Functional Variant in 3′UTR of <i>FAM13A</i> Is Potentially Associated with Susceptibility and Survival of Lung Squamous Carcinoma

Yu, Yuhui; Mao, Liping; Lü, Xiao; Yuan, Wei; Chen, Yujia; Jiang, Liying; Ding, Li; Sang, Lingli; Xu, Zhengcheng; Tian, Tian; Wu, Shuangshuang; Zhuang, Xun; Chu, Minjie

doi:10.1089/dna.2019.4892

Cited by 15 publications

(11 citation statements)

References 39 publications

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“…26 The hypoxia signaling pathway is known to regulate multiple steps of tumorigenesis and keys oncogenes, such as FAM13A played a key role in lung cancer under hypoxia. [27][28][29] Gastric cancer was also reported to display hypoxia, which could be a potential therapeutic target. 30 Previous studies indicated that the cross-talk between Wnt/b-catenin and hypoxia signaling pathway, but the mechanism has not well documented due to the complexity of the network between Wnt/b-catenin and hypoxia signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia Activates SOX5/Wnt/β-Catenin Signaling by Suppressing MiR-338-3p in Gastric Cancer

Zheng

Que

et al. 2020

Technol Cancer Res Treat

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MicroRNAs are known to be important in a variety of cancer types. The specific expression and roles of miR-338-3p in the context of gastric cancer, however, remains largely unknown. In this study, we found that miR-338-3p was expressed significantly lower in established/primary human gastric cancer cells than that in human gastric epithelial cells; miR-338-3p is also decreased in human gastric cancer tissues and was positively associated with the worse prognosis of patients with gastric cancer. Enforced expression of miR-338-3p could inhibit cell growth, survival, and proliferation, while inducing cell apoptosis. In addition, miR-338-3p negatively regulated SOX5 expression through directly binding to the 3′-untranslated region of SOX5, and an inverse correlation was found between miR-338-3p and SOX5 messenger RNA expression in gastric cancer tissues. Furthermore, miR-338-3p-induced inactivation of Wnt/β-catenin signaling was greatly abrogated by SOX5 upregulation. Finally, we found that hypoxic conditions were linked with reduced miR-338-3p expression in the context of gastric cancer. In conclusion, miR-338-3p acts as a tumor suppressor in gastric cancer, possibly by directly targeting SOX5 and blocking Wnt/β-catenin signaling. These findings might provide novel therapeutic targets for gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Hypoxia Activates SOX5/Wnt/β-Catenin Signaling by Suppressing MiR-338-3p in Gastric Cancer

Zheng

Que

et al. 2020

Technol Cancer Res Treat

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“…The first is that we found that ESR2 was also upregulated by miR22-5p, but it was not through the regulation of promoter region methylation of ESR2; hence, the regulatory mechanisms are needed to be further studied. In addition, some studies have revealed the functions of miR22-5p in other diseases [32,33]. However, this study only focused on that miR22-5p dysregulates directly the expression of TET2 in the eutopic endometrium of endometriosis without the exploration of specific functions of miR22-5p.…”

Section: Plos Onementioning

confidence: 99%

MicroRNA22-5p targets ten-eleven translocation and regulates estrogen receptor 2 expression in infertile women with minimal/mild endometriosis during implantation window

et al. 2020

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Based on microRNA (miR) microarray analysis, we previously found that miR22-5p expression is decreased in the mid-luteal endometrium of women with minimal/mild endometriosis. Bioinformatics analysis predicted that miR22-5p targets ten-eleven translocation (TET2) 3 0-untranslated region. This study aimed to determine the regulation and roles of miR22-5p in the pathogenesis of minimal/mild endometriosis-associated infertility. MiR22-5p and TET2 expression in the mid-luteal endometrium from women with or without minimal/mild endometriosis was analyzed. After transfection with miR22-5p mimics or inhibitor, TET2 expression was analyzed by quantitative reverse transcription (RT-q) PCR, western blotting and immunohistochemistry. 5-Hydroxymethylcytosine was determined by immunofluorescence and dot blotting. Expression and promoter methylation of estrogen receptor 2 (ESR2) was measured by RT-qPCR and western blotting, and by bisulfite sequencing, respectively. We first established that miR22-5p expression decreased and TET2 expression increased in minimal/mild endometriosis during implantation window. TET2 was found to be a direct target of miR22-5p. MiR22-5p regulated the expression of ESR2, but did not directly affect methylation of its promoter region (-197/+359). Our results suggest that an imbalance in miR22-5p expression in the midluteal endometrium may be involved in minimal/mild endometriosis-associated infertility.

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“…Meanwhile, FAM13A is a susceptibility gene for lung cancer [ 52 ]. Its rs9224 site can change the susceptibility of squamous cell carcinoma by affecting the binding of miRNA-22-5p [ 53 ]. Our in vitro results showed that TGF-β1 stimulation upregulated FAM13A expression in BEAS-2B cells in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Family with sequence similarity 13 member A mediates TGF-β1-induced EMT in small airway epithelium of patients with chronic obstructive pulmonary disease

et al. 2021

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Background To explore the role of family with sequence similarity 13 member A (FAM13A) in TGF-β1-induced EMT in the small airway epithelium of patients with chronic obstructive pulmonary disease (COPD). Methods Small airway wall thickness and protein levels of airway remodeling markers, EMT markers, TGF-β1, and FAM13A were measured in lung tissue samples from COPD and non-COPD patients. The correlations of FAM13A expression with COPD severity and EMT marker expression were evaluated. Gain- and loss-of-function assays were performed to explore the functions of FAM13A in cell proliferation, motility, and TGF-β1-induced EMT marker alterations in human bronchial epithelial cell line BEAS-2B. Results Independent of smoking status, lung tissue samples from COPD patients exhibited significantly increased small airway thickness and collagen fiber deposition, along with enhanced protein levels of remodeling markers (collagen I, fibronectin, and MMP-9), mesenchymal markers (α-SMA, vimentin, and N-cadherin), TGF-β1, and FAM13A, compared with those from non-COPD patients. FAM13A expression negatively correlated with FEV1% and PO2 in COPD patients. In small airway epithelium, FAM13A expression negatively correlated with E-cadherin protein levels and positively correlated with vimentin protein levels. In BEAS-2B cells, TGF-β1 dose-dependently upregulated FAM13A protein levels. FAM13A overexpression significantly promoted cell proliferation and motility in BEAS-2B cells, whereas FAM13A silencing showed contrasting results. Furthermore, FAM13A knockdown partially reversed TGF-β1-induced EMT marker protein alterations in BEAS-2B cells. Conclusions FAM13A upregulation is associated with TGF-β1-induced EMT in the small airway epithelium of COPD patients independent of smoking status, serving as a potential therapeutic target for anti-EMT therapy in COPD.

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Functional Variant in 3′UTR of FAM13A Is Potentially Associated with Susceptibility and Survival of Lung Squamous Carcinoma

Cited by 15 publications

References 39 publications

Hypoxia Activates SOX5/Wnt/β-Catenin Signaling by Suppressing MiR-338-3p in Gastric Cancer

Hypoxia Activates SOX5/Wnt/β-Catenin Signaling by Suppressing MiR-338-3p in Gastric Cancer

MicroRNA22-5p targets ten-eleven translocation and regulates estrogen receptor 2 expression in infertile women with minimal/mild endometriosis during implantation window

Family with sequence similarity 13 member A mediates TGF-β1-induced EMT in small airway epithelium of patients with chronic obstructive pulmonary disease

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