LncRNA DLX6-AS1/miR-129-5p/DLK1 axis aggravates stemness of osteosarcoma through Wnt signaling

Zhang, Rongmou; Tang, Ting; Yu, Haiming; Yao, Xuedong

doi:10.1016/j.bbrc.2018.11.019

Cited by 60 publications

(51 citation statements)

References 20 publications

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“…Recently, several studies have shown the participation of Wnt6, Barx1, ptprz1, and other genes in the regulation of Wnt/β-catenin signalling and their involvement in the development of malignant tumours [31][32][33][34][35][36][37][38][39][40][41]. These ndings support our hypothesis that dlx6-as1 may affect the mRNA expression of Wnt6, Barx1, ptprz1 and other genes through ceRNA network to regulate Wnt/β-catenin signalling and participate in the distant bone metastasis of breast cancer.…”

Section: Discussionsupporting

confidence: 88%

“…In our study, we found the activation of mast cells was correlated with Wnt6 expression. Zhang et al proved that Wnt signal is often activated under the action of dlx6-as1 [34]. Therefore, we speculate that Wnt pathway may be important for the impact of dlx6-as1 on the composition of immune cells.…”

Section: Discussionmentioning

confidence: 62%

“…Guo et al demonstrated dlx6-as1 upregulation in cell lines and tissues from bladder cancer patients, which augmented the proliferation, invasion, and migration of these cells by regulating EMT process and the activity of Wnt/β-catenin signalling [35]. dlx6-as1's impact on the characteristics of cancer stem cells in osteosarcoma has also been investigated and was found to positively correlate with more advanced disease and poorer survival [36]. Similar ndings have been demonstrated in prostate cancer patients.…”

Section: Discussionmentioning

confidence: 99%

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ceRNA Network Development and Tumour-infiltrating Immune Cell Analysis in Metastatic Breast Cancer of Bone

Liu

Song

Zhou

et al. 2020

Preprint

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Background: Advanced breast cancer commonly metastasises to the bone and the molecular mechanism explaining the bone affinity of breast cancer cells is unclear. Thus, we developed nomograms based on a competing endogenous RNA (ceRNA) network and analysed tumour-infiltrating immunecells to elucidate the molecular pathways that may predict the prognosis of breast cancer patients.Methods: We obtained the RNA expression profile of 1091 primary breast cancer samples from The Cancer Genome Atlas database, 58 of which had bone metastasis. We analysed differential RNA expression patterns between breast cancer with and without bone metastasis and developed a ceRNA network. Cibersort was employed to differentiate between immune cell types based on tumour transcripts. Nomograms were then established using the ceRNA network and immune cell analysis. The value of prognostic factors was evaluated by Kaplan-Meier survival analysis and Cox proportional risk model.Results: There were significant differences in lncRNAs, 18 miRNAs, and 20mRNAs between breast cancer with and without bone metastasis, which were used to construct a ceRNA network. We found that the protein-coding genes gjb3, cammv, ptprz1,and fbn3 were significant in our Kaplan-Meier analysis. We also observed significant differences in plasma cell and follicular helper T cell populations between the two groups. In addition, the proportions of mast cells, gamma delta T cells, and plasma cells differed depending on disease location and stage. Our analysis revealed that a high proportion of follicular helper T cells and a low proportion of eosinophils promoted survival and that dlx6-as1, wnt6,and gabbr2expression may be related to bone metastasis of breast cancer.Conclusions: We provided a bioinformatic basis for exploring the molecular mechanism of bone metastasis in breast cancer patients and identified factors that may predict this.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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ceRNA Network Development and Tumour-infiltrating Immune Cell Analysis in Metastatic Breast Cancer of Bone

Liu

Song

Zhou

et al. 2020

Preprint

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“…[14][15][16] Regarding OS, extensive evidence has demonstrated that many lncRNAs are dysregulated and that this dysregulation is important in tumor onset and development. [17][18][19] For instance, FBXL19-AS1, 20 GClnc1, 21 and DLX6-AS1 22 are highly expressed in OS and play cancer-promoting roles in regulating cancer aggressiveness. On the contrary, TUSC7, 23 AWPPH, 24 and HAND2-AS1 25 are weakly expressed in OS and restrain malignant cancer cell phenotypes.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA ASB16-AS1 Functions as a miR-760 Sponge to Facilitate the Malignant Phenotype of Osteosarcoma by Increasing HDGF Expression</p>

