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Metabolic Regulation: Cell Growth and Proliferation

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (30 August 2023) | Viewed by 29482

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Dr. Debabrata Banerjee

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Department of Pharmacology, Rutgers, Robert Wood Johnson Medical School (RWJMS), Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA
Interests: metabolic cooperation between tumor cells and stromal cells; role of carcinoma associated fibroblasts
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Dr. Deepshikha Mishra

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Department of Pharmacology, Rutgers, Robert Wood Johnson Medical School (RWJMS), Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA
Interests: cancer development and progression; tumor microenvironment; tumor-stroma interaction; carcinoma associated fibroblasts; animal model; identifying novel molecular targets; systems biology
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Special Issue Information

Dear Colleagues,

Advancements in the last few decades have set a firm foundation for emergence of metabolism as a key cancer hallmark. It is not surprising to see metabolic regulations as fundamental mechanisms fostering additional energy and nutrient demands of the cancer cell. To support tumor growth and proliferation in an altered environment, a broader metabolic rewiring is necessary thus helping to acquire additional glucose and other nutrients including, amino acids, nucleotides, and lipids indispensable for the sustenance of cell growth. These metabolites fulfill energy demands and serve as substrates for biomass generation. Other factors that influence metabolic adaptations include specific cell types and the microenvironment. Interestingly, many of the metabolites also impact molecular signaling by regulating gene and protein expression. Further, they also influence the neighboring non-transformed cells in the vicinity of the tumor.

Cellular metabolism is highly complex and multifactorial making it extremely difficult to fully understand its regulation. However, state-of-the-art techniques like metabolic flux analysis are highly efficient in identifying and tracing the precise metabolites through metabolic pathways. Metabolic rewiring also causes changes in cellular bioenergetics which allows cancer cells to endure high proliferation rates. A deeper knowledge of cellular bioenergetics is advantageous for understanding of cancerous cell physiology. Measuring oxygen consumption rate (OCR) and extracellular acidification rate or rate of acid efflux (ECAR) are helpful in determining mitochondrial respiration and amount of lactic acid produced during glycolytic metabolism.

A deeper understanding of metabolic regulation has further sparked interest in identifying cancer-specific metabolic signatures that render more direct and substantial effects to encourage cancer cell proliferation and survival. The era of metabolomics has fueled the identification of pathways and metabolic markers that are causative in cancer generation and progression. Further, external factors like diet and exercise also directly influence metabolic regulation. Metabolomic, transcriptomic and proteomic profiling enables the identification of alterations associated with cancer and these approaches provide a complete picture of discrepancies observed in regulation at molecular and pathway levels. Targeting altered metabolic regulation to diminish tumor growth and energy reservoir is now a major focus of future research and could be more advantageous and effective in advanced cancer therapeutics. A better understanding of the principles of metabolic regulation may improve ways to treat different cancers but also other metabolic diseases that rely on such pathways.

Dr. Debabrata Banerjee
Dr. Deepshikha Mishra
Guest Editors

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Keywords

cancer
metabolic regulation
lactate
tumor stroma
fibroblasts
molecular signatures
mitochondria
metabolic biomarkers
animal model
tumorigenesis
metabolomics
transcriptomics
proteomics

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Metabolic Regulation: Cell Growth and Proliferation—2nd Edition in Cells

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Research

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18 pages, 3740 KiB

Open AccessArticle

Survival Pathways of HIF-Deficient Tumour Cells: TCA Inhibition, Peroxisomal Fatty Acid Oxidation Activation and an AMPK-PGC-1α Hypoxia Sensor

by Monika A. Golinska, Marion Stubbs, Adrian L. Harris, Laszlo G. Boros, Madhu Basetti, Dominick J. O. McIntyre and John R. Griffiths

