MicroRNA‑34a inhibits liver cancer cell growth by reprogramming glucose metabolism

Zhang, Haifeng; Wang, Yi‐Cheng; Han, Yidi

doi:10.3892/mmr.2018.8399

Cited by 32 publications

(32 citation statements)

References 45 publications

(56 reference statements)

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“…Previous studies have suggested that miR-34a expression is lost or downregulated in numerous types of cancer, including HCC (28,29). miR-34a inhibits HCC glycolysis by targeting lactate dehydrogenase A, leading to reduced cell proliferation and invasion (28). However, aside from glucose metabolism, the role of miR-34a during HCC has not been previously reported.…”

Section: Discussionmentioning

confidence: 99%

“…The present study indicated that miR-34a was negatively regulated by SNHG7 in liver cancer. Previous studies have suggested that miR-34a expression is lost or downregulated in numerous types of cancer, including HCC (28,29). miR-34a inhibits HCC glycolysis by targeting lactate dehydrogenase A, leading to reduced cell proliferation and invasion (28).…”

Section: Discussionmentioning

confidence: 99%

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Long non‑coding RNA SNHG7 inhibits NLRP3‑dependent pyroptosis by targeting the miR‑34a/SIRT1 axis in liver cancer

Chen

et al. 2020

Oncol Lett

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Long non-coding RNA small nucleolar RNA host gene 7 (SNHG7) is involved in a variety of different types of cancer; however, the role of SNHG7 during liver cancer progression is not completely understood. The aim of the present study was to investigate the functional role and regulatory mechanism underlying SNHG7 during liver cancer. A total of 25 paired hepatocellular carcinoma (HCC) tumor tissues and adjacent normal tissues were collected. Reverse transcription-quantitative PCR and western blotting were performed to detect the expression levels of SNHG7, microRNA (miR)-34a, sirtuin 1 (SIRT1) and pyroptosis-related targets. RNA fluorescence in situ hybridization was performed to detect the expression of SNHG7 in HCC tissues. SNHG7 expression was upregulated in HCC tissues and liver cancer cells compared with normal tissues and normal liver cell lines. High expression of SNHG7 inhibited NLR family pyrin domain containing 3 (NLRP3)-dependent pyroptosis in HepG2 and SK-hep-1 cells. Bioinformatics analysis and dual-luciferase reporter assays were performed to investigate the interactions between miR-34a and SNHG7 or SIRT1. SNHG7 served as a competing endogenous RNA of miR-34a, and SIRT1 was identified as a direct target of miR-34a. Cell pyroptosis was evaluated by TUNEL and lactate dehydrogenase release assays. SNHG7 knockdown reduced SIRT1 expression, but increased the expression levels of NLRP3, caspase-1 and interleukin-1β, leading to pyroptosis. SNHG7 knockdown-induced effects were enhanced by miR-34a upregulation. In summary, the present study indicated that the SNHG7/miR-34a/SIRT1 axis contributed to NLRP3-dependent pyroptosis during liver cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA SNHG7 inhibits NLRP3‑dependent pyroptosis by targeting the miR‑34a/SIRT1 axis in liver cancer

Chen

et al. 2020

Oncol Lett

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“…High expression of glycolysis-related genes, such as glucose transporter 1 (GLUT1), have been found in several carcinoma tissues [8,9]. Intriguingly, recent research has identified a potential strategy for the treatment of cancer by lowering the metabolic pathway of glucose [10,11].…”

mentioning

confidence: 99%

Kallikrein-related peptidase (KLK10) cessation blunts colorectal cancer cell growth and glucose metabolism by regulating the PI3K/Akt/mTOR pathway

