Arsenic trioxide-induced upregulation of miR-1294 suppresses tumor growth in hepatocellular carcinoma by targeting TEAD1 and PIM1

Cai, Xiaoniao; Yu, Leilei; Chen, Zhe; Ye, Fangpeng; Ren, Zhigang; Jin, Peisheng

doi:10.3233/cbm-190490

Cited by 16 publications

(10 citation statements)

References 37 publications

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“…Notably, the upregulation of miR-1294 expression levels was demonstrated to inhibit the proliferation and promote the apoptosis of HCC cells (10). 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).…”

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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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: 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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“…The authors further found that As2O3 can induce differentiation of HCC cancer stem cells, inhibit recurrence and prolong survival after hepatectomy by targeting GLI1 expression ( 74 ). As2O3 can also inhibit the growth of hepatocellular carcinoma by up-regulating Mir-1294 expression ( 75 ). In addition, As2O3 inhibits MCM7 transcription by targeting serum reaction factor (SRF)/microchromosome maintenance protein 7 (MCM7) complex, thus inhibiting the function and metastasis of liver cancer stem cells ( 84 ).…”

Section: Treatment Statusmentioning

confidence: 99%

Hepatocellular Carcinoma Differentiation: Research Progress in Mechanism and Treatment

Song

Zhou

et al. 2022

Front. Oncol.

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Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. Although progress has been made in diagnosis and treatment, morbidity and mortality continue to rise. Chronic liver disease and liver cirrhosis are still the most important risk factors for liver cancer. Although there are many treatments, it can only be cured by orthotopic liver transplantation (OLT) or surgical resection. And the worse the degree of differentiation, the worse the prognosis of patients with liver cancer. Then it can be considered that restoring a better state of differentiation may improve the prognosis. The differentiation treatment of liver cancer is to reverse the dedifferentiation process of hepatocytes to liver cancer cells by means of drugs, improve the differentiation state of the tumor, and restore the normal liver characteristics, so as to improve the prognosis. Understanding the mechanism of dedifferentiation of liver cancer can provide ideas for drug design. Liver enrichment of transcription factors, imbalance of signal pathway and changes of tumor microenvironment can promote the occurrence and development of liver cancer, and restoring its normal level can inhibit the malignant behavior of tumor. At present, some drugs have been proved to be effective, but more clinical data are needed to support the effectiveness and reliability of drugs. The differentiation treatment of liver cancer is expected to become an important part of the treatment of liver cancer in the future.

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“…Li et al (86) reported that varying concentrations of As 2 O 3 significantly inhibited cell proliferation, activation of caspase-3 (mediator of cell death), and JNk activation (86) in hepatocellular carcinoma (HepG2) cells. Antiproliferative effects of As on hepatocellular carcinoma have been studied extensively over the years and reported in several papers (87)(88)(89). However, recent findings by Chen et al (90) suggest that hypoxic hepatocellular carcinoma cells develop resistance against As 2 O 3 due to upregulation of the transcription factor HIF-1α.…”

Section: Mechanism Of Genotoxicitymentioning

confidence: 99%

Metabolic and genetic derangement: a review of mechanisms involved in arsenic and lead toxicity and genotoxicity

Rodríguez-Seijo

2022

Archives of Industrial Hygiene and Toxicology

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Urbanisation and industrialisation are on the rise all over the world. Environmental contaminants such as potentially toxic elements (PTEs) are directly linked with both phenomena. Two PTEs that raise greatest concern are arsenic (As) and lead (Pb) as soil and drinking water contaminants, whether they are naturally occurring or the consequence of human activities. Both elements are potential carcinogens. This paper reviews the mechanisms by which As and Pb impair metabolic processes and cause genetic damage in humans. Despite efforts to ban or limit their use, due to high persistence both continue to pose a risk to human health, which justifies the need for further toxicological research.

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Arsenic trioxide-induced upregulation of miR-1294 suppresses tumor growth in hepatocellular carcinoma by targeting TEAD1 and PIM1

Cited by 16 publications

References 37 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

Hepatocellular Carcinoma Differentiation: Research Progress in Mechanism and Treatment

Metabolic and genetic derangement: a review of mechanisms involved in arsenic and lead toxicity and genotoxicity

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