Cells 2022, 11(22), 3595; https://doi.org/10.3390/cells11223595 - 14 Nov 2022

Cited by 2 | Viewed by 3151

Abstract

The HIF-1 and HIF-2 (HIF1/2) hypoxia responses are frequently upregulated in cancers, and HIF1/2 inhibitors are being developed as anticancer drugs. How could cancers resist anti-HIF1/2 therapy? We studied metabolic and molecular adaptations of HIF-1β-deficient Hepa-1c4, a hepatoma model lacking HIF1/2 signalling, which mimics a cancer treated by a totally effective anti-HIF1/2 agent. [1,2-¹³C₂]-D-glucose metabolism was measured by SiDMAP metabolic profiling, gene expression by TaqMan, and metabolite concentrations by ¹H MRS. HIF-1β-deficient Hepa-1c4 responded to hypoxia by increasing glucose uptake and lactate production. They showed higher glutamate, pyruvate dehydrogenase, citrate shuttle, and malonyl-CoA fluxes than normal Hepa-1 cells, whereas pyruvate carboxylase, TCA, and anaplerotic fluxes decreased. Hypoxic HIF-1β-deficient Hepa-1c4 cells increased expression of PGC-1α, phospho-p38 MAPK, and PPARα, suggesting AMPK pathway activation to survive hypoxia. They had higher intracellular acetate, and secreted more H₂O₂, suggesting increased peroxisomal fatty acid β-oxidation. Simultaneously increased fatty acid synthesis and degradation would have “wasted” ATP in Hepa-1c4 cells, thus raising the [AMP]:[ATP] ratio, and further contributing to the upregulation of the AMPK pathway. Since these tumour cells can proliferate without the HIF-1/2 pathways, combinations of HIF1/2 inhibitors with PGC-1α or AMPK inhibitors should be explored. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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15 pages, 2879 KiB

Open AccessEditor’s ChoiceArticle

The HSF1-CPT1a Pathway Is Differentially Regulated in NAFLD Progression

by Wiebke Breternitz, Friedrich Sandkühler, Frauke Grohmann, Jochen Hampe, Mario Brosch, Alexander Herrmann, Clemens Schafmayer, Christian Meinhardt, Stefan Schreiber, Alexander Arlt and Claudia Geismann

Cells 2022, 11(21), 3504; https://doi.org/10.3390/cells11213504 - 4 Nov 2022

Cited by 3 | Viewed by 2615

Abstract

Obesity and obesity-associated diseases represent one of the key health challenges of our time. In this context, aberrant hepatic lipid accumulation is a central pathological aspect of non-alcoholic fatty liver disease (NAFLD). By comparing methylation signatures of liver biopsies before and after bariatric surgery, we recently demonstrated the strong enrichment of differentially methylated heat shock factor 1 (HSF1) binding sites (>400-fold) in the process of liver remodeling, indicating a crucial role of HSF1 in modulating central aspects of NAFLD pathogenesis. Using cellular models of NAFLD, we were able to show that HSF1 is activated during fat accumulation in hepatocytes, mimicking conditions in patients before bariatric surgery. This induction was abolished by starving the cells, mimicking the situation after bariatric surgery. Regarding this connection, carnitine palmitoyltransferase 1 isoform A (CTP1a), a central regulator of lipid beta-oxidation, was identified as a HSF1 target gene by promoter analysis and HSF1 knockdown experiments. Finally, pharmacological activation of HSF1 through celastrol reduced fat accumulation in the cells in a HSF1-dependent manner. In conclusion, we were able to confirm the relevance of HSF1 activity and described a functional HSF1-CPT1a pathway in NAFLD pathogenesis. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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12 pages, 2197 KiB

Open AccessArticle

Targeting Asparagine Synthetase in Tumorgenicity Using Patient-Derived Tumor-Initiating Cells

by Gen Nishikawa, Kenji Kawada, Keita Hanada, Hisatsugu Maekawa, Yoshiro Itatani, Hiroyuki Miyoshi, Makoto Mark Taketo and Kazutaka Obama

