Study of Tumor Growth under Hyperthermia Condition

Zhu, Qing; Zhang, Aili; Liu, Ping; Xu, Lisa X.

doi:10.1155/2012/198145

Cited by 6 publications

(5 citation statements)

References 45 publications

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“…The number of cancer cells is directly linked to the metabolism, where the growth rate depends on the intracellular concentrations of three primary metabolites known to influence cell proliferation: glucose, glutamine and ATP (Venkatasubramanian et al, 2008 ; Zhu et al, 2012 ). The dependence on these three metabolites is modeled assuming Monod-type functions (Higuera et al, 2009 ) (Equation 2).…”

Section: Methodsmentioning

confidence: 99%

Computational Model Predicts the Effects of Targeting Cellular Metabolism in Pancreatic Cancer

Roy

Finley

2017

Front. Physiol.

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Reprogramming of energy metabolism is a hallmark of cancer that enables the cancer cells to meet the increased energetic requirements due to uncontrolled proliferation. One prominent example is pancreatic ductal adenocarcinoma, an aggressive form of cancer with an overall 5-year survival rate of 5%. The reprogramming mechanism in pancreatic cancer involves deregulated uptake of glucose and glutamine and other opportunistic modes of satisfying energetic demands in a hypoxic and nutrient-poor environment. In the current study, we apply systems biology approaches to enable a better understanding of the dynamics of the distinct metabolic alterations in KRAS-mediated pancreatic cancer, with the goal of impeding early cell proliferation by identifying the optimal metabolic enzymes to target. We have constructed a kinetic model of metabolism represented as a set of ordinary differential equations that describe time evolution of the metabolite concentrations in glycolysis, glutaminolysis, tricarboxylic acid cycle and the pentose phosphate pathway. The model is comprised of 46 metabolites and 53 reactions. The mathematical model is fit to published enzyme knockdown experimental data. We then applied the model to perform in silico enzyme modulations and evaluate the effects on cell proliferation. Our work identifies potential combinations of enzyme knockdown, metabolite inhibition, and extracellular conditions that impede cell proliferation. Excitingly, the model predicts novel targets that can be tested experimentally. Therefore, the model is a tool to predict the effects of inhibiting specific metabolic reactions within pancreatic cancer cells, which is difficult to measure experimentally, as well as test further hypotheses toward targeted therapies.

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Section: Methodsmentioning

confidence: 99%

Computational Model Predicts the Effects of Targeting Cellular Metabolism in Pancreatic Cancer

Roy

Finley

2017

Front. Physiol.

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“…21 Moreover, the dysregulated cellular glucose metabolism has been shown to provide survival advantages of cancer cells under chemo-or/and radio-therapies, resulting in tumor occurrence. 22 Recent studies reported that mild HT treatment accelerated glucose metabolism and induced oxidative stress, 9,23 thus suggesting that blocking the HT-promoted anerobic glycolysis might be an effective approach against tumors. In this study, we characterized the HT-mediated glucose metabolism of colon cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Blocking the IGF2BP1-promoted glucose metabolism of colon cancer cells via direct de-stabilizing mRNA of the LDHA enhances anticancer effects

Zhang

Jiao

et al. 2021

Molecular Therapy - Nucleic Acids

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Colorectal cancer (CRC) is a commonly diagnosed cancer with poor prognosis and high mortality rate. Hyperthermia (HT) is an adjunctive therapy to enhance the antitumor effects of traditional chemo-or radio-therapy. Here, we report that a cluster of essential regulator genes and speed-limit enzymes of glucose metabolism were significantly elevated under HT from a glucose metabolism PCR array analysis. Under low glucose supply or glucose metabolism inhibition, CRC cells displayed increased sensitivity to HT treatments. By transcript sequencing from the established HT resistant (HTR) colon cancer cell line LoVo HTR, we observed that IGF2BP1, an RNAbinding protein, was significantly upregulated in HTR cells compared with parental cells. Furthermore, LDHA mRNA was identified as an IGF2BP1 direct target. An RNA immunoprecipitation assay and RNA pull-down assay consistently illustrated IGF2BP1 specifically bonds to the 3 0 UTR of LDHA mRNA, leading to enhanced stability of LDHA mRNA. Finally, we demonstrated that inhibiting the IGF2BP1-promoted glycolysis sensitized colon cancer cells to HT treatment via both in vitro and in vivo experiments. Our findings suggest that targeting the IGF2BP1-LDHA-glycolysis pathway might be a promising therapeutic approach to enhance the anti-cancer effects of HT treatment.

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“…Generally, the antitumor effectiveness of thermotherapy is dependent on the temperature and duration of therapy [ 48 ]. Specifically, in the melanoma when the antenna is tuned at 2.4 GHz at 10 W ( Figure 13 a), the temperature can activate apoptotic mechanisms at the 9th minute of the therapy.…”

Section: Resultsmentioning

confidence: 99%

Prediction of Gold Nanoparticle and Microwave-Induced Hyperthermia Effects on Tumor Control via a Simulation Approach

et al. 2019

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Hyperthermia acts as a powerful adjuvant to radiation therapy and chemotherapy. Recent advances show that gold nanoparticles (Au-NPs) can mediate highly localized thermal effects upon interaction with laser radiation. The purpose of the present study was to investigate via in silico simulations the mechanisms of Au-NPs and microwave-induced hyperthermia, in correlation to predictions of tumor control (biological endpoints: tumor shrinkage and cell death) after hyperthermia treatment. We also study in detail the dependence of the size, shape and structure of the gold nanoparticles on their absorption efficiency, and provide general guidelines on how one could modify the absorption spectrum of the nanoparticles in order to meet the needs of specific applications. We calculated the hyperthermia effect using two types of Au-NPs and two types of spherical tumors (prostate and melanoma) with a radius of 3 mm. The plasmon peak for the 30 nm Si-core Au-coated NPs and the 20 nm Au-NPs was found at 590 nm and 540 nm, respectively. Considering the plasmon peaks and the distribution of NPs in the tumor tissue, the induced thermal profile was estimated for different intervals of time. Predictions of hyperthermic cell death were performed by adopting a three-state mathematical model, where “three-state” includes (i) alive, (ii) vulnerable, and (iii) dead states of the cell, and it was coupled with a tumor growth model. Our proposed methodology and preliminary results could be considered as a proof-of-principle for the significance of simulating accurately the hyperthermia-based tumor control involving the immune system. We also propose a method for the optimization of treatment by overcoming thermoresistance by biological means and specifically through the targeting of the heat shock protein 90 (HSP90), which plays a critical role in the thermotolerance of cells and tissues.

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Study of Tumor Growth under Hyperthermia Condition

Cited by 6 publications

References 45 publications

Computational Model Predicts the Effects of Targeting Cellular Metabolism in Pancreatic Cancer

Computational Model Predicts the Effects of Targeting Cellular Metabolism in Pancreatic Cancer

Blocking the IGF2BP1-promoted glucose metabolism of colon cancer cells via direct de-stabilizing mRNA of the LDHA enhances anticancer effects

Prediction of Gold Nanoparticle and Microwave-Induced Hyperthermia Effects on Tumor Control via a Simulation Approach

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