Dauricine upregulates the chemosensitivity of hepatocellular carcinoma cells: Role of repressing glycolysis via miR-199a:HK2/PKM2 modulation

Li, Wei; Qiu, Yunhan; Jiang, Hao; Zhao, Chi; Deng, Xukun; Gao, Shu

doi:10.1016/j.fct.2018.08.030

Cited by 33 publications

(28 citation statements)

References 44 publications

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“…It has been reported that inhibiting the expression or activity of key glycolytic enzymes can effectively inhibit tumor cell proliferation and even kill tumor cells. Such enzymes include lactate dehydrogenase (LDHA), hexokinase 2 (HK2), phosphofructokinase (PFK) and M2 type acetone kinase (PKM2) (6,7). Given the increasing incidence of this cancer and its lack of effective therapeutic targets, there is an urgent requirement to identify the potential mechanisms by which clear cell RCC (ccRCC) behavior is regulated.…”

Section: Introductionmentioning

confidence: 99%

Aryl hydrocarbon receptor nuclear translocator promotes the proliferation and invasion of clear cell renal cell carcinoma cells potentially by affecting the glycolytic pathway

et al. 2020

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Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that has been reported to play a vital role in regulating glycolysis, angiogenesis and apoptosis. Recently, ARNT has been reported to a play role in pancreatic-islet function in type 2 diabetes. However, the role of ARNT in kidney cancer has not yet been investigated. In the present study, ARNT expression was detected in tissues from patients with renal cell carcinoma (RCC) and in RCC cell lines. Oncomine, The Cancer Genome Atlas and cBioPortal were used to investigate the roles of ARNT in RCC. Cell migration and invasion assays were used to explore the molecular mechanisms involved. It was found that ARNT protein expression was elevated both in tissues from patients with clear cell RCC (ccRCC) and in different RCC cell lines. ARNT disruption using siRNA knockdown inhibited the migratory abilities and cell proliferation, potentially by altering the glycolysis pathway in vitro, as evidenced by decreased M2 type acetone kinase, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 and hexokinase 2 expression. Taken together, the findings in the present study revealed a novel function of ARNT in ccRCC and indicated that ARNT promotes the proliferation and invasion of ccRCC, possibly through changes to the glycolytic pathway.

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Section: Introductionmentioning

confidence: 99%

Aryl hydrocarbon receptor nuclear translocator promotes the proliferation and invasion of clear cell renal cell carcinoma cells potentially by affecting the glycolytic pathway

et al. 2020

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“…In c-Myc-driven HCC, glucose catabolism through glycolysis is elevated via the activation of pyruvate kinase (33). Inhibition of glycolysis and increase in oxidative phosphorylation can re-sensitize HCC cells to chemotherapeutics such as sorafenib, cisplatin, and isoliensinine (34). HIF1α activates the transcription of genes encoding angiogenic cytokines, for example, VEGF, and glycolytic enzymes, such as hexokinase 1, hexokinase 2, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase.…”

Section: Cellular Metabolismmentioning

confidence: 99%

“…Moreover, natural products can also increase the sensitivity of HCC cells to anticancer drugs by regulating cellular metabolism. Li and colleagues demonstrated that dauricine dose-dependently suppressed glucose glycolysis and increased oxidative phosphorylation by downregulating the expression of hexokinase 2 and pyruvate kinase M2, consequently increasing the sensitivities of HCC to cisplatin, sorafenib, and isoliensinie (34).…”

Section: Natural Productsmentioning

confidence: 99%

Multidrug Resistance in Hepatocellular Carcinoma

Duan

Huang

Bai

et al. 2019

Hepatocellular Carcinoma

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Although there has been tremendous progress in the treatment of hepatocellular carcinoma over the past decades, multidrug resistance to chemotherapy and targeted therapy remains a major hindrance in its successful management. Multidrug resistance, whether intrinsic or extrinsic, is a multifactorial process that includes enhanced drug efflux, decreased drug uptake, intracellular sequestration, metabolic alterations, aberrant apoptotic and autophagic signaling, changes in tumor microenvironment, and acquisition of stem cell-like properties by the cancer cells. Although many experimental strategies have been developed to overcome drug resistance, translation of the knowledge to the clinic has not been crowned with success. This chapter provides an overview of the role of multidrug resistance in hepatocellular carcinoma and the potential approaches to overcome this obstacle.

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“…One possibility is that the thyroid hormone induces miR-214 to suppress Bim expression through negatively regulating the transcription factor Forkhead box protein O1 (FoxO1) to avoid liver cell apoptosis and ROS-induced stress [110]. In addition to miR-214, there are many miRNAs that have the potential to affect the apoptosis of liver cancer cells, such as miR-155, miR-4417, miR-199a, and miR-122 [59,77,115,116]. Among them, the expression levels of miR-199a and miR-122 are associated with thyroid hormone and oxidative stress (Table 2 and Table 3) [27].…”

Section: Effect Of Thyroid Hormone On the Role Of Oxidative Stressmentioning

confidence: 99%

Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

Huang

Wang

Yeh

et al. 2019

IJMS

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Oxidative stress occurs as a result of imbalance between the generation of reactive oxygen species (ROS) and antioxidant genes in cells, causing damage to lipids, proteins, and DNA. Accumulating damage of cellular components can trigger various diseases, including metabolic syndrome and cancer. Over the past few years, the physiological significance of microRNAs (miRNA) in cancer has been a focus of comprehensive research. In view of the extensive level of miRNA interference in biological processes, the roles of miRNAs in oxidative stress and their relevance in physiological processes have recently become a subject of interest. In-depth research is underway to specifically address the direct or indirect relationships of oxidative stress-induced miRNAs in liver cancer and the potential involvement of the thyroid hormone in these processes. While studies on thyroid hormone in liver cancer are abundantly documented, no conclusive information on the potential relationships among thyroid hormone, specific miRNAs, and oxidative stress in liver cancer is available. In this review, we discuss the effects of thyroid hormone on oxidative stress-related miRNAs that potentially have a positive or negative impact on liver cancer. Additionally, supporting evidence from clinical and animal experiments is provided.

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Dauricine upregulates the chemosensitivity of hepatocellular carcinoma cells: Role of repressing glycolysis via miR-199a:HK2/PKM2 modulation

Cited by 33 publications

References 44 publications

Aryl hydrocarbon receptor nuclear translocator promotes the proliferation and invasion of clear cell renal cell carcinoma cells potentially by affecting the glycolytic pathway

Aryl hydrocarbon receptor nuclear translocator promotes the proliferation and invasion of clear cell renal cell carcinoma cells potentially by affecting the glycolytic pathway

Multidrug Resistance in Hepatocellular Carcinoma

Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

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