Yin

Liu

Zhao

et al. 2020

OTT

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Purpose: ASB16 antisense RNA 1 (ASB16-AS1) is a cancer-associated long non-coding RNA that contributes to tumorigenesis and tumor development. Nevertheless, to the best of our knowledge, whether and how ASB16-AS1 is implicated in osteosarcoma (OS) malignancy remains unclear and therefore warrants exploration. Our current study focused on making in-depth investigation of ASB16-AS1 in OS. In the present study, the expression pattern of ASB16-AS1 in OS tissues and cell lines was analyzed. In addition, we examined the clinical value of ASB16-AS1 for OS patients. Furthermore, we explored the impacts of ASB16-AS1 on the malignant phenotype of OS cells in vitro and in vivo as well as the underlying mechanism. Methods: ASB16-AS1, microRNA-760 (miR-760) and hepatoma-derived growth factor (HDGF) expressions were measured using reverse transcription-quantitative PCR. Cell proliferation and apoptosis were evaluated using CCK-8 and flow cytometry analyses, respectively, and cell migration and invasion were determined via cell migration and invasion assays. Results: ASB16-AS1 expression was significantly elevated in OS tissues and cell lines, and increased ASB16-AS1 expression was related to patients' tumor size, TNM stage, and distant metastasis. The overall survival rate of OS patients presenting high ASB16-AS1 expression was shorter than that of patients presenting low ASB16-AS1 expression. Reduced ASB16-AS1 expression inhibited OS cell proliferation, migration, and invasion; promoted cell apoptosis; and impaired tumor growth in vivo. Mechanistically, ASB16-AS1 served as a sponge for miR-760 and positively modulated the expression of its target HDGF. Finally, inhibiting miR-760 and restoring HDGF expression abolished the impacts of ASB16-AS1 knockdown on the malignant characteristics of OS cells. Conclusion: ASB16-AS1 is a novel oncogenic lncRNA in OS cells. ASB16-AS1 increased HDGF expression by sponging miR-760, thereby conferring cancer-promoting roles in OS. ASB16-AS1 is a potential early diagnostic and therapeutic target in OS.

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“…Similarly, lncRNA TTN-AS1 facilitates MBTD1 expression by binding miR-134-5p, thereby regulating cell growth and apoptosis in OS (24). Zhang et al (25) suggested that lncRNA DLX6-AS1/miR-129-5p/DLK1 axis deteriorate stemness of OS. In considering the role of lncRNA/miRNA/mRNA axis in phenotypes of OS, we therefore further explore roles of NORAD/miR-26a-5p/NAMPT axis in proliferation and apoptosis of OS cells.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA NORAD/MiR-26a-5p/NAMPT (Visfatin) Axis Regulates Proliferation and Apoptosis of Human Osteosarcoma Cells

Gong

Huang

Cao

et al. 2020

Preprint

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Background: Visfatin is a novel adipokine, also known as a nicotinamide phosphorybosyltransferase (NAMPT) that is reported to promote the progression of osteosarcoma. The research sought to determine the regulatory network underlying NAMPT on osteosarcoma (OS).Method: The OS tissues and paired normal controls were collected from 45 OS patients. The binding relationship between microRNA-26a-5p (miR-26a-5p) and two genes (NAMPT and NORAD) were predicted by TargetScan V7.2 and confirmed by dual-luciferase reporter assay. To reveal the function of long noncoding RNA NORAD/miR-26a-5p/NAMPT axis on cell viability, cell cycle and apoptosis of U2OS cells, CCK-8 and flow cytometry assays, examination of apoptosis-associated molecules (Bcl-2, Bax, cleaved (C)-caspase-3) were performed. The mRNA and protein levels were separately examined by RT-qPCR and Western blot. Results: NAMPT and NORAD expressions were increased in OS tissue samples, while miR-26a-5p expression was decreased. Functionally, NORAD functions as a ceRNA of miR-136-5p to competitively target NAMPT. Furthermore, miR-26a-5p overexpression inhibited viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating NAMPT along with change the expressions of apoptosis-related molecules. NORAD overexpression promoted viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating MiR-26a-5p along with changes of the expressions of apoptosis-related molecules.Conclusion: LncRNA NORAD, serving as a ceRNA of miR-26a-5p, promoted proliferation and apoptosis resistance of U2OS cells by upregulation of NAMPT.

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LncRNA DLX6-AS1/miR-129-5p/DLK1 axis aggravates stemness of osteosarcoma through Wnt signaling

Cited by 60 publications

References 20 publications

ceRNA Network Development and Tumour-infiltrating Immune Cell Analysis in Metastatic Breast Cancer of Bone

ceRNA Network Development and Tumour-infiltrating Immune Cell Analysis in Metastatic Breast Cancer of Bone

<p>Long Non-Coding RNA ASB16-AS1 Functions as a miR-760 Sponge to Facilitate the Malignant Phenotype of Osteosarcoma by Increasing HDGF Expression</p>

Long Noncoding RNA NORAD/MiR-26a-5p/NAMPT (Visfatin) Axis Regulates Proliferation and Apoptosis of Human Osteosarcoma Cells

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