Cells 2022, 11(20), 3273; https://doi.org/10.3390/cells11203273 - 18 Oct 2022

Cited by 5 | Viewed by 2517

Abstract

Reprogramming of energy metabolism is regarded as one of the hallmarks of cancer; in particular, oncogenic RAS has been shown to be a critical regulator of cancer metabolism. Recently, asparagine metabolism has been heavily investigated as a novel target for cancer treatment. For example, Knott et al. showed that asparagine bioavailability governs metastasis in a breast cancer model. Gwinn et al. reported the therapeutic vulnerability of asparagine biosynthesis in KRAS-driven non-small cell lung cancer. We previously reported that KRAS-mutated CRC cells can adapt to glutamine depletion through upregulation of asparagine synthetase (ASNS), an enzyme that synthesizes asparagine from aspartate. In our previous study, we assessed the efficacy of asparagine depletion using human cancer cell lines. In the present study, we evaluated the clinical relevance of asparagine depletion using a novel patient-derived spheroid xenograft (PDSX) mouse model. First, we examined ASNS expression in 38 spheroid lines and found that 12 lines (12/37, 32.4%) displayed high ASNS expression, whereas 26 lines (25/37, 67.6%) showed no ASNS expression. Next, to determine the role of asparagine metabolism in tumor growth, we established ASNS-knockdown spheroid lines using lentiviral short hairpin RNA constructs targeting ASNS. An in vitro cell proliferation assay demonstrated a significant decrease in cell proliferation upon asparagine depletion in the ASNS-knockdown spheroid lines, and this was not observed in the control spheroids lines. In addition, we examined asparagine inhibition with the anti-leukemia drug L-asparaginase (L-Asp) and observed a considerable reduction in cell proliferation at a low concentration (0.1 U/mL) in the ASNS-knockdown spheroid lines, whereas it exhibited limited inhibition of control spheroid lines at the same concentration. Finally, we used the PDSX model to assess the effects of asparagine depletion on tumor growth in vivo. The nude mice injected with ASNS-knockdown or control spheroid lines were administered with L-Asp once a day for 28 days. Surprisingly, in mice injected with ASNS-knockdown spheroids, the administration of L-Asp dramatically inhibited tumor engraftment. On the other hands, in mice injected with control spheroids, the administration of L-Asp had no effect on tumor growth inhibition at all. These results suggest that ASNS inhibition could be critical in targeting asparagine metabolism in cancers. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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23 pages, 4704 KiB

Open AccessArticle

Omics Analysis of Chemoresistant Triple Negative Breast Cancer Cells Reveals Novel Metabolic Vulnerabilities

by Dimitris Kordias, Christina E. Kostara, Styliani Papadaki, John Verigos, Eleni Bairaktari and Angeliki Magklara

Cells 2022, 11(17), 2719; https://doi.org/10.3390/cells11172719 - 31 Aug 2022

Cited by 6 | Viewed by 2618

Abstract

The emergence of drug resistance in cancer poses the greatest hurdle for successful therapeutic results and is associated with most cancer deaths. In triple negative breast cancer (TNBC), due to the lack of specific therapeutic targets, systemic chemotherapy is at the forefront of treatments, but it only benefits a fraction of patients because of the development of resistance. Cancer cells may possess an innate resistance to chemotherapeutic agents or develop new mechanisms of acquired resistance after long-term drug exposure. Such mechanisms involve an interplay between genetic, epigenetic and metabolic alterations that enable cancer cells to evade therapy. In this work, we generated and characterized a chemoresistant TNBC cell line to be used for the investigation of mechanisms that drive resistance to paclitaxel. Transcriptomic analysis highlighted the important role of metabolic-associated pathways in the resistant cells, prompting us to employ ¹H-NMR to explore the metabolome and lipidome of these cells. We identified and described herein numerous metabolites and lipids that were significantly altered in the resistant cells. Integrated analysis of our omics data revealed MSMO1, an intermediate enzyme of cholesterol biosynthesis, as a novel mediator of chemoresistance in TNBC. Overall, our data provide a critical insight into the metabolic adaptations that accompany acquired resistance in TNBC and pinpoint potential new targets. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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20 pages, 2839 KiB

Open AccessArticle

p73α1, an Isoform of the p73 Tumor Suppressor, Modulates Lipid Metabolism and Cancer Cell Growth via Stearoyl-CoA Desaturase-1

by Zachary Rabow, Kyra Laubach, Xiangmudong Kong, Tong Shen, Shakur Mohibi, Jin Zhang, Oliver Fiehn and Xinbin Chen

Cells 2022, 11(16), 2516; https://doi.org/10.3390/cells11162516 - 13 Aug 2022

Cited by 4 | Viewed by 2428

Abstract

Altered lipid metabolism is a hallmark of cancer. p73, a p53 family member, regulates cellular processes and is expressed as multiple isoforms. However, the role of p73 in regulating lipid metabolism is not well-characterized. Previously, we found that loss of p73 exon 12 (E12) leads to an isoform switch from p73α to p73α1, the latter of which has strong tumor suppressive activity. In this study, comprehensive untargeted metabolomics was performed to determine whether p73α1 alters lipid metabolism in non-small cell lung carcinoma cells. RNA-seq and molecular biology approaches were combined to identify lipid metabolism genes altered upon loss of E12 and identify a direct target of p73α1. We found that loss of E12 leads to decreased levels of phosphatidylcholines, and this was due to decreased expression of genes involved in phosphatidylcholine synthesis. Additionally, we found that E12-knockout cells had increased levels of phosphatidylcholines containing saturated fatty acids (FAs) and decreased levels of phosphatidylcholines containing monounsaturated fatty acids (MUFAs). We then found that p73α1 inhibits cancer cell viability through direct transcriptional suppression of Stearoyl-CoA Desaturase-1 (SCD1), which converts saturated FAs to MUFAs. Finally, we showed that p73α1-mediated suppression of SCD1 leads to increased ratios of saturated FAs to MUFAs. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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14 pages, 3325 KiB

