&lt;p&gt;Protein kinase C-iota-mediated glycolysis promotes non-small-cell lung cancer progression&lt;/p&gt;

Liu, Liu; Liu, Bei; Wang, Lihua; Chang, Cheng; Yang, Hao; Li, Jianjun; Huang, Gang; Xie, Wenhui

doi:10.2147/ott.s207211

Cited by 19 publications

(15 citation statements)

References 51 publications

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“…It was investigated that glycolysis was regulated by the long non-coding RNA HOTTIP/ miR-615-3p/HMGB3 axis to impact tumor cell behaviors in non-small cell lung carcinoma (45). Another study revealed that glycolysis metabolism could be controlled by protein kinase C-iota, due to the progression of non-small-cell lung carcinoma (46). PCK1 is another gene that participates in cell glycolysis metabolism.…”

Section: Discussionmentioning

confidence: 99%

High PD‑L1 expression drives glycolysis via an Akt/mTOR/HIF‑1α axis in acute myeloid leukemia

Xing

Han

et al. 2020

Oncol Rep

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Acute myeloid leukemia (AML) is a hematological malignancy derived from immature myeloid cells, which have the characteristics of abnormal proliferation and differentiation. Glycolysis has been a popular topic of research in recent years, with increasing uptake and consumption of glucose. The present study aimed to investigate the glycolysis of tumor cells in patients with AML; in particular, how programmed cell death 1 ligand 1 (PD-L1) regulates tumor cells glycolysis using real time PCR (RT-PCR), western blotting and flow cytometry. PD-L1 high expression predicted poor outcome in patients with AML in the public database Gene Expression Profiling Interactive Analysis. PD-L1 expression was decreased in the samples from patients with AML with complete remission compared to that in patients with relapsed or refractory AML. In AML cell lines, glycolysis-associated genes ALDOA, PGK1, LDHA and HK2 were highly expressed in a PD-L1 high-expressed cell line. Overexpressed PD-L1 enhanced glucose consumption and the extracellular acidification rate, accompanied by decreased apoptosis and accumulation of cells in the S phase. In contrast, the apoptosis rate of tumor cells and the percentage of cells in the S phase were significantly increased following PD-L1 knockdown in the THP1 cell line. HK2 and LDHA expression decreased after AML tumor cells were treated with Akt inhibitor or rapamycin. In addition, the PD-L1-overexpressed cell line (PD-L1-OV) MOLM-13 exhibited rapid tumor progression. Glycolysis-associated genes were highly expressed in tumor tissues of PD-L1-OV MOLM-13, with increased Ki67. Based on these findings, PD-L1 may be considered as a suitable marker for prognosis and treatment in the clinical setting.

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Section: Discussionmentioning

confidence: 99%

High PD‑L1 expression drives glycolysis via an Akt/mTOR/HIF‑1α axis in acute myeloid leukemia

Xing

Han

et al. 2020

Oncol Rep

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“…Besides, β-AR activation depressed endothelial oxidative phosphorylation and turned on the angiogenic switch for tumor progression in a rodent prostate cancer model (Zahalka et al, 2017). Additionally, the activations of PKC and PKA can lead to unfavorable metabolic alterations and fuel cancer progression (Aggarwal et al, 2019;Liu et al, 2019;Vergara et al, 2020).…”

Section: Metabolismmentioning

confidence: 99%

Chronic Stress: Impacts on Tumor Microenvironment and Implications for Anti-Cancer Treatments

Tian

Liu

Cao

et al. 2021

Front. Cell Dev. Biol.

