miR-1294 alleviates epithelial–mesenchymal transition by repressing FOXK1 in gastric cancer

Wang, Yaru; Sun, Shijuan; Qin, Junjie

doi:10.1007/s13258-019-00899-3

Cited by 18 publications

(19 citation statements)

References 39 publications

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“…Previous studies reported that miR-1294 expression levels were downregulated in gastric, esophageal, epithelial ovarian and cervical cancers, while miR-1294 overexpression inhibited the cell proliferation and cell cycle progression of cancer cells (13,(30)(31)(32). The results of the current study revealed that the expression levels of miR-1294 and miR-186-5p were downregulated in HCC cells.…”

Section: Discussionmentioning

confidence: 99%

“…miR-186-5p expression levels were reported to be downregulated in HCC tissues and cells, which promoted the tumorigenesis and metastasis of HCC, while the overexpression of miR-186-5p suppressed the viability and increased the apoptosis and autophagy of the cancer cells (11,12). In addition, multiple previous studies have suggested that both miR-1294 and miR-186-5p could regulate the expression levels of forkhead box K1 (FOXK1) (13,14). FOXK1 expression levels were discovered to be upregulated in liver cancer cells, which regulated glycolysis and subsequently affected the viability of liver cancer cells (15).…”

Section: Introductionmentioning

confidence: 99%

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circ-PRKCI targets miR-1294 and miR-186-5p by downregulating FOXK1 expression to suppress glycolysis in hepatocellular carcinoma

Chen

Zhong

et al. 2021

Mol Med Rep

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Numerous human circular RNAs (circRNAs/circ) have been functionally characterized. However, the potential role of circ-protein kinase C iota (PRKCI) in hepatocellular carcinoma (HCC) remains unknown. The effects of each transfection and expression levels of circ-PRKCI, microRNA (miR)-1294, miR-186-5p and forkhead box K1 (FOXK1) in HCC cells were analyzed using reverse transcription-quantitative PCR analysis. The interactions between circ-PRKCI and miR-1294 or miR-186-5p, and miR-1294 or miR-186-5p and FOXK1 were validated using dual luciferase reporter assays. The viability, invasion and migration of HCC cells were determined using Cell Counting Kit-8, Transwell and wound healing assays, respectively. The expression levels of FOXK1, hexokinase-2 (HK2), glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA) in HCC cells were analyzed using western blotting. The levels of glucose and lactic acid in the cultured supernatant were detected using commercially available kits. The results of the present study revealed that miR-1294 and miR-186-5p expression levels were downregulated in the HCC cell line, HCCLM3, and were subsequently downregulated by circ-PRKCI overexpression and upregulated by the knockdown of circ-PRKCI. circ-PRKCI overexpression promoted the viability, invasion and migration of HCCLM3 cells, which was also reversed by the overexpression of miR-1294 and miR-186-5p. In addition, the overexpression of circ-PRKCI upregulated FOXK1 expression levels, while the overexpression of miR-1294 and miR-186-5p downregulated FOXK1 expression levels. Conversely, the knockdown of circ-PRKCI expression downregulated FOXK1 expression levels, while the knockdown of miR-1294 and miR-186-5p upregulated FOXK1 expression levels. Furthermore, circ-PRKCI was identified to target miR-1294 and miR-186-5p, and miR-1294 and miR-186-5p were subsequently found to target FOXK1. The overexpression of circ-PRKCI also increased glucose and lactic acid levels, while the knockdown of FOXK1 decreased glucose and lactic acid levels. The knockdown of circ-PRKCI decreased glucose and lactic acid levels, which were reversed by FOXK1 overexpression. In conclusion, the findings of the present study suggested that circ-PRKCI may promote the viability, invasion and migration of HCC cells by sponging miR-1294 and miR-186-5p to upregulate FOXK1 expression levels.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

circ-PRKCI targets miR-1294 and miR-186-5p by downregulating FOXK1 expression to suppress glycolysis in hepatocellular carcinoma

Chen

Zhong

et al. 2021

Mol Med Rep

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“…For instance, AWPPH played an accelerative role in the progression of non-small cell lung cancer by the upregulation of CDK6 via sponging miR-204 [31] while PVT1 facilitated colorectal cancer cell proliferation and invasion by sequestering miR-214-3p to affect the IRS1 level [21]. Previous studies have suggested that microRNA-1294 (miR-1294) was down-regulated in GC and inhibited the epithelial-mesenchymal transition process via targeting FOXK1 [22,30]. Serine/threonine kinase 1 (AKT1) belongs to the AKT family and has crucial modulation in multiple cancers [6,11].…”

