Linking tumor glycolysis and immune evasion in cancer: Emerging concepts and therapeutic opportunities

Ganapathy-Kanniappan, Shanmugasundaram

doi:10.1016/j.bbcan.2017.04.002

Cited by 97 publications

(73 citation statements)

References 95 publications

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“…Therefore, in the tumor microenvironment, JNK may activate immune evasion mechanisms by modulating TGF‐β, toll‐like receptors, INF‐γ, and/or other immunosuppressive cytokines to promote tumor survival. Future studies should investigate the potential role of JNK signaling in tumor immune evasion, which may be important for the design of cancer therapies …”

Section: Mechanisms By Which Jnk Regulates Cancer Cell Survivalmentioning

confidence: 99%

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JNK signaling in cancer cell survival

et al. 2019

Medicinal Research Reviews

247

146

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c‐Jun N‐terminal kinase (JNK) is involved in cancer cell apoptosis; however, emerging evidence indicates that this Janus signaling promotes cancer cell survival. JNK acts synergistically with NF‐κB, JAK/STAT, and other signaling molecules to exert a survival function. JNK positively regulates autophagy to counteract apoptosis, and its effect on autophagy is related to the development of chemotherapeutic resistance. The prosurvival effect of JNK may involve an immune evasion mechanism mediated by transforming growth factor‐β, toll‐like receptors, interferon‐γ, and autophagy, as well as compensatory JNK‐dependent cell proliferation. The present review focuses on recent advances in understanding the prosurvival function of JNK and its role in tumor development and chemoresistance, including a comprehensive analysis of the molecular mechanisms underlying JNK‐mediated cancer cell survival. There is a focus on the specific “Yin and Yang” functions of JNK1 and JNK2 in the regulation of cancer cell survival. We highlight recent advances in our knowledge of the roles of JNK in cancer cell survival, which may provide insight into the distinct functions of JNK in cancer and its potential for cancer therapy.

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Section: Mechanisms By Which Jnk Regulates Cancer Cell Survivalmentioning

confidence: 99%

“…Future studies should investigate the potential role of JNK signaling in tumor immune evasion, which may be important for the design of cancer therapies. 124,125…”

Section: Tumor Immune Evasion May Be Involved In Jnk-mediated Cancementioning

confidence: 99%

JNK signaling in cancer cell survival

et al. 2019

Medicinal Research Reviews

247

146

View full text Add to dashboard Cite

show abstract

“…More importantly, it reduces the mitochondrial burden. Similarly, it has been established that highly proliferative cells such as cancer cells also adopt the 'glycolytic' phenotype as shown by elegant reviews [32][33][34][35]. Thus, irrespective of the cell type or the disease condition, an increase in energy demand in general facilitates metabolic shift to glycolysis, a rapid energy-producing pathway.…”

Section: Resultsmentioning

confidence: 98%

Elevated mitochondrial activity distinguishes fibrogenic hepatic stellate cells and sensitizes for selective inhibition by mitotropic doxorubicin

Gajendiran

Vega

Itoh

et al. 2018

J Cellular Molecular Medi

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Activation of hepatic stellate cells (HSCs) is an integral component of the wound‐healing process in liver injury/inflammation. However, uncontrolled activation of HSCs leads to constant secretion of collagen‐rich extracellular matrix (ECM) proteins, resulting in liver fibrosis. The enhanced ECM synthesis/secretion demands an uninterrupted supply of intracellular energy; however, there is a paucity of data on the bioenergetics, particularly the mitochondrial (mito) metabolism of fibrogenic HSCs. Here, using human and rat HSCs in vitro, we show that the mito‐respiration, mito‐membrane potential (Δψm) and cellular ‘bioenergetic signature’ distinguish fibrogenic HSCs from normal, less‐active HSCs. Ex vivo, HSCs from mouse and rat models of liver fibrosis further confirmed the altered ‘bioenergetic signature’ of fibrogenic HSCs. Importantly, the distinctive elevation in mito‐Δψm sensitized fibrogenic HSCs for selective inhibition by mitotropic doxorubicin while normal, less‐active HSCs and healthy human primary hepatocytes remained minimally affected if not, unaffected. Thus, the increased mito‐Δψm may provide an opportunity to selectively target fibrogenic HSCs in liver fibrosis.

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“…BT-474 and SKBR-3 are HER2 positive cell lines, and secreted exosomes highly enriched with proteins involved in antigen presenting (HSPA5, CALR, PSME1,2, PSMA 3,6, PSMB 2,4, and HLA-C) and glycolytic metabolism (G6PD, TP1, and PGAM1). These proteins could lead to cancer immune-surveillance and malfunctioned energy synthesis in breast cancer microenvironment [91][92][93]. In addition, BT-474-derived exosomal proteins have a strong relation with neutrophil GO terms; DDX3X, VCP, HSP90AA1, ILF2, HSPA8, PNP, MME, MME2, PAB37, SERPINB6, GDI2, ALDOA, PGAM1, and GPI, which are related with neutrophil degranulation, mediated immunity and neutrophil activation.…”

Section: Cell Ultracentrifugementioning

confidence: 99%

Exploring the key communicator role of exosomes in cancer microenvironment through proteomics

Kim

Cho

2019

Proteome Sci

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There have been many attempts to fully understand the mechanism of cancer behavior. Yet, how cancers develop and metastasize still remain elusive. Emerging concepts of cancer biology in recent years have focused on the communication of cancer with its microenvironment, since cancer cannot grow and live alone. Cancer needs to communicate with other cells for survival, and thus they secrete various messengers, including exosomes that contain many proteins, miRNAs, mRNAs, etc., for construction of the tumor microenvironment. Moreover, these intercellular communications between cancer and its microenvironment, including stromal cells or distant cells, can promote tumor growth, metastasis, and escape from immune surveillance. In this review, we summarized the role of proteins in the exosome as communicators between cancer and its microenvironment. Consequently, we present cancer specific exosome proteins and their unique roles in the interaction between cancer and its microenvironment. Clinically, these exosomes might provide useful biomarkers for cancer diagnosis and therapeutic tools for cancer treatment.

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Linking tumor glycolysis and immune evasion in cancer: Emerging concepts and therapeutic opportunities

Cited by 97 publications

References 95 publications

JNK signaling in cancer cell survival

JNK signaling in cancer cell survival

Elevated mitochondrial activity distinguishes fibrogenic hepatic stellate cells and sensitizes for selective inhibition by mitotropic doxorubicin

Exploring the key communicator role of exosomes in cancer microenvironment through proteomics

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