MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3

Tan, Pei-Yi; Wen, Li; Li, Hua-Nan; Chai, Shiwei

doi:10.1007/s10616-020-00418-3

Cited by 20 publications

(17 citation statements)

References 36 publications

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“…Transfection of HepG2 cells was conducted using lipofectamine 2000 transfection reagent (Thermo Fisher Scientific, USA), and HepG2 cells were cultured in 6-well plates for 48 h and collected for subsequent analyses. 28 …”

Section: Methodsmentioning

confidence: 99%

miR-140-5p Aggravates Insulin Resistance via Directly Targeting GYS1 and PPP1CC in Insulin-Resistant HepG2 Cells

Yan

Wang

et al. 2021

DMSO

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Background Much attention has been paid to the regulatory role of microRNA (miRNA) in insulin resistance. Nevertheless, how miR-140-5p regulates insulin resistance remains unclear. In this research, we aim to investigate the roles of miR-140-5p in insulin resistance. Methods qRT-PCR is used to analyze the expression level of miR-140-5p in insulin-resistant HepG2 cells. Glucose consumption and glucose uptake are detected to study the effect of miR-140-5p knockdown in insulin-resistant HepG2 cells and miR-140-5p overexpression in HepG2 cells. Bioinformatic analysis, luciferase reporter assay and confirmatory experiments are applied to identify the target gene bound with miR-140-5p and study the effect of miR-140-5p on the downstream substrates of target genes. Rescue experiments have verified the roles of miR-140-5p and target gene in glucose metabolism. Results The expression level of miR-140-5p was upregulated in insulin-resistant HepG2 cells and was significantly correlated with cellular glucose metabolism. Functionally, miR-140-5p overexpression induced impairment of glucose consumption and glucose uptake. Besides, bioinformatics analysis indicated that glycogen synthetase (GYS1) and protein phosphatase 1 catalytic subunit gamma (PPP1CC) were the target genes of miR-140-5p. Western blotting and qRT-PCR results revealed a negative correlation between GYS1, PPP1CC and miR-140-5p. The glycogen detection results showed that miR140-5p inhibited the production of the downstream substrates of the target gene. Rescue experiments showed that inhibition of GYS1 or PPP1CC partially enhanced the insulin-resistant effects of miR-140-5p knockdown in insulin-resistant HepG2 cells. Conclusion miR-140-5p overexpression augments the development of insulin resistance and miR-140-5p may be served as a therapeutic target of metabolic diseases.

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Section: Methodsmentioning

confidence: 99%

miR-140-5p Aggravates Insulin Resistance via Directly Targeting GYS1 and PPP1CC in Insulin-Resistant HepG2 Cells

Yan

Wang

et al. 2021

DMSO

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“…MiR-340-5p expression is reduced in BC, and miR-340-5p overexpression represses the aggressiveness of BC cells by targeting SOX4 [ 14 ]. Besides, it is reported that E2F transcription factor 3 (E2F3) expression is elevated in BC, and E2F3 overexpression facilitates BC cell proliferation and metastasis [ 15 ]. In this study, bioinformatics analysis showed that miR-340-5p could target the 3’UTR of E2F3.…”

Section: Introductionmentioning

confidence: 99%

Long intergenic non-protein coding RNA 1094 (LINC01094) promotes the progression of breast cancer (BC) by regulating the microRNA-340-5p (miR-340-5p)/E2F transcription factor 3 (E2F3) axis

Chen

2021

Bioengineered

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The present study was targeted at investigating the effects of long intergenic non-protein coding RNA 1094 on breast cancer (BC) cell proliferation, apoptosis, and cell cycle and its related mechanism. In this study, Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to detect the expressions of LINC01094, microRNA (miRNA, miR)-340-5p, and E2F transcription factor 3 (E2F3) in BC tissues and cells. With transfection, LINC01094 and miR-340-5p expressions were selectively up-regulated or down-regulated in BC cell lines, and then cell proliferation, cell cycle, and apoptosis were examined by cell counting kit-8 (CCK-8), 5-bromo-2'-deoxyuridine (BrdU), and flow cytometry assays. Bioinformatics was utilized to predict the targeted relationships between miR-340-5p and LINC01094, as well as miR-340-5p and E2F3 mRNA 3'-untranslated region (3'UTR), and RNA immunoprecipitation (RIP) assay and dual-luciferase reporter gene assay were employed to validate them. It was revealed that, LINC01094 expression was enhanced in BC cells and tissues, and LINC01094 overexpression promoted BC cell proliferation, accelerated cell cycle progression, and inhibited apoptosis while knocking down LINC01094 worked oppositely. LINC01094 directly targeted miR-340-5p and negatively regulated its expression in BC cells. Besides, E2F3 was substantiated to be the target gene of miR-340-5p, and E2F3 expression could be indirectly and positively modulated by LINC01094. All in all, LINC01094 promotes BC cell proliferation and cell cycle progression and inhibits apoptosis via modulating miR-340-5p/E2F3 molecular axis.

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“…Overexpression of miR-34a and miR-214 was also found to inhibit the proliferation of hepatoma cells by downregulating the expression of E2F3 [16]. Generally, E2F1/E2F3, as an important node molecule of cell signaling network, participate in the transcriptional regulation of many important genes through dialogue with other signaling pathways, including NF-κB, and are tumor therapy targets [17,18].…”

Section: Discussionmentioning

confidence: 99%

Valeric acid acts as a novel HDAC3 inhibitor against prostate cancer

Han

Yang

et al. 2022

Med Oncol

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Prostate cancer is the second cause of cancer-related deaths in men worldwide, and new agents for curing the disease are still needed. In this study, we theoretically and experimentally demonstrated that valeric acid (VA) was a HDAC inhibitor, and anti-cancer efficacy of VA in prostate cancer cells was also observed using either 2D or 3D culture systems. VA was cytotoxic for prostate cancer cells but low toxic to normal cells. VA significantly inhibited E2F1/E2F3 expression but increased CASP3 activity. In vivo mouse models further showed its anti-cancer activity and potential property of chemosensitizer with promoting apoptosis. The findings suggest that VA acts as a HDAC3 inhibitor with anti-cancer effect on prostate cancer by regulating E2F1/E2F3/CASP3 axis.

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MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3

Cited by 20 publications

References 36 publications

miR-140-5p Aggravates Insulin Resistance via Directly Targeting GYS1 and PPP1CC in Insulin-Resistant HepG2 Cells

miR-140-5p Aggravates Insulin Resistance via Directly Targeting GYS1 and PPP1CC in Insulin-Resistant HepG2 Cells

Long intergenic non-protein coding RNA 1094 (LINC01094) promotes the progression of breast cancer (BC) by regulating the microRNA-340-5p (miR-340-5p)/E2F transcription factor 3 (E2F3) axis

Valeric acid acts as a novel HDAC3 inhibitor against prostate cancer

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