MiR-646 inhibited cell proliferation and EMT-induced metastasis by targeting FOXK1 in gastric cancer

Zhang, P; Tang, Weimei; Zhang, H; Li, Y Q; Peng, Ying; Wang, J; Liu, G N; Huang, Xiaoting; Zhao, Jian; Li, G; Li, A M; Bai, Yang; Chen, Y; Ren, Yue-Xin; Li, G X; Wang, Y D; liu, shiwei; Wang, J D

doi:10.1038/bjc.2017.181

Cited by 83 publications

(83 citation statements)

References 40 publications

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“…Ectopic expression of FOXK1 markedly enhances cell proliferation, migration, and invasion in gastrointestinal cancer cells [15,26]. We recently demonstrated that FOXK1 induces EMT progression and predicts poor prognosis in human gastric cancer [15,34]. The Snail super family of zinc-finger transcription factors is involved in processes that cause pronounced cell movements, both during embryonic development and in the acquisition of invasive and migratory properties during tumor progression [16][17][18].…”

Section: Discussionmentioning

confidence: 99%

Snail/FOXK1/Cyr61 Signaling Axis Regulates the Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer

Huang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Metastasis is the primary cause of colorectal cancer (CRC)-related death. However, the molecular mechanisms underlying metastasis in CRC remain unclear. Methods: We evaluated mRNA and protein expression levels by quantitative real-time reverse transcription PCR, western blotting, immunofluorescence, tissue microarrays, and immunohistochemistry assays. We also assessed the migration and invasion abilities of CRC cells in vitro by wound healing assays, invasion and migration assays, western blot analysis, and immunofluorescence. Tumor metastasis was evaluated in nude mice in vivo. Results: A positive correlation was observed between the expression patterns of Forkhead box k1 (FOXK1) and Snail in CRC. Luciferase reporter and chromatin immunoprecipitation assays demonstrated that Snail directly bound to and activated the human FOXK1 gene promoter. Moreover, the Snail-FOXK1 axis promote epithelial mesenchymal transition (EMT)-mediated CRC cell invasion and metastasis. FOXK1 and Snail expression levels were correlated with tumor progression and served as significant predictors of overall survival in patients with CRC. Furthermore, overexpression of FOXK1 induced the EMT by upregulating the expression of cysteine-rich angiogenic inducer 61 (Cyr61). Luciferase assays showed that Cyr61 was a direct transcriptional target of FOXK1. Down regulation of Cyr61 decreased FOXK1-enhanced “CRC cell” migration, invasion, and metastasis. Additionally, FOXK1 expression was positively correlated with Cyr61 expression and was associated with poor prognosis. Conclusions: The Snail/FOXK1/Cyr61 signaling axis regulates the EMT and metastasis of CRC.

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Section: Discussionmentioning

confidence: 99%

Snail/FOXK1/Cyr61 Signaling Axis Regulates the Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer

Huang

et al. 2018

Cell Physiol Biochem

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“…29 During EMT process, the expression of several proteins is alteration, such as epithelial marker E-cadherin, mesenchymal markers N-cadherin and vimentin, EMT-associated transcription factors TWIST, Snail and Slug. 30 Multiple studies have demonstrated that FOXK1 acts as a critical mediator of EMT in certain tumors, such as gastric cancer, 31 colorectal cancer 32 and prostate cancer, 33 indicating that FOXK1 regulates the EMT process and may serve as the core protein during EMT in human cancers. MicroRNAs (miRNAs) are a class of 22-nucleotide noncoding RNAs encoded by endogenous genes.…”

Section: Discussionmentioning

confidence: 99%

<p>FOXK1, Regulated by miR-365-3p, Promotes Cell Growth and EMT Indicates Unfavorable Prognosis in Breast Cancer</p>

Gao¹,

Tian²

2020

OTT

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Background: Forkhead box K1 (FOXK1) is members of the FOX transcription factor family. Previous work has found out that FOXK1 promotes cell proliferation, migration and invasion in several cancers, such as gastric cancer, glioma cancer and lung cancer; however, the exact role of FOXK1 in breast cancer is still poorly known. Methods: Here, the association between FOXK1 expression and the clinicopathological characteristics of patients with breast cancer was identified. To further decipher the functional roles of FOXK1, it was overexpressed or knocked down in MCF-7, MDA-MB-231 and MCF-10A cells. Cell Counting Kit-8, colony formation and cell cycle assays were performed to examine the proliferation of breast cancer cells. Moreover, wound-healing and Transwell invasion analyses were carried out to explore the effect of FOXK1 on breast cancer cell migration and invasion. Results: Our findings discovered that FOXK1 promotes cell proliferation, migration and invasion in breast cancer. In addition, consistent with the previous report, FOXK1 also facilitates EMT in breast cancer. TargetScan was used to predict upstream of FOXK1, indicating that miR-365-3p could regulate FOXK1 expression in breast cancer. Conclusion: The findings of the present study demonstrated that miR-365-3p-FOXK1 axis plays a key role in breast cancer.

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“…In gastric cancer, several studies demonstrated that FOXK1 was a target for some certain miRNAs (e.g. MiR-646, miR-4492, miR-137) which could inhibit the gastric cancer progression by mediating the cell proliferation, migration and invasion [32][33][34] . Given that the gastric cancer progression was correlated with the expression levels of miR-498 and FOXK1, our study also demonstrated that the miRNA-498 targets on FOXK1 and negatively regulates its expression in the gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

miR-498 inhibits cell proliferation and metastasis by targeting FOXK1 in gastric cancer

Liu¹,

Huang²,

Wu³

et al. 2020

Preprint

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Objective: MiR-498 has emerged as a potential molecular target for several cancer. In this study, we aimed to investigate the important function and mechanisms of miR-498 in gastric cancer.Methods: To detect the important roles of miR-498 in gastric cancer, we first measured its expression by RT-qPCR in gastric cancer cell lines. The impact of the miR-498 on gastric cancer cell proliferation were detected by CCK-8 and colony formation assays. The effect of the miR-498 on the cell apoptosis and cell cycle were detected by flow cytometry. We also used the scratch and transwell chamber assays to measure the cell migration and invasion. The expression levels of related proteins were assessed by western blot. The bioinformatics analysis was used to explore the target gene of miR-498. RT-qPCR and western blot assays were used to detect the expression levels of FOXK1 in response to miR-498 overexpression. In order to prove the role of FOXK1 in mediating the effect of miR-498 on the gastric cancer, CCK-8, colony formation, transwell chamber and flow cytometry assays were used for the further investigations.Results: The expression level of miR-498 is downregulated in gastric cancer cell lines. Overexpression of miR-498 inhibited proliferation and migration/invasion, while promoted the apoptosis of gastric cancer cells. Bioinformatics analysis indicated that miR-498 targeted on FOXK1 to inhibit the gastric cancer in vitro.Conclusion: MiR-498/FOXK1 axis may be a potential therapeutic target for the treatment of gastric cancers.

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MiR-646 inhibited cell proliferation and EMT-induced metastasis by targeting FOXK1 in gastric cancer

Cited by 83 publications

References 40 publications

Snail/FOXK1/Cyr61 Signaling Axis Regulates the Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer

Snail/FOXK1/Cyr61 Signaling Axis Regulates the Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer

<p>FOXK1, Regulated by miR-365-3p, Promotes Cell Growth and EMT Indicates Unfavorable Prognosis in Breast Cancer</p>

miR-498 inhibits cell proliferation and metastasis by targeting FOXK1 in gastric cancer

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