Section: Introductionmentioning

confidence: 99%

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

Wang

et al. 2020

Open Medicine

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Long non-coding RNAs (lncRNAs) were reported to promote the development of gastric cancer (GC). Nuclear-enriched abundant transcript 1 (NEAT1) played a great role in diverse cancers, but the mechanism of NEAT1 in GC remains indistinct. NEAT1 and AKT1 were distinctly up-regulated and miR-1294 was down-regulated in GC tissues and cells. Cell proliferation and metastasis were refrained but apoptosis was promoted in GC cells after knockdown of NEAT1. NEAT1 negatively regulated miR-1294 expression, and the miR-1294 inhibitor reverted the si-NEAT1-induced effect on GC cells. NEAT1 modulated AKT1 expression through miR-1294, and the si-NEAT1-induced effect was relieved by AKT1. NEAT1 affected phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway via regulating miR-1294 and AKT1. NEAT1 could modulate cell proliferation, apoptosis, and metastasis in GC cells by regulating the PI3K/AKT/mTOR signaling pathway via the miR-1294/AKT1 axis, showing the great potential for NEAT1 as a valid biomarker in the progression and treatment of GC.

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“…High expression of FOXK1 is identified in various human cancers and may be deeply involved in tumor oncogenicity, such as gastric [ 24 ], pancreatic [ 26 ], colorectal [ 27 ] cancers, and osteosarcoma [ 25 ]. In line with the previous results, an increased expression of FOXK1 was determined in OC tissues in this study, which suggested that FOXK1 is an oncogene in OC.…”

Section: Discussionmentioning

confidence: 99%

“…Forkhead box k1 (FOXK1), a transcription factor in tumorigenesis, is reported to serve as an oncogene regulated by miRNAs to promote tumor progression in various human cancers, such as gastric cancer [ 24 ], osteosarcoma [ 25 ], pancreatic cancer [ 26 ], and colorectal cancer [ 27 ]. In addition, through enhancement FOXK1 expression, Aurora-A/SOX8 axis promotes the chemosensitivity and inhibits cell senesence in OC [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

Repression of lncRNA PART1 attenuates ovarian cancer cell viability, migration and invasion through the miR-503-5p/FOXK1 axis

Li¹,

Lou²,

Zhang³

et al. 2022

BMC Cancer

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Background Ovarian cancer (OC) is a female malignant tumor with a high fatality rate. Long non-coding RNAs (lncRNAs) are deeply involved in OC progression. The aim of this study is to explore the specific mechanism of lncRNA prostate androgen-regulated transcript 1 (PART1) in OC. Methods Quantitative real time PCR was utilized to determine the expression levels of PART1, microRNA (miR)-503-5p and forkhead-box k1 (FOXK1) in OC tissues and/or cells. The cell viability, migration, and invasion in OC were evaluated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-h-tetrazolium bromide assay, wound healing assay and transwell invasion assay, respectively. Flow cytometry was used to analyze the cell apoptosis. The xenograft tumor was conducted in nude mice to verify the effect of PART1 knockdown on OC in vivo. The target relationships among PART1, miR-503-5p and FOXK1 were predicted by StarBase, and verified by luciferase reporter assay. The level of FOXK1 was assessed by western blot. Results Increased expression of PART1 and FOXK1 was observed in OC tissues or cells, whereas miR-503-5p was downregulated. PART1 silencing or miR-503-5p overexpression repressed the cell viability, migration and invasion, and protomed apoptosis. Meanwhile, miR-503-5p was a target of PART1, and FOXK1 was a direct target gene of miR-503-5p. Both downregulation of miR-503-5p and upregulation of FOXK1 partly relieved the suppressive effects of PART1 knockdown on the oncogenicity of OC in vitro. Conclusion Decreased PART1 represses the cell viability, migration and invasion of OC via regulating the miR-503-5p/FOXK1 axis, which provided an underlying target for treating OC.

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miR-1294 alleviates epithelial–mesenchymal transition by repressing FOXK1 in gastric cancer

Cited by 18 publications

References 39 publications

circ-PRKCI targets miR-1294 and miR-186-5p by downregulating FOXK1 expression to suppress glycolysis in hepatocellular carcinoma

circ-PRKCI targets miR-1294 and miR-186-5p by downregulating FOXK1 expression to suppress glycolysis in hepatocellular carcinoma

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

Repression of lncRNA PART1 attenuates ovarian cancer cell viability, migration and invasion through the miR-503-5p/FOXK1 axis

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