Paradoxical role of Id proteins in regulating tumorigenic potential of lymphoid cells

Roy, Sumedha; Zhuang, Yuan

doi:10.1007/s11684-018-0652-x

Cited by 4 publications

(4 citation statements)

References 121 publications

(199 reference statements)

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“…The inflammatory responses of a developing tumor may include a different leukocyte category. As a result doi: 10.7243/2054-9903-7-1 of these diversitytypes of inflammation, the cancer microenvironment has innate immune cells (including neutrophils, macrophages, dendritic cells, mast cells, myeloid-derived suppressor cells and natural killer cells) and adaptive immune cells (B and T lymphocytes) in addition to the cancer cells and their embracing stroma which formed from fibroblasts, endothelial cells, pericytes and mesenchymal cells [10]. Table 2 summarized the role of most inflammatory cells in antitumor and tumor-promoting cancer.…”

Section: Review Inflammatory Cell Component Of Tumorsmentioning

confidence: 99%

Inflammation and cancer interconnection; simply as we think

Hussein¹,

Darwish²,

Soliman³

2020

Appl Sci Rep

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Microbiota variety is site specific depending on its location in the body and this diversity can get together with human health. At the last decades, inflammation is a primary protective response that sometimes goes away and becomes a main cofactor in the pathogenesis of numerous chronic human diseases, including malignant tumor. As well, microbes have the potency power to influence tumor growth and progression through a wide forms of routes; including alteration of tumor microenvironment, prolonged activation of inflammation, induction of genotoxic restraints and metabolism. In this review, we will set a general overview of inflammation has suspected to provide a major role in the pathogenesis and development of cancer as an important object for advanced cancer biology. Semin Cancer Biol. 2015; 35 Suppl:S151-S184. | Article | PubMed Abstract | PubMed FullText 50. Nickoloff BJ, Ben-Neriah Y and Pikarsky E. Inflammation and cancer: is the link as simple as we think? J Invest Dermatol. 2005; 124:x-xiv. | Article | PubMed Citation: Hussein AM, Darwish ZE and Soliman OH. Inflammation and cancer interconnection; simply as we think. Appl Sci Rep. 2020; 7:1. http://dx.

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Section: Review Inflammatory Cell Component Of Tumorsmentioning

confidence: 99%

Inflammation and cancer interconnection; simply as we think

Hussein¹,

Darwish²,

Soliman³

2020

Appl Sci Rep

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“…Furthermore, the systemic administration of tumor-suppressing CM to a mouse model of breast cancer and bone metastasis is reported to inhibit the growth of mammary tumors and the osteolytic destruction of tumor-invaded bone [ 37 , 38 , 39 ]. An emerging paradigm is that some of the oncogenes have a double-edged role as a tumor enhancer as well as a tumor suppressor [ 40 , 41 , 42 ]. Although paradoxical, a provocative question is whether a novel therapeutic strategy could be developed not by inhibiting those proto-oncogenes but by utilizing their neighbor-removing capabilities.…”

Section: Introductionmentioning

confidence: 99%

The Double-Edged Proteins in Cancer Proteomes and the Generation of Induced Tumor-Suppressing Cells (iTSCs)

Huo

et al. 2023

Proteomes

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Unlike a prevalent expectation that tumor cells secrete tumor-promoting proteins and stimulate the progression of neighboring tumor cells, accumulating evidence indicates that the role of tumor-secreted proteins is double-edged and context-dependent. Some of the oncogenic proteins in the cytoplasm and cell membranes, which are considered to promote the proliferation and migration of tumor cells, may inversely act as tumor-suppressing proteins in the extracellular domain. Furthermore, the action of tumor-secreted proteins by aggressive “super-fit” tumor cells can be different from those derived from “less-fit” tumor cells. Tumor cells that are exposed to chemotherapeutic agents could alter their secretory proteomes. Super-fit tumor cells tend to secrete tumor-suppressing proteins, while less-fit or chemotherapeutic agent-treated tumor cells may secrete tumor-promotive proteomes. Interestingly, proteomes derived from nontumor cells such as mesenchymal stem cells and peripheral blood mononuclear cells mostly share common features with tumor cell-derived proteomes in response to certain signals. This review introduces the double-sided functions of tumor-secreted proteins and describes the proposed underlying mechanism, which would possibly be based on cell competition.

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“…12,13 These proteins promote cell division and repress differentiation by dimerizing with and inhibiting the action of bHLH transcription factors, including those that bind to E-box motifs. 14,15 In addition, under appropriate physiological conditions, these proteins are potent regulators of apoptosis. 16 All four ID protein members (namely, ID1, ID2, ID3 and ID4) are expressed in the testis.…”

Section: Introductionmentioning

confidence: 99%

“…ID proteins are required for the G1‐ to S‐phase transition of the cell cycle 12,13 . These proteins promote cell division and repress differentiation by dimerizing with and inhibiting the action of bHLH transcription factors, including those that bind to E‐box motifs 14,15 . In addition, under appropriate physiological conditions, these proteins are potent regulators of apoptosis 16 .…”

Section: Introductionmentioning

confidence: 99%

Elevated Id2 expression causes defective meiosis and spermatogenesis in mice

He,

Yan,

Shang

et al. 2023

Developmental Dynamics

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BackgroundInhibitors of DNA binding (ID) proteins mainly inhibit gene expression and regulate cell fate decisions by interacting with E‐proteins. All four ID proteins (ID1–4) are present in the testis, and ID4 has a particularly important role in spermatogonial stem cell fate determination. Several lines of evidence indicate that ID proteins are involved in meiosis; however, functional experiments have not been conducted to validate this observation.ResultsIn this study, we report that ID2 is enriched in spermatocytes and that forced ID2 expression in germ cells causes defects in spermatogenesis. A detailed analysis demonstrated that Id2 overexpression (Id2 OE) decreased the total number of spermatogonia and changed the dynamics of meiosis progression. Specifically, spermatocytes were enriched in the zygotene stage, and the proportion of pachytene spermatocytes was significantly decreased, indicating defects in the zygotene–pachytene transition. The number of MLH1‐positive foci per cell was decreased in pachytene spermatocytes from Id2 OE testes, suggesting abnormalities in recombination. Transcriptome analysis revealed that forced Id2 expression changed the expression of a list of genes mainly associated with meiosis and spermatid development.ConclusionsID2 protein is expressed in spermatocytes, and its genetic ablation in the germline does not affect spermatogenesis, likely due to genetic compensation of its family members. However, forced Id2 expression changes meiosis progression and causes defects in spermiogenesis. These data provide important evidence that ID proteins play pivotal roles in male meiosis and spermatid development.

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Paradoxical role of Id proteins in regulating tumorigenic potential of lymphoid cells

Cited by 4 publications

References 121 publications

Inflammation and cancer interconnection; simply as we think

Inflammation and cancer interconnection; simply as we think

The Double-Edged Proteins in Cancer Proteomes and the Generation of Induced Tumor-Suppressing Cells (iTSCs)

Elevated Id2 expression causes defective meiosis and spermatogenesis in mice

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