Open AccessArticle

Uridine Diphosphate Glucuronosyl Transferase 2B28 (UGT2B28) Promotes Tumor Progression and Is Elevated in African American Prostate Cancer Patients

by Anindita Ravindran, Kimiko L. Krieger, Akash K. Kaushik, Hélène Hovington, Sadia Mehdi, Danthasinghe Waduge Badrajee Piyarathna, Vasanta Putluri, Paul Basil, Uttam Rasaily, Franklin Gu, Truong Dang, Jong Min Choi, Rajni Sonavane, Sung Yun Jung, Lisha Wang, Rohit Mehra, Nancy L. Weigel, Nagireddy Putluri, David R. Rowley, Ganesh S. Palapattu, Chantal Guillemette, Louis Lacombe, Éric Lévesque and Arun Sreekumar Show full author list Hide full author list

Cells 2022, 11(15), 2329; https://doi.org/10.3390/cells11152329 - 29 Jul 2022

Viewed by 2396

Abstract

Prostate cancer (PCa) is the second most diagnosed cancer in the United States and is associated with metabolic reprogramming and significant disparities in clinical outcomes among African American (AA) men. While the cause is likely multi-factorial, the precise reasons for this are unknown. Here, we identified a higher expression of the metabolic enzyme UGT2B28 in localized PCa and metastatic disease compared to benign adjacent tissue, in AA PCa compared to benign adjacent tissue, and in AA PCa compared to European American (EA) PCa. UGT2B28 was found to be regulated by both full-length androgen receptor (AR) and its splice variant, AR-v7. Genetic knockdown of UGT2B28 across multiple PCa cell lines (LNCaP, LAPC-4, and VCaP), both in androgen-replete and androgen-depleted states resulted in impaired 3D organoid formation and a significant delay in tumor take and growth rate of xenograft tumors, all of which were rescued by re-expression of UGT2B28. Taken together, our findings demonstrate a key role for the UGT2B28 gene in promoting prostate tumor growth. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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14 pages, 2949 KiB

Open AccessArticle

Differences in Antioxidant and Lipid Handling Protein Expression Influence How Cells Expressing Distinct Mutant TP53 Subtypes Maintain Iron Homeostasis

by Cameron J. Cardona, Evan R. Hermann, Kate N. Kouplen, Steven D. Hartson and McKale R. Montgomery

Cells 2022, 11(13), 2064; https://doi.org/10.3390/cells11132064 - 29 Jun 2022

Cited by 1 | Viewed by 2291

Abstract

The tumor suppressor TP53 is the most commonly mutated gene in human cancers, and iron is necessary for cancer cell growth and proliferation, but there is a significant gap in knowledge for how the two cooperate to affect cellular physiology. Elucidating this role is complicated, however, because each TP53 mutation subtype exhibits unique phenotypic responses to changes in iron availability. The goal of this work was to determine how cells expressing distinct TP53 mutation subtypes respond to iron restriction. Utilizing a reverse genetics approach, we generated eight isogenic cell lines that either lacked TP53 expression, expressed wild-type TP53, or expressed one of the six most common TP53 “hotspot” mutations. We then employed isobaric peptide labeling and mass spectrometry to quantitively measure changes in global protein expression, both in response to induction of mutant TP53 expression, and in response to iron chelation. Our findings indicate that mutant TP53-dependent sensitivities to iron restriction are not driven by differences in responsiveness to iron chelation, but more so by mutant TP53-dependent differences in cellular antioxidant and lipid handling protein expression. These findings reinforce the importance of distinguishing between TP53 mutation subtypes when investigating approaches to target mutant TP53. We also identify unique TP53-dependent perturbances in protein expression patterns that could be exploited to improve iron-targeted chemotherapeutic strategies. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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Review

