Crosstalk Between Long Non-coding RNAs, Micro-RNAs and mRNAs: Deciphering Molecular Mechanisms of Master Regulators in Cancer

López–Urrutia, Eduardo; Bustamante-Montes, Lilia Patricia; Cervantes, Diego Ladrón de Guevara; Pérez‐Plasencia, Carlos; Campos‐Parra, Alma D.

doi:10.3389/fonc.2019.00669

Cited by 198 publications

(143 citation statements)

References 76 publications

Supporting

Mentioning

143

Contrasting

Order By: Relevance

“…Accumulative evidence reveal a clear involvement of the individual lnRNAs of the 8q24.21 gene desert in tumorigenesis (Table 1), a concept that is supported by the emerging roles of lnRNAs in tumorigenesis via complex mechanisms [44,45]. Upregulations of PRNCR1 (prostate cancer non-coding RNA1) occurred in prostate cancer (PC), and precancerous lesions PINs (prostatic intraepithelial neoplasia) and knockdown of PRNCR1 reduced the survival of PC cells and the expression of androgen receptor (AR), indicating an important role of PRNCR1 in facilitating PC via AR signaling (Table 1) [46].…”

Section: Association Of the 8q2421 Gene Desert With Oncogenesismentioning

confidence: 94%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

View full text Add to dashboard Cite

FAM84B is a risk gene in breast and prostate cancers. Its upregulation is associated with poor prognosis of prostate cancer, breast cancer, and esophageal squamous cell carcinoma. FAM84B facilitates cancer cell proliferation and invasion in vitro, and xenograft growth in vivo. The FAM84B and Myc genes border a 1.2 Mb gene desert at 8q24.21. Co-amplification of both occurs in 20 cancer types. Mice deficient of a 430 Kb fragment within the 1.2 Mb gene desert have downregulated FAM84B and Myc expressions concurrent with reduced breast cancer growth. Intriguingly, Myc works in partnership with other oncogenes, including Ras. FAM84B shares similarities with the H-Ras-like suppressor (HRASLS) family over their typical LRAT (lecithin:retinal acyltransferase) domain. This domain contains a catalytic triad, H23, H35, and C113, which constitutes the phospholipase A 1/2 and O-acyltransferase activities of HRASLS1-5. These enzymatic activities underlie their suppression of Ras. FAM84B conserves H23 and H35 but not C113 with both histidine residues residing within a highly conserved motif that FAM84B shares with HRASLS1-5. Deletion of this motif abolishes FAM84B oncogenic activities. These properties suggest a collaboration of FAM84B with Myc, consistent with the role of the gene desert in strengthening Myc functions. Here, we will discuss recent research on FAM84B-derived oncogenic potential.Genes 2020, 11, 312 2 of 15 non-coding RNA (lnRNA), and on its upstream or centromeric side sits a 1.2 Mb gene desert with the centromeric side bordered by the FAM84B or LRATD2 gene ( Figure 1). The unique feature of this gene desert is the existence of multiple (lnRNAs) (PCAT1, PCAT2, POU5F1B, CCAT1, CCAT2, CASC8, CASC11, CASC19, and CASC21) with FAM84B and Myc being the only protein coding genes (Figure 1) [12][13][14]. In view of Myc being the most-well-studied oncogene and the 8q24 gene desert as a region that is frequently amplified in cancer, FAM84B stands as a promising target for oncogenic activities; nonetheless, its impact on tumorigenesis remained unknown until recently. As the oncogenic potential of the non-coding RNAs of PVT1 and those within the gene desert (Figure 1) has been recently reviewed [13][14][15][16][17], we will focus on the emerging role of FAM84B in tumorigenesis in this review. We will briefly discuss the 8q24 gene desert with respect to oncogenesis to set the stage for the following systemic examination of the evidence pertinent to FAM84B-derived tumorigenesis. The main materials used in this review were chosen based on the PRISMA (preferred reporting items for systematic reviews and meta-analyses) Guidelines [18,19]. A literature search of the PubMed database for (1) "8q24 gene desert", revealed 28 papers with 6 irrelevant to tumorigenesis (Figure 2A) and (2) "FAM84B", identified 21 articles, including non-English papers (n = 1) and articles not directly related to FAM84B and cancer (n = 2) ( Figure 2B). After excluding these items, 22 articles on 8q24 gene desert and 18 papers related to the FAM84B topic h...

show abstract

Section: Association Of the 8q2421 Gene Desert With Oncogenesismentioning

confidence: 94%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

View full text Add to dashboard Cite

show abstract

“…Long noncoding RNAs (lncRNAs) are novel class of regulatory RNAs, which are involved in numerous biological processes via interaction with mRNAs and miRNAs, such as miRNA and lncRNA competition for the same mRNA target, and lncRNAs acting as decoys (or sponges) for miRNAs [ 154 ]. By RNA sequencing of hypertrophic and leaner broilers, Li et al identified a novel lncRNA, termed lncIRS1, is upregulated in hypertrophic muscles.…”

Section: Atrophy-related Mirs and Their Potential Regulation Of Imentioning

confidence: 99%

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

Yoshida

Delafontaine

2020

Cells

382

209

View full text Add to dashboard Cite

Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration.

show abstract

“…Evaluation of circulating miRNAs and lncRNAs trough liquid biopsies is appealing and has been extensively performed in a variety of cancers, where these molecules have often shown prognostic and predictive roles [45]. In PDAC, both overexpression and downregulation of specific miRNAs have been associated with poor prognosis.…”

Section: Microrna and Long Non-coding Rnamentioning

confidence: 99%

Prognostic and predictive factors in pancreatic cancer

et al. 2020

View full text Add to dashboard Cite

Pancreatic cancer is one of the leading causes of cancer death worldwide. Its high mortality rate has remained unchanged for years. Radiotherapy and surgery are considered standard treatments in early and locally advanced stages. Chemotherapy is the only option for metastatic patients. Two treatment regimens, i. e. the association of 5-fluorouracil-irinotecan-oxaliplatin (FOLFIRINOX) and the association of nabpaclitaxel with gemcitabine, have been shown to improve outcomes for metastatic pancreatic adenocarcinoma patients. However, there are not standardized predictive biomarkers able to identify patients who benefit most from treatments. CA19-9 is the most studied prognostic biomarker, its predictive role remains unclear. Other clinical, histological and molecular biomarkers are emerging in prognostic and predictive settings. The aim of this review is to provide an overview of prognostic and predictive markers used in clinical practice and to explore the most promising fields of research in terms of treatment selection and tailored therapy in pancreatic cancer.

show abstract

Crosstalk Between Long Non-coding RNAs, Micro-RNAs and mRNAs: Deciphering Molecular Mechanisms of Master Regulators in Cancer

Cited by 198 publications

References 76 publications

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

Prognostic and predictive factors in pancreatic cancer

Contact Info

Product

Resources

About