FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment

Zhong, Zhaoming; Zhang, Hongxing; Hong, Mei; Sun, Chuanzheng; Xu, Yuanyuan; Chen, Xiao; Gao, Change; He, Minjie; Liu, Weiqing

doi:10.3892/or.2018.6231

Cited by 23 publications

(30 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

“…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 . In addition, Fan et al found that there was a binding site for miR‐143 in the 3′‐UTR region of FNDC3B , which was involved in the regulation of prostate cancer metastasis 29 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

Yang

et al. 2020

Cancer Science

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…FNDC3B is mainly composed of fibronectin III (FNIII) domain [27], which has been widely reported to be upregulated in cancer as a oncogene [28], such as hepatocellular carcinoma [27], oral tongue squamous cell carcinoma [29] and gastric cancer [30]. This may be due to that the domain of FNIII was involved in cell adhesion [31,32], which can promote cell proliferation and migration, especially in the development of tumor [33].…”

Section: Discussionmentioning

confidence: 99%

MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B

Wang

Zhang

et al. 2020

Open Medicine

View full text Add to dashboard Cite

This study attempted to research the molecular mechanism underlying the inhibitory role of miR-1225-5p in the malignant progression of glioblastoma. Bioinformatics analyses based on the gene expression omnibus (GEO) and Chinese glioma genome atlas (CGGA) databases showed that miR-1225-5p, as a favorable prognostic factor, was expressed at low levels in glioblastoma, and its expression was also related to WHO grade and age. The subsequent CCK-8 assay indicated that miR-1225-5p might prevent the malignant progression of glioblastoma, which was represented by that miR-1225-5p mimic reduced the viability of glioblastoma cells. Then, we predicted that FNDC3B might be a potential target gene of miR-1225-5p, and it was negatively correlated with the level of miR-1225-5p, which were confirmed by dual-luciferase reporter assay, qRT-PCR and western blot assays. Moreover, based on the analyses of the cancer genome atlas (TCGA), Oncomine and CGGA databases, FNDC3B was enriched in glioblastoma and high expression of FNDC3B led to poor prognosis. Finally, CCK8 and transwell experiments showed that the ability of miR-1225-5p to inhibit glioblastoma cell viability, invasion and migration was at least partially achieved by targeting FNDC3B. In general, these results revealed that the miR-1225-5p/FNDC3B axis contributes to inhibiting the malignant phenotype of glioblastoma cells, which lays a foundation for molecular diagnosis and treatment of glioblastoma.

show abstract

“…Fibronectin type III domain containing 3B (FNDC3B, also FAD104), a member of FNDC3 family, was previously identified as a modulator of osteoblast and adipocyte differentiation. 5,6 The fibronectin type III domain is a main structural component of FNDC3B, along with the transmembrane region and proline-rich region. 7 As the fibronectin type III domain has the ability to combine with various proteins, FNDC3B plays an important role in multiple cell processes, including cell adhesion, proliferation and growth signaling.…”

Section: Introductionmentioning

confidence: 99%

<p>FNDC3B, Targeted by miR-125a-5p and miR-217, Promotes the Proliferation and Invasion of Colorectal Cancer Cells via PI3K/mTOR Signaling</p>

Yang

Wang

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Fibronectin type III domain containing 3B (FNDC3B) acts as an oncogene in various cancers, and abnormal expression of FNDC3B has been found in colorectal cancer (CRC). Our study aimed to illustrate the role of FNDC3B in CRC development. Methods: Through RT-qPCR and western blotting assays, the mRNA and protein expressions of target genes were measured. CCK-8 and MTT methods were used to detect cell proliferation. Invasion ability was determined using Transwell assay. TargetScan platform and luciferase reporter gene assay were performed to predict and validate the bindings between FNDC3B and miR-125a-5p or miR-217. Besides, the expression correlation was measured by Pearson's Correlation analysis. Results: We found that FNDC3B was significantly upregulated in CRC tissues and tumor cell lines, and high expression of FNDC3B predicted a poor survival outcome. The bindings between FNDC3B and miR-125a-5p and miR-217 were respectively at the motifs of CUCAGGG and AUGCAGU. MiR-125a-5p and miR-217 were downregulated in CRC tissues, and both were negatively correlated with FNDC3B expression. Subsequently, the downregulated miR-125a-5p and miR-217 were confirmed as contributors FNDC3B upregulation in CRC. A loss-of-function assay demonstrated that FNDC3B knockdown inhibited the proliferation of CRC cells, while FNDC3B overexpression promoted the proliferation and invasion of tumor cells. Besides, we validated that PI3K/mTOR signaling was involved in the regulation of FNDC3B on the proliferation and invasion of CRC cells. Conclusion: Generally, our findings demonstrated that FNDC3B facilitated cell proliferation and invasion via PI3K/mTOR signaling, and further promoted CRC progression. The novel miR-125a-5p/FNDC3B and miR-217/FNDC3B axes might be new targets for CRC prognosis and therapy.

show abstract

FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment

Cited by 23 publications

References 26 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

MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B

<p>FNDC3B, Targeted by miR-125a-5p and miR-217, Promotes the Proliferation and Invasion of Colorectal Cancer Cells via PI3K/mTOR Signaling</p>

Contact Info

Product

Resources

About