Paradoxical role of high mobility group box 1 in glioma: a suppressor or a promoter?

Seidu, Richard A.; Wu, Min; Su, Zhaoliang; Xu, Huaxi

doi:10.4081/oncol.2017.325

Cited by 34 publications

(34 citation statements)

References 63 publications

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“…In cancer, excessive HMGB1 release is known to contribute to angiogenesis, evasion of programmed cell death (apoptosis), inflammation, tissue invasion, and metastasis [ 201 ]. When serum levels of HMGB1 are high, its hyperacetylated and disulfide isoforms have been shown to be sensitive disease biomarkers and contribute to the different disease stages [ 202 ].…”

Section: Necrosis Promotes Tumor Progressionmentioning

confidence: 99%

Regulation of Tumor Progression by Programmed Necrosis

Lee

Jeon

et al. 2018

Oxidative Medicine and Cellular Longevity

177

137

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Rapidly growing malignant tumors frequently encounter hypoxia and nutrient (e.g., glucose) deprivation, which occurs because of insufficient blood supply. This results in necrotic cell death in the core region of solid tumors. Necrotic cells release their cellular cytoplasmic contents into the extracellular space, such as high mobility group box 1 (HMGB1), which is a nonhistone nuclear protein, but acts as a proinflammatory and tumor-promoting cytokine when released by necrotic cells. These released molecules recruit immune and inflammatory cells, which exert tumor-promoting activity by inducing angiogenesis, proliferation, and invasion. Development of a necrotic core in cancer patients is also associated with poor prognosis. Conventionally, necrosis has been thought of as an unregulated process, unlike programmed cell death processes like apoptosis and autophagy. Recently, necrosis has been recognized as a programmed cell death, encompassing processes such as oncosis, necroptosis, and others. Metabolic stress-induced necrosis and its regulatory mechanisms have been poorly investigated until recently. Snail and Dlx-2, EMT-inducing transcription factors, are responsible for metabolic stress-induced necrosis in tumors. Snail and Dlx-2 contribute to tumor progression by promoting necrosis and inducing EMT and oncogenic metabolism. Oncogenic metabolism has been shown to play a role(s) in initiating necrosis. Here, we discuss the molecular mechanisms underlying metabolic stress-induced programmed necrosis that promote tumor progression and aggressiveness.

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Section: Necrosis Promotes Tumor Progressionmentioning

confidence: 99%

Regulation of Tumor Progression by Programmed Necrosis

Lee

Jeon

et al. 2018

Oxidative Medicine and Cellular Longevity

177

137

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“…Furthermore, glioma invasiveness is piquantly interconnected to the proteolytic exploits of MMPs (44,90,100). It is now clear that MMP-2 and MMP-9 secretion are associated with the development, advancement spread as well as the level of malignancy of gliomas in human beings (41,44,121). Nevertheless, the secretion of MMP-1, MMP-11 and MMP-19 has also been implicated in the WHO categorization of malignant gliomas in human beings (44,131,153).…”

