Overexpression of fibronectin type�III domain containing�3B is correlated with epithelial‑mesenchymal transition and predicts poor prognosis in lung adenocarcinoma

Bian, Tingting; Zheng, Liangfeng; Jiang, Daishan; Liu, Jian; Zhang, Jianguo; Feng, Jia; Zhang, Qing; Li, Qian; Qiu, Hongmei; Liu, Yifei; Yao, Sumei

doi:10.3892/etm.2019.7370

Cited by 21 publications

(27 citation statements)

References 33 publications

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“…FNDC3B , also known as FAD104 (factor for adipocyte differentiation 104), is located at 3q26, and is amplified in more than 20% of human tumors 24,25 . Recently, FNDC3B was found to serve as an oncogene and it can promote tumorigenesis and metastasis in various cancer types 24‐28 . FNDC3B can promote cell migration and metastasis by cooperating with annexin A2 (ANXA2) in hepatocellular carcinoma 26 .…”

Section: Discussionmentioning

confidence: 99%

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FNDC3B 3′‐UTR shortening escapes from microRNA‐mediated gene repression and promotes nasopharyngeal carcinoma progression

Yang

et al. 2020

Cancer Science

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Alternative polyadenylation (APA), which induces shortening of the 3′‐UTR, is emerging as an important feature in cancer development and progression. Nevertheless, the effects and mechanisms of APA‐induced 3′‐UTR shortening in nasopharyngeal carcinoma (NPC) remain largely unclear. Fibronectin type III domain containing 3B (FNDC3B) tended to use proximal polyadenylation site and produce shorter 3′‐UTR according to our previous sequencing study. Herein, we found that FNDC3B with shorter 3′‐UTR could escape from miRNA‐mediated gene repression, and caused its increased expression in NPC. Knocking down of FNDC3B inhibited NPC cell proliferation, migration, invasion, and metastasis in vitro and in vivo. Overexpression of FNDC3B, especially those with shorter 3′‐UTR, promoted NPC progression. Furthermore, the mechanism study revealed that FNDC3B could bind to and stabilize myosin heavy chain 9 (MYH9) to activate the Wnt/β‐catenin signaling pathway. In addition, MYH9 could reverse the inhibitory effects of FNDC3B knockdown in NPC. Altogether, our results suggested that the 3′‐UTR shortening of FNDC3B mRNA mediated its overexpression in NPC and promoted NPC progression by targeting MYH9. This newly identified FNDC3B‐MYH9‐Wnt/β‐catenin axis could represent potential targets for individualized treatment in NPC.

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Section: Discussionmentioning

confidence: 99%

“…FNDC3B can promote cell migration and metastasis by cooperating with annexin A2 (ANXA2) in hepatocellular carcinoma 26 . FNDC3B is correlated with poor survival and can promote epithelial‐mesenchymal transition in lung adenocarcinoma 27 . FNDC3B can promote migration and invasion in tongue squamous cell carcinoma 28 .…”

Section: Discussionmentioning

confidence: 99%

FNDC3B 3′‐UTR shortening escapes from microRNA‐mediated gene repression and promotes nasopharyngeal carcinoma progression

Yang

et al. 2020

Cancer Science

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“…Consistent with its oncogenic role in multiple cancer types, the overexpression of FNDC3B could malignantly transform mammary and kidney epithelial cells and hepatocytes [ 28 ]. FNDC3B may trigger either apoptotic or survival signals by the recruitment of different sets of molecules [ 29 ]. Overexpression of FNDC3B in HCC cell lines enhanced cell migration and invasion, knockdown of FNDC3B using shRNA reduced tumor nodule formation in intra- and extra-hepatic metastasis [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia–reperfusion injury by regulating FNDC3B/TGF-β1

Zhou

et al. 2020

Renal Failure

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Renal ischemia-reperfusion injury is a leading cause of acute kidney injury, but its underlying mechanism remains poorly understood and effective therapies are still lacking. Here, we identified lncRNA XLOC_032768 as a novel target in renal ischemia-reperfusion injury by analyzing differentially expressed genes of the transcriptome data. PCR results show that XLOC_032768 was markedly downregulated in the kidney during renal ischemia-reperfusion in mice and in cultured kidney cells during hypoxia. Upon induction in vitro, XLOC_032768 overexpression repressed the expression of fibronectin type III domain containing 3B (FNDC3B) and tubular epithelial cells apoptosis. Administration of XLOC_032768 preserved FNDC3B expression and attenuated renal tubular epithelial cells apoptosis, resulting in protection against kidney injury in mice. Knockdown of FNDC3B markedly reduced the expression of TGF-b1 and apoptosis of renal tubular cells. Thus, XLOC_032768/FNDC3B/TGF-b1signaling pathway in ischemia-reperfusion injury may be targeted for therapy.

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“…The expression constructs were confirmed by DNA sequencing. The transfection process was as described before (10).…”

Section: Construction Of Plasmids and Transfectionmentioning

confidence: 99%

Molecular and Immune Characteristics for Lung Adenocarcinoma Patients With ERLIN2 Overexpression

et al. 2020

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BackgroundEndoplasmic reticulum lipid raft-associated protein 2 (ERLIN2) is protein contained in the membrane of the endoplasmic reticulum. In lung adenocarcinoma (LUAD), the molecular function of ERLIN2 and the correlation between ERLIN2 and tumor-infiltrating immune cells have been unclear. The aim of our study was to determine the role of ERLIN2 in LUAD development to provide a better understanding of the molecular pathogenesis of this disease and identify new therapeutic targets for its treatment.MethodsImmunohistochemistry, Western blotting, and real-time quantitative polymerase chain reaction were used to detect protein and mRNA levels of ERLIN2 in LUAD and adjacent normal tissues. Using the A549, H1299 cell line, ERLIN2-short hairpin RNA was applied to silence ERLIN2 to determine its role in LUAD cell proliferation and invasion. Based on mRNA expression of ERLIN2 from the Cancer Genome Atlas (TCGA) database, we identified ERLIN2-related protein-coding genes and analyzed the Kyoto Encyclopedia of Genes and Genomes pathway to explore its potential biological functions and determined the correlation between ERLIN2 and tumor-infiltrating immune cells.ResultsERLIN2 was abnormally expressed in a variety of tumor tissues and is highly expressed in LUAD. This overexpression was associated with histological grade (P = 0.044), TNM stage (P = 0.01), and lymph node metastasis (P = 0.038). Patient overall survival was poorer with ERLIN2 overexpression. Downregulation of ERLIN2 inhibited LUAD cell proliferation and invasion in vitro. Based on mRNA expression of ERLIN2 from the TCGA database, 13 ERLIN2-related genes and 10 pathways were identified and showed a correlation between ERLIN2 and naive B cells and neutrophils.ConclusionERLIN2 could serve as a potential diagnostic and prognostic biomarker for LUAD and has demonstrated to be correlated with immune infiltrates, which suggests that it may represent a new therapeutic target for LUAD.

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Overexpression of fibronectin type�III domain containing�3B is correlated with epithelial‑mesenchymal transition and predicts poor prognosis in lung adenocarcinoma

Cited by 21 publications

References 33 publications

FNDC3B 3′‐UTR shortening escapes from microRNA‐mediated gene repression and promotes nasopharyngeal carcinoma progression

FNDC3B 3′‐UTR shortening escapes from microRNA‐mediated gene repression and promotes nasopharyngeal carcinoma progression

Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia–reperfusion injury by regulating FNDC3B/TGF-β1

Molecular and Immune Characteristics for Lung Adenocarcinoma Patients With ERLIN2 Overexpression

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