Deleted in Breast Cancer 1 as a Novel Prognostic Biomarker for Digestive System Cancers: A Meta-Analysis

Liu, Jingting; Meng, Chunyan; Li, Changcan; Tang, Kaifeng; Tang, Hongchao; Liao, Jiyuan

doi:10.7150/jca.26935

Cited by 2 publications

(2 citation statements)

References 44 publications

(71 reference statements)

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“…The tumor-promoting role of CCAR2 is further supported by recent meta-analyses 105 , 106 . Upregulation of CCAR2 is associated with short overall survival and relapse-free survival in various human cancers, suggesting that CCAR2 can be used as a prognostic marker for the survival of cancer patients and as a novel target for cancer therapy.…”

Section: Dual Function Of Ccar2 As a Tumor Suppressor And Tumor Promotermentioning

confidence: 76%

Mechanistic insights into the dual role of CCAR2/DBC1 in cancer

Kim,

Moon,

Kim

2023

Exp Mol Med

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Cell cycle and apoptosis regulator 2 (CCAR2), also known as deleted in breast cancer 1 (DBC1), has been recently identified as a master regulator of transcriptional processes and plays diverse roles in physiology and pathophysiology, including as a regulator of apoptosis, DNA repair, metabolism, and tumorigenesis. CCAR2 functions as a coregulator of various transcription factors and a critical regulator of numerous epigenetic modifiers. Based on its ability to stimulate apoptosis by activating and stabilizing p53, CCAR2 was initially considered to be a tumor suppressor. However, an increasing number of studies have shown that CCAR2 also functions as a tumor-promoting coregulator by activating oncogenic transcription factors and regulating the enzymatic activity of epigenetic modifiers, indicating that CCAR2 may play a dual role in cancer progression by acting as a tumor suppressor and tumor promoter. Here, we review recent progress in understanding the dual tumor-suppressing and oncogenic roles of CCAR2 in cancer. We discuss CCAR2 domain structures, its interaction partners, and the molecular mechanisms by which it regulates the activities of transcription factors and epigenetic modifiers.

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Section: Dual Function Of Ccar2 As a Tumor Suppressor And Tumor Promotermentioning

confidence: 76%

Mechanistic insights into the dual role of CCAR2/DBC1 in cancer

Kim,

Moon,

Kim

2023

Exp Mol Med

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“…Cancer is one of the leading causes of human disease-related death, and much attention regarding cancer treatment has focused on targeting and killing the tumor itself, e.g., radiation, chemotherapy, and targeted therapy. [1][2][3][4][5] Recently, cancer immunotherapy has become one of the most promising therapeutic pillars in improving patient survival. 6, 7 Unlike other cancer treatments, cancer immu-notherapy activates the host's immune system or relieves "immune exhaustion" in the tumor environment to eliminate cancer cells.…”

Section: Introductionmentioning

confidence: 99%

The Combination of LPS and Melatonin Induces M2 Macrophage Apoptosis to Prevent Lung Cancer

Gao¹,

Lin²,

Zhang³

et al. 2022

Explor Res Hypothesis Med

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Background and objectives: Lasting LPS stimulation changes macrophages toward the M2 phenotype therefore resulting in immunodepression. Melatonin can improve sleep, adjust the time difference, regulate immunity, and anti-tumor. This study is to observe whether melatonin can induce M2 macrophage apoptosis to reverse lasting LPS-induced immunodepression for lung cancer prevention and explore the possible mechanism. Methods:The effects of LPS alone or in combination with melatonin on macrophage phenotypes were assessed by surface markers, morphological changes, cytokines, autophagy, and autophagic efflux. The anti-cancer effect was evaluated in the lung carcinogenic model and lung cancer allograft model. Melatonin-related targets and pathways were predicted by network pharmacology.Results: Single LPS stimulation polarized macrophages to M1 phenotype, whereas LPS stimulation lasting for 7d polarized macrophages to M2 phenotype. However, combination treatment of lasting LPS and 10 µM melatonin inhibited the polarization of macrophages towards an M2-like phenotype and exerted a continuous antitumor effect. In the urethane-induced lung carcinoma model, long-lasting LPS administration (>4 times) facilitated macrophage polarization toward the M2 phenotype and promoted lung carcinogenesis, which was abrogated by macrophage depletion, while melatonin alone or in combination with lasting LPS could decrease M2-like macrophages and prevented carcinogenesis. In the Lewis lung cancer allograft model, melatonin decreased M2 macrophages and promoted the tumor-suppressing effect of short-term LPS administration (<4 times). Network pharmacology indicated that melatonin regulates macrophages by targeting the multi-protein network.Conclusions: Melatonin as a key maintainer of macrophage phenotype can induce LPS-stimulated M2 macrophage apoptosis to reverse system immunodepression for lung cancer prevention.

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Deleted in Breast Cancer 1 as a Novel Prognostic Biomarker for Digestive System Cancers: A Meta-Analysis

Cited by 2 publications

References 44 publications

Mechanistic insights into the dual role of CCAR2/DBC1 in cancer

Mechanistic insights into the dual role of CCAR2/DBC1 in cancer

The Combination of LPS and Melatonin Induces M2 Macrophage Apoptosis to Prevent Lung Cancer

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