Section: Resveratrol and Matrix Metalloproteinasementioning

confidence: 99%

The Therapeutic Potential of Resveratrol in Gliomas

Richard¹

2019

ABCMed

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Resveratrol (RSV) is found in most human foods especially fruits such as grapes, peanuts, strawberry, blueberry, cranberry, mulberry, lingberry, sparkleberry, bilberry and in flowers as well as leaves like butterfly orchid tree, eucalyptus, spruce, lily, gnetum and so many others. Functionally, RSV has the propensity to safeguard DNA as well as the induction of DNA repair. RSV is precipitously metabolized in the liver via phase-II detoxification enzymes leading to its principal urine excretion. RSV steered growth inhibition, induction of apoptosis and G0/G1phase cell cycle arrest in an experiment involving glioma cells. RVS can block the triggering of signal transducer and activator of transcription (STAT3) signaling of glioma cells. RSV subdues STAT3 signaling via the inhibition of SRC or Janus kinase (JAK2) induction, thereby inducing growth inhibitory and apoptotic properties. RSV explicitly blocks both COX-1 and COX-2 invitro. In the cancer inflammatory milieu, the blockade effects of RSV on NF-κB could also lead to the blockade of TNF-α resulting in inhibition of cancer advancement as well as metastasis.Individually, RSV has proven to very potent in glioma cells. It is able to down-regulate glioma angiogenesis as well as metastasis. In combination with other agents, RVS augment its potency in glioma. RVS is able to cross the blood brain barrier (BBB) via gap junctions making it very efficient central nervous system medication. RVS after oral administration peaks in the blood stream after one hour meaning it acts very fast. This review focuses on the neuropharmacological role of RVS in glioma.proven to have chemo-preventive effects on numerous human ailments like osteoporosis and gastric ulcers besides the cardioprotective effect mentioned above (27,32). STRUCTURE AND FUNCTIONS OF RESVERATROLRSV is a white powder with a feeble yellow cast. It is a stilbene with a natural polyphenol configuration analogous to diethylstilbestrol and estradiol (32,86). Its molecular formula is C 14 H 12 O 3 and it is commonly referred to as 3,5,4'thihydroxystilbene. Other unconventional terms use to describe this compound are: 3,4',5-stilbenetriol, (E)-5-(7-hydroxystyryl) resorcinol, (E)-5-(4-hydroxystyryl) benzene-1,3-diol. RSV occurs innately as both cis-and trans-isomers. The trans-isomer is often used in classic laboratory studies because its more physical available have has higher biological activity than the cis-isomer. On the other hand, the cis-isomer is unstably and not commercial accessible (32,144).Functionally, RSV has the propensity to safeguard DNA as well as the induction of DNA repair (17,89). Studies have proven that, at high dose, RSV does not only suppress cancer advancement but also inhibits the synthesis of RNA, DNA and

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“…The upsurge in HMGB1 levels has shown to directly stimulate cancer development [79]. Furthermore, HMGB1 partakes in all fundamental hallmarks of cancer including unlimited proliferation, angiogenesis, invasion and metastasis [80,81].…”

Section: Mdscs High Mobility Group Box 1 and Cancermentioning

confidence: 99%

Myeloid-derived Suppressor Cells in Cancer: A Review on the Pathogenesis and Therapeutic Potentials

Richard¹

2018

TOCIJ

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Myeloid-Derived Suppressor Cells (MDSCs) are multifarious group of immature cells that arise from the myeloid and amass in individuals with cancer, sepsis, burns, or chronic inflammation. It has been evidenced that these group of cells are efficient in modifying adaptive and innate immune responses, coherent with their assumed key biological roles. It is evidenced that MDSCs inter-communicate with Tumor-Associated Macrophages (TAM), Tumor-Associated Neutrophils (TAN), Dendritic Cells (DCs), Receptor for Advanced Glycation End-products (RAGE), Toll-Like Receptors (TLRs), Matrix Metalloproteinase (MMPs) as well as High Mobility Group Box 1 (HMGB1) during carcinogenesis. This interaction although elaborated in various studies and reviews still does not explain in details as to how their interplay results in cancer pathogenesis. We noted that MDSC contributed to cancer immune suppressionviaTLR-4 receptor and lipopolysaccharideas (LPS). Furthermore, MDSC contributed to cancer developmentviaMMPs (MMP-9 and MMP1-12) as well as RAGE. In the cancer microenvironment, HMGB1-driven MDSC amassment expedites cancer development and metastasisviaPMN-MDSCs, macrophages, DCs and Immature Myeloid Cells (IMC). Also, HMGB1 intermediation with MDSCsviaRAGE and/or TLR-4 leading to cancer development. Nevertheless, MDSCs have already proven potent in some cancers and are currently been used as treatment options although further studies are needed in some other cancers. Our review, therefore, explores the pivotal pathogenic and therapeutic roles of MDSCs in cancer.

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Paradoxical role of high mobility group box 1 in glioma: a suppressor or a promoter?

Cited by 34 publications

References 63 publications

Regulation of Tumor Progression by Programmed Necrosis

Regulation of Tumor Progression by Programmed Necrosis

The Therapeutic Potential of Resveratrol in Gliomas

Myeloid-derived Suppressor Cells in Cancer: A Review on the Pathogenesis and Therapeutic Potentials

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