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17 pages, 1060 KiB

Open AccessFeature PaperReview

Secretome of Stromal Cancer-Associated Fibroblasts (CAFs): Relevance in Cancer

by Deepshikha Mishra and Debabrata Banerjee

Cells 2023, 12(4), 628; https://doi.org/10.3390/cells12040628 - 15 Feb 2023

Cited by 9 | Viewed by 3064

Abstract

The cancer secretome reflects the assortment of proteins released by cancer cells. Investigating cell secretomes not only provides a deeper knowledge of the healthy and transformed state but also helps in the discovery of novel biomarkers. Secretomes of cancer cells have been studied in the past, however, the secretome contribution of stromal cells needs to be studied. Cancer-associated fibroblasts (CAFs) are one of the predominantly present cell populations in the tumor microenvironment (TME). CAFs play key role in functions associated with matrix deposition and remodeling, reciprocal exchange of nutrients, and molecular interactions and signaling with neighboring cells in the TME. Investigating CAFs secretomes or CAFs-secreted factors would help in identifying novel CAF-specific biomarkers, unique druggable targets, and an improved understanding for personalized cancer diagnosis and prognosis. In this review, we have tried to include all studies available in PubMed with the keywords “CAFs Secretome”. We aim to provide a comprehensive summary of the studies investigating role of the CAF secretome on cancer development, progression, and therapeutic outcome. However, challenges associated with this process have also been addressed in the later sections. We have highlighted the functions and clinical relevance of secretome analysis in stromal CAF-rich cancer types. This review specifically discusses the secretome of stromal CAFs in cancers. A deeper understanding of the components of the CAF secretome and their interactions with cancer cells will help in the identification of personalized biomarkers and a more precise treatment plan. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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17 pages, 809 KiB

Open AccessReview

Modeling Obesity-Driven Pancreatic Carcinogenesis—A Review of Current In Vivo and In Vitro Models of Obesity and Pancreatic Carcinogenesis

by Sally Kfoury, Patrick Michl and Laura Roth

Cells 2022, 11(19), 3170; https://doi.org/10.3390/cells11193170 - 10 Oct 2022

Cited by 1 | Viewed by 2958

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is the most common pancreatic malignancy with a 5-year survival rate below 10%, thereby exhibiting the worst prognosis of all solid tumors. Increasing incidence together with a continued lack of targeted treatment options will cause PDAC to be the second leading cause of cancer-related deaths in the western world by 2030. Obesity belongs to the predominant risk factors for pancreatic cancer. To improve our understanding of the impact of obesity on pancreatic cancer development and progression, novel laboratory techniques have been developed. In this review, we summarize current in vitro and in vivo models of PDAC and obesity as well as an overview of a variety of models to investigate obesity-driven pancreatic carcinogenesis. We start by giving an overview on different methods to cultivate adipocytes in vitro as well as various in vivo mouse models of obesity. Moreover, established murine and human PDAC cell lines as well as organoids are summarized and the genetically engineered models of PCAC compared to xenograft models are introduced. Finally, we review published in vitro and in vivo models studying the impact of obesity on PDAC, enabling us to decipher the molecular basis of obesity-driven pancreatic carcinogenesis. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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14 pages, 1062 KiB

Open AccessReview

Therapeutic Drug-Induced Metabolic Reprogramming in Glioblastoma

by Trang T. T. Nguyen, Enyuan Shang, Mike-Andrew Westhoff, Georg Karpel-Massler and Markus D. Siegelin

Cells 2022, 11(19), 2956; https://doi.org/10.3390/cells11192956 - 22 Sep 2022

Cited by 16 | Viewed by 3656

Abstract

Glioblastoma WHO IV (GBM), the most common primary brain tumor in adults, is a heterogenous malignancy that displays a reprogrammed metabolism with various fuel sources at its disposal. Tumor cells primarily appear to consume glucose to entertain their anabolic and catabolic metabolism. While less effective for energy production, aerobic glycolysis (Warburg effect) is an effective means to drive biosynthesis of critical molecules required for relentless growth and resistance to cell death. Targeting the Warburg effect may be an effective venue for cancer treatment. However, past and recent evidence highlight that this approach may be limited in scope because GBM cells possess metabolic plasticity that allows them to harness other substrates, which include but are not limited to, fatty acids, amino acids, lactate, and acetate. Here, we review recent key findings in the literature that highlight that GBM cells substantially reprogram their metabolism upon therapy. These studies suggest that blocking glycolysis will yield a concomitant reactivation of oxidative energy pathways and most dominantly beta-oxidation of fatty acids. Full article

(This article belongs to the Special Issue Metabolic Regulation: Cell Growth and Proliferation)

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