Pigment epithelium-derived factor inhibits lung cancer migration and invasion by upregulating exosomal thrombospondin 1

Huang, Wen-Cheng; Chong, Inn Wen; Chen, Hsiu-Lin; Li, Chia-Yang; Hsieh, Chong Chao; Kuo, Hsuan Fu; Chang, Chia Yuan; Chen, Yung‐Hsiang; Liu, Yu Peng; Lu, Cheng-Hsien; Liu, Yu Ru; Liu, Po Len

doi:10.1016/j.canlet.2018.10.031

Cited by 54 publications

(48 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The back regulator and signaling involved need to be further identified through high-throughput sequencing. PEDF was widely considered as a tumor suppressor in solid tumors as it exhibits antiangiogenic and antimetastatic activities ( Baxter-Holland and Dass, 2018 ; Nardi et al, 2018 ; Ansari et al, 2019 ; Honrubia-Gomez et al, 2019 ; Huang et al, 2019 ). Its role in hematologic malignancies such as leukemia, lymphoma, and multiple myeloma remains unclear.…”

Section: Discussionmentioning

confidence: 99%

The m6A Methyltransferase METTL3 Is Functionally Implicated in DLBCL Development by Regulating m6A Modification in PEDF

Cheng

Wang

et al. 2020

Front. Genet.

View full text Add to dashboard Cite

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of lymphoma, whose treatment still has a major challenge of achieving a satisfactory curative effect. The underlying mechanisms also have not been fully illustrated. N 6-Methyladenosine (m6A) has been identified as the most prevalent internal modification of mRNAs present in eukaryotes, which is involved in the pathogenesis of cancers. It remains unclear how m6A mRNA methylation is functionally linked to the pathogenesis of DLBCL. In this study, we sought to explore the roles of METTL3 on DLBCL development. The results showed that m6A level for RNA methylation and the expression level of METTL3 were upregulated in DLBCL tissues and cell lines. Functionally, downregulated METTL3 expression in DLBCL cells inhibited the cell proliferation ability. Further mechanism analysis indicated that METTL3 knockdown abates the m6A methylation and total mRNA level of pigment epithelium-derived factor (PEDF). However, Wnt/β-catenin signaling was not thus activated. Overexpressed PEDF abrogates the inhibition of cell proliferation in DLBCL cells that is caused by METTL3 silence. In summary, the abovementioned results demonstrated that the METTL3 promotes DLBCL progression by regulating the m6A level of PEDF.

show abstract

Section: Discussionmentioning

confidence: 99%

The m6A Methyltransferase METTL3 Is Functionally Implicated in DLBCL Development by Regulating m6A Modification in PEDF

Cheng

Wang

et al. 2020

Front. Genet.

View full text Add to dashboard Cite

show abstract

“…Recent studies have shown that exosomes play an important role in the metastasis of lung cancer cells (5)(6)(7)(8). Characterized by inflammation, angiogenesis, immunosuppression, and organotropism, pre-metastatic niche is used to spread tumor cells (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Exosome-Derived LncRNAs in Lung Cancer

Fan

Sun

2020

Front. Oncol.

View full text Add to dashboard Cite

As extracellular vesicles, exosomes are released from most cells to perform cell-cell communication. Recent studies have shown that exosomes could be released into tumor microenvironment and blood to promote tumor progression through packaging and transmitting various bioactive molecules, such as cholesterol, proteins, lipids, miRNAs, mRNAs, and long non-coding RNAs (lncRNAs) to distant cells. LncRNAs have emerged as a major class of non-coding transcripts. A lot of LncRNAs have been discovered during the past few years of research on genomics. They have been proven to participate in various biological functions and disease processes through multiple mechanisms. In this review, we analyzed the role of exosome-derived lncRNAs in lung carcinogenesis and metastasis. We also highlight opportunities for the clinical potential of exosomes with specific lncRNAs as biomarkers and therapeutic intervention in lung cancer.

show abstract

“…28 A recent analysis identified THBS1 release in LUAC cell-derived exosomes, which are involved in NSCLC cell migration; cloud-based computing was used as a source of biomarkers. 29,30 GO analysis revealed that these genes are high correlated with elements of the cell division process, such as cell adhesion, extracellular matrix organization, and the positive regulation of transforming growth factor beta1 production.…”

Section: Discussionmentioning

confidence: 99%

<p>FTO Facilitates Lung Adenocarcinoma Cell Progression by Activating Cell Migration Through mRNA Demethylation</p>

Ding¹,

Qi²,

Wang³

et al. 2020

OTT

View full text Add to dashboard Cite

These authors contributed equally to this workBackground: The fat mass and obesity-associated protein (FTO) was identified as a critical demethylase involved in regulating cellular mRNA stability by removing N6methyladenosine (m6A) residues from mRNA. Emerging evidence has revealed that FTO is deeply implicated in lung cancer. However, knowledge of the function of FTO in lung adenocarcinoma (LUAC) is limited. Methods: FTO and FTO R96Q (R96Q), an FTO missense mutant lacking demethylase activity, were ectopically overexpressed, and FTO was knocked down via siRNA in A549 and H1299 cells. The relationships between FTO with cell characteristics and mRNA m6A levels were explored. Furthermore, RNA sequencing was performed on A549 cells. Results: FTO overexpression enhanced the proliferation, migration, and invasion ability of A549 and H1299 cells, decreased mRNA m6A levels. Interestingly, overexpression of R96Q, blunted the effects of FTO overexpression on cell proliferation and invasion. Through RNA sequencing analysis of A549 cells overexpressing FTO or R96Q and control A594 cells, 45 genes were identified as affected by m6A mRNA demethylation. Most of these genes were related to lung cancer, such as laminin γ2, thrombospondin 1, nerve growth factor inducible, integrin alpha11, and proprotein convertase subtilisin/kexin type 9. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses suggested that these genes are fundamental to cancer development processes, such as cell migration and extracellular matrix organization. Conclusion: Our research shows that FTO facilitates LUAC cell progression by activating cell migration through m6A demethylation; however, further research on the mechanism underlying FTO activity in LUAC is necessary.

show abstract

Pigment epithelium-derived factor inhibits lung cancer migration and invasion by upregulating exosomal thrombospondin 1

Cited by 54 publications

References 39 publications

The m6A Methyltransferase METTL3 Is Functionally Implicated in DLBCL Development by Regulating m6A Modification in PEDF

The m6A Methyltransferase METTL3 Is Functionally Implicated in DLBCL Development by Regulating m6A Modification in PEDF

Exosome-Derived LncRNAs in Lung Cancer

<p>FTO Facilitates Lung Adenocarcinoma Cell Progression by Activating Cell Migration Through mRNA Demethylation</p>

Contact Info

Product

Resources

About