The miR-1185-2-3p—GOLPH3L pathway promotes glucose metabolism in breast cancer by stabilizing p53-induced SERPINE1

Xu, Youqin; Chen, Wancheng; Liang, Jing; Zeng, Xiaoqi; Ji, Kaiyuan; Zhou, Jianlong; Liao, Shijun; Wu, Jiexian; Xing, Kongyang; He, Zhiwei; Yang, Yang; Liu, Qianzhen; Zhu, Paikun; Liu, Yuchang; Li, Li; Liu, Minfeng; Huang, Wenhua

doi:10.1186/s13046-020-01767-9

Cited by 21 publications

(15 citation statements)

References 40 publications

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“…Real-time PCR analysis was performed using the StepOnePlus Real-Time PCR System (Applied Biosystems) with FastStart Universal SYBR Green Master (Roche) as previously reported (25). The primer sets used are as follows:…”

Section: Quantitative Pcr Analysismentioning

confidence: 99%

Inhibition of RFX6 Suppresses the Invasive Ability of Tumor Cells Through the Notch Pathway and Affects Tumor Immunity in Hepatocellular Carcinoma

Kuerban

Zhao

et al. 2021

Front. Oncol.

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BackgroundThe DNA-binding protein RFX6 was overexpressed in hepatocellular carcinoma, and its expression level was correlated with the prognosis and immune cell infiltration in liver hepatocellular carcinoma. However, the mechanism of the abnormal expression and the biological effects of RFX6 in liver cancer remains unknown.MethodsTo understand the specific expression mechanism of RFX6 in liver cancer, we performed bioinformatic prediction, CHIP-qPCR assay, co-IP, and dual-luciferase assay to assess the regulating mechanism of RFX6. In the meantime, a series of biological experiments in vivo and in vitro were conducted to analyze the biological significance of RFX6 in hepatocellular carcinoma.ResultsWe demonstrated that knockdown of RFX6 in liver cancer cells significantly suppressed the proliferation, migration, and invasion of cancer cells. Moreover, inhibition of RFX6 could affect the immune response of T cells. Among a number of interacting proteins, we revealed that RFX6 directly binds to DTX2, a regulator of the Notch signaling pathway by targeting NOTCH1, and helps in its transcription stability. Furthermore, we discovered that miRNA-542-3p, the expression of which was decreased in hepatocellular carcinoma, was directly involved in the negative regulation of the expression of RFX6.ConclusionIn summary, we discovered that the miRNA-542-3p–RFX6–DTX2–NOTCH1 regulatory pathway played significant roles in the tumor progression of liver hepatocellular carcinoma.

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Section: Quantitative Pcr Analysismentioning

confidence: 99%

Inhibition of RFX6 Suppresses the Invasive Ability of Tumor Cells Through the Notch Pathway and Affects Tumor Immunity in Hepatocellular Carcinoma

Kuerban

Zhao

et al. 2021

Front. Oncol.

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“…6 c). Coincidentally, published reports and the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway database indicated that Serpine1 could be regulated by p53 [ 32 ]. The mRNA and protein levels of Serpine1 in circ-GALNT16 knockdown and overexpressing cells revealed that Serpine1 could be antagonistically regulated by circ-GALNT16 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Circ-GALNT16 restrains colorectal cancer progression by enhancing the SUMOylation of hnRNPK

