K
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PVT1
Bone remodeling
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: Long non-coding RNAs (lncRNAs) belong to an extremely heterogeneous class of non-coding RNAs with a length ranging from 200 to 100,000 bp. They modulate a series of cellular pathways in both physiological and pathological context. It is no coincidence that they are expressed in an aberrant way in pathologies such as cancer, so as to deserve to be subclassified as oncogenes or tumor suppressors. These molecules are also involved in the regulation of cancer cell proliferation. Several lncRNAs are able to modulate cell growth both positively and negatively, and in this review we have focused on a small group of them, characterized by the simultaneous action on different pathways regulating cell proliferation. They have been considered in the light of their behavior in three different subtypes of proliferative pathways that we can define as (I) tumor suppressor, (II) oncogenic and (III) transcriptionally-driven. More specifically, we have characterized some lncRNAs considered oncogenes (such as H19, linc-ROR, MALAT1, HULC, HOTAIR and ANRIL), tumor suppressors (such as MEG3 and lincRNA-p21), and both oncogenes/tumor suppressors (UCA1 and TUG1) in a little more detail. As can be understood from the review, the interactions between lncRNAs and their molecular targets, only in the context of controlling cell proliferation, give rise to an intricate molecular network, the understanding of which, in the future, will certainly be of help for the treatment of molecular diseases such as cancer.
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PVT1
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MALAT1
MEG3
GAS5
Competing Endogenous RNA
Macrophage polarization
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Non-coding RNAs (ncRNAs) are reported to be expressed in human cancer, including pancreatic ductal adenocarcinoma (PDAC). They affect the growth, migration and invasion of tumor cells by regulating cell cycle and apoptosis, as well as play an important role on epigenetic modification, transcription and post-transcriptional regulation. However, whether ncRNAs alteration results in PDAC remains largely unknown. Because of this, analysis based on existing data on ncRNAs, which are crucial for modulating pancreatic tumorigenesis, will be important for the future research on PDAC. We identify non-coding RNAs with tumor-promoting function: HOTAIR, HOTTIP, MALAT1, lncRNA H19, lncRNA PVT1, circ-RNA ciRS-7, circ-0030235, circ-RNA_100782, circ-LDLRAD3, circ-0007534, circRHOT1, circZMYM2, circ-IARS, circ-RNA PDE8A, miR-21, miR-155, miR-221/222, miR-196b, miR-10a. While others including GAS5, MEG3 and lncRNA ENST00000480739, has_circ_0001649, miR-34a, miR-100, miR-217, miR-143 inhibit the proliferation and invasion of PDAC. Hence, we summarized the function of ncRNAs' role in the occurrence, development and metastasis of PDAC, aiming to provide guidance for the clinical diagnosis and treatment of PDAC.
MALAT1
PVT1
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GAS5
Competing Endogenous RNA
HOTAIR
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HOTAIR
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MALAT1
GAS5
PVT1
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