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Chronic stress is common among cancer patients due to the psychological, operative, or pharmaceutical stressors at the time of diagnosis or during the treatment of cancers. The continuous activations of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS), as results of chronic stress, have been demonstrated to take part in several cancer-promoting processes, such as tumorigenesis, progression, metastasis, and multi-drug resistance, by altering the tumor microenvironment (TME). Stressed TME is generally characterized by the increased proportion of cancer-promoting cells and cytokines, the reduction and malfunction of immune-supportive cells and cytokines, augmented angiogenesis, enhanced epithelial-mesenchymal transition, and damaged extracellular matrix. For the negative effects that these alterations can cause in terms of the efficacies of anti-cancer treatments and prognosis of patients, supplementary pharmacological or psychotherapeutic strategies targeting HPA, SNS, or psychological stress may be effective in improving the prognosis of cancer patients. Here, we review the characteristics and mechanisms of TME alterations under chronic stress, their influences on anti-cancer therapies, and accessory interventions and therapies for stressed cancer patients.

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“…Glut1, HK2, and LDH-A proteins are key molecules in the glycolysis process of cancer cells, which can affect the glucose uptake and lactic acid production of cancer cells. 24 However, up-regulation of FOXO6 expression can significantly promote glycolysis in HCC cells. Some studies 25 suggested that FOXO6 produced a marked effect in the metabolism of cancer cells, which was validated in the present study.…”

Section: Discussionmentioning

confidence: 99%

<p>Knockdown of FOXO6 Inhibits Glycolysis and Reduces Cell Resistance to Paclitaxel in HCC Cells via PI3K/Akt Signaling Pathway</p>

Gao

Mao

et al. 2020

OTT

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Purpose: Previous studies have reported that FOXO6 is highly expressed in hepatocellular carcinoma (HCC) tissues and is associated with the prognosis of HCC patients. However, little research has been carried out to explore the role of FOXO6 in glycolysis of HCC cells and paclitaxel resistance. Today, along with the increasing incidence and mortality of HCC, chemotherapy resistance of HCC also poses a serious challenge. Therefore, this study was set out to investigate the effect of FOXO6 on glycolysis and cytotoxicity of paclitaxel in HCC cells and its potential mechanism. Patients and Methods: The levels of FOXO6 mRNA and protein were detected by qRT-PCR and Western blot, respectively. In addition, paclitaxel-resistant cell lines of HCC cells were established, whose activity was assessed by CCK-8 assay, among which the invasion ability was assessed by Transwell and the apoptosis rate by flow cytometry. What is more, glycolysis levels were evaluated by measuring glucose consumption and lactic acid production, and the protein levels of p-PI3K and p-protein kinase B (Akt) were determined by Western blot. Results: Compared with normal human hepatocytes, FOXO6 was highly expressed in HCC cells, which was of high real value for HCC. FOXO6 knockdown inhibited the proliferation and invasion and induced apoptosis of HCC cells. In addition, FOXO6 knockdown suppressed glycolysis, reversed resistance to chemotherapy in Hep3B/PTX cells and inactivated PI3K and Akt proteins, thus inhibiting the PI3K/Akt signaling pathway. Furthermore, it was found that when activated by 740Y-P, PI3K/Akt signaling pathway could resist the effects of FOXO6 knockdown on the cytotoxicity and glycolysis of paclitaxel in HCC cells. Vice versa, inhibition of PI3K/Akt pathway by LY294002 could resist the effect of FOXO6 overexpression on chemotherapy, cytotoxicity and glycolysis of HCC cells. Conclusion: FOXO6 knockdown can inhibit glycolysis of HCC cells and reduce their resistance to chemotherapy by inhibiting the PI3K/Akt signaling pathway, which may be a new target for the treatment of HCC.

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<p>Protein kinase C-iota-mediated glycolysis promotes non-small-cell lung cancer progression</p>

Cited by 19 publications

References 51 publications

High PD‑L1 expression drives glycolysis via an Akt/mTOR/HIF‑1α axis in acute myeloid leukemia

High PD‑L1 expression drives glycolysis via an Akt/mTOR/HIF‑1α axis in acute myeloid leukemia

Chronic Stress: Impacts on Tumor Microenvironment and Implications for Anti-Cancer Treatments

<p>Knockdown of FOXO6 Inhibits Glycolysis and Reduces Cell Resistance to Paclitaxel in HCC Cells via PI3K/Akt Signaling Pathway</p>

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