Peng

Tan

Yang

et al. 2021

J Exp Clin Cancer Res

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Background Recent studies have investigated the role of circular RNAs (circRNAs) as significant regulatory factors in multiple cancer progression. Nevertheless, the biological functions of circRNAs and the underlying mechanisms by which they regulate colorectal cancer (CRC) progression remain unclear. Methods A novel circRNA (circ-GALNT16) was identified by microarray and qRT-PCR. A series of in vitro and in vivo phenotype experiments were performed to investigate the role of circ-GALNT16 in CRC. The FISH, RNA pulldown assay, RIP assay, RNA sequencing, coimmunoprecipitation, and ChIP were performed to investigate the molecular mechanisms of circ-GALNT16 in CRC progression. Results Circ-GALNT16 was downregulated in CRC and was negatively correlated with poor prognosis. Circ-GALNT16 suppressed the proliferation and metastatic ability of CRC cells in vitro and in vivo. Mechanistically, circ-GALNT16 could bind to the KH3 domain of heterogeneous nuclear ribonucleoprotein K (hnRNPK), which promoted the SUMOylation of hnRNPK. Additionally, circ-GALNT16 could enhance the formation of the hnRNPK-p53 complex by facilitating the SUMOylation of hnRNPK. RNA sequencing assay identified serpin family E member 1 as the target gene of circ-GALNT16 at the transcriptional level. Rescue assays revealed that circ-GALNT16 regulated the expression of Serpine1 by inhibiting the deSUMOylation of hnRNPK mediated by SUMO-specific peptidase 2 and then regulating the sequence-specific DNA binding ability of the hnRNPK-p53 transcriptional complex. Conclusions Circ-GALNT16 suppressed CRC progression by inhibiting Serpine1 expression through regulating the sequence-specific DNA binding ability of the SENP2-mediated hnRNPK-p53 transcriptional complex and might function as a biomarker and therapeutic target for CRC.

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“…SERPINE1, encoding plasminogen activator inhibitor 1 (PAI-1), is an essential inhibitor of tissue plasminogen activator and urokinase (uPA). Previous studies have focused on the effect of SERPINE1 on human thrombosis, cardiac fibrosis, inflammatory injury, ageing and metabolism ( 53 – 57 ). However, current studies report on the importance of SERPINE1 in promoting tumor malignant progression, distant metastasis and chemotherapy resistance through multiple pathways.…”

Section: Discussionmentioning

confidence: 99%

BAP1-Related ceRNA (NEAT1/miR-10a-5p/SERPINE1) Promotes Proliferation and Migration of Kidney Cancer Cells

Liu

et al. 2022

Front. Oncol.

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BackgroundBAP1 is an important tumor suppressor involved in various biological processes and is commonly lost or inactivated in clear-cell renal cell carcinoma (ccRCC). However, the role of the BAP1-deficient tumor competing endogenous RNA (ceRNA) network involved in ccRCC remains unclear. Thus, this study aims to investigate the prognostic BAP1-related ceRNA in ccRCC.MethodsRaw data was obtained from the TCGA and the differentially expressed genes were screened to establish a BAP1-related ceRNA network. Subsequently, the role of the ceRNA axis was validated using phenotypic experiments. Dual-luciferase reporter assays and fluorescence in situ hybridization (FISH) assays were used to confirm the ceRNA network.ResultsNuclear enriched abundant transcript 1 (NEAT1) expression was significantly increased in kidney cancer cell lines. NEAT1 knockdown significantly inhibited cell proliferation and migration, which could be reversed by miR-10a-5p inhibitor. Dual-luciferase reporter assay confirmed miR-10a-5p as a common target of NEAT1 and Serine protease inhibitor family E member 1 (SERPINE1). FISH assays revealed the co-localization of NEAT1 and miR-10a-5p in the cytoplasm. Additionally, the methylation level of SERPINE1 in ccRCC was significantly lower than that in normal tissues. Furthermore, SERPINE1 expression was positively correlated with multiple immune cell infiltration levels.ConclusionsIn BAP1-deficient ccRCC, NEAT1 competitively binds to miR-10a-5p, indirectly upregulating SERPINE1 expression to promote kidney cancer cell proliferation. Furthermore, NEAT1/miR-10a-5p/SERPINE1 were found to be independent prognostic factors of ccRCC.

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The miR-1185-2-3p—GOLPH3L pathway promotes glucose metabolism in breast cancer by stabilizing p53-induced SERPINE1

Cited by 21 publications

References 40 publications

Inhibition of RFX6 Suppresses the Invasive Ability of Tumor Cells Through the Notch Pathway and Affects Tumor Immunity in Hepatocellular Carcinoma

Inhibition of RFX6 Suppresses the Invasive Ability of Tumor Cells Through the Notch Pathway and Affects Tumor Immunity in Hepatocellular Carcinoma

Circ-GALNT16 restrains colorectal cancer progression by enhancing the SUMOylation of hnRNPK

BAP1-Related ceRNA (NEAT1/miR-10a-5p/SERPINE1) Promotes Proliferation and Migration of Kidney Cancer Cells

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