Wei

Dong

Shen

2020

neo

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Colorectal cancer (CRC) is a common aggressive carcinoma with a proverbial feature of metabolic reprogramming that is essential for cancer cell growth. Recent research corroborates the controversial function of kallikrein-related peptidase 10 (KLK10) in cancer. However, its role and underlying mechanism in CRC remains elusive. In the present study, high expression of KLK10 was detected in CRC cell lines. Knockdown of KLK10 expression by a specific siRNA inhibited cell proliferation, evoked cell apoptosis, and increased caspase-3 activity in HT29 CRC cells. Furthermore, KLK10 suppression also afforded the suppressive effects on glycolysis in CRC cells as the data showed that targeting KLK10 restrained glucose uptake, lactate production, and glycolysis-related glucose transporter 1 (Glut1) expression. Mechanism analysis corroborated that cessation of KLK10 muted the PI3K/AKT-mTOR signaling. Intriguingly, reactivating the PI3K/AKT-mTOR pathway by its agonist IGF-1 notably reversed the inhibitory effects of KLK10 cessation on CRC cell growth and glucose metabolism. More important, preconditioning with PI3K/AKT inhibitor LY294002 or mTOR inhibitor rapamycin both aggravated KLK10 knockdown-suppressed cancer cell growth and glucose metabolism. These findings suggest that KLK10 silencing may attenuate the progression of CRC by inhibiting cell growth and glycolysis via the PI3K/AKT/mTOR signaling, supporting a potential and promising target for CRC therapy.

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“…LDH is a key factor for HCC tumor proliferation and invasion. Analysis of HCC patients’ serum samples suggested the use of serum LDH as a prognostic factor [ 30 , 31 , 32 , 33 , 34 , 35 ]. High levels of MCT4 and CD147, a transmembrane glycoprotein able to induce matrix metalloprotease (MMP) production and to interact with MCT4 for lactate secretion, were detected in HCC tissues [ 36 , 37 , 38 , 39 ].…”

Section: Hcc and Glucose Metabolismmentioning

confidence: 99%

Glucose Metabolism and Oxidative Stress in Hepatocellular Carcinoma: Role and Possible Implications in Novel Therapeutic Strategies

Mossenta

Busato

et al. 2020

Cancers

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Hepatocellular carcinoma (HCC) metabolism is redirected to glycolysis to enhance the production of metabolic compounds employed by cancer cells to produce proteins, lipids, and nucleotides in order to maintain a high proliferative rate. This mechanism drives towards uncontrolled growth and causes a further increase in reactive oxygen species (ROS), which could lead to cell death. HCC overcomes the problem generated by ROS increase by increasing the antioxidant machinery, in which key mechanisms involve glutathione, nuclear factor erythroid 2-related factor 2 (Nrf2), and hypoxia-inducible transcription factor (HIF-1α). These mechanisms could represent optimal targets for innovative therapies. The tumor microenvironment (TME) exerts a key role in HCC pathogenesis and progression. Various metabolic machineries modulate the activity of immune cells in the TME. The deregulated metabolic activity of tumor cells could impair antitumor response. Lactic acid–lactate, derived from the anaerobic glycolytic rate of tumor cells, as well as adenosine, derived from the catabolism of ATP, have an immunosuppressive activity. Metabolic reprogramming of the TME via targeted therapies could enhance the treatment efficacy of anti-cancer immunotherapy. This review describes the metabolic pathways mainly involved in the HCC pathogenesis and progression. The potential targets for HCC treatment involved in these pathways are also discussed.

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MicroRNA‑34a inhibits liver cancer cell growth by reprogramming glucose metabolism

Cited by 32 publications

References 45 publications

Long non‑coding RNA SNHG7 inhibits NLRP3‑dependent pyroptosis by targeting the miR‑34a/SIRT1 axis in liver cancer

Long non‑coding RNA SNHG7 inhibits NLRP3‑dependent pyroptosis by targeting the miR‑34a/SIRT1 axis in liver cancer

Kallikrein-related peptidase (KLK10) cessation blunts colorectal cancer cell growth and glucose metabolism by regulating the PI3K/Akt/mTOR pathway

Glucose Metabolism and Oxidative Stress in Hepatocellular Carcinoma: Role and Possible Implications in Novel Therapeutic Strategies

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