Berberine exerts anti-tumor activity in diffuse large B-cell lymphoma by modulating c-myc/CD47 axis

Ren, Shuai; Cai, Yin; Hu, Shunfeng; Liu, Jiarui; Zhao, Yi; Ding, Mingmin; Chen, Xiaomin; Zhan, Linquan; Zhou, Xiangxiang; Wang, Xin

doi:10.1016/j.bcp.2021.114576

Cited by 27 publications

(18 citation statements)

References 54 publications

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“…CD47 is located on the surface of cancer cells and interacts with signal-regulatory protein alpha (SIRP-α) to induce tolerance in immune cells, prevent cancer cells phagocytosis, and prolong cancer cells survival in pancreatic cancer. 120 , 121 CD47 blockade enhanced the antitumor function of CD8 + T cells and macrophages in the mice model of pancreatic cancer. 122 Likewise, immunotherapy with CD47-CAR-T cells significantly reduced pancreatic cancer cells population and prevent pancreatic cancer growth in mice.…”

Section: The Effect Of C-myc On Cancer Cells Metabolismmentioning

confidence: 96%

Target c-Myc to treat pancreatic cancer

Ala

2022

Cancer Biology & Therapy

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C-Myc overexpression is a common finding in pancreatic cancer and predicts the aggressive behavior of cancer cells. It binds to the promoter of different genes, thereby regulating their transcription. C-Myc is downstream of KRAS and interacts with several oncogenic and proliferative pathways in pancreatic cancer. C-Myc enhances aerobic glycolysis in cancer cells and regulates glutamate biosynthesis from glutamine. It provides enough energy for cancer cells’ metabolism and sufficient substrate for the synthesis of organic molecules. C-Myc overexpression is associated with chemoresistance, intra-tumor angiogenesis, epithelial-mesenchymal transition (EMT), and metastasis in pancreatic cancer. Despite its title, c-Myc is not “undruggable” and recent studies unveiled that it can be targeted, directly or indirectly. Small molecules that accelerate c-Myc ubiquitination and degradation have been effective in preclinical studies. Small molecules that hinder c-Myc-MAX heterodimerization or c-Myc/MAX/DNA complex formation can functionally inhibit c-Myc. In addition, c-Myc can be targeted through transcriptional, post-transcriptional, and translational modifications.

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Section: The Effect Of C-myc On Cancer Cells Metabolismmentioning

confidence: 96%

Target c-Myc to treat pancreatic cancer

Ala

2022

Cancer Biology & Therapy

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“…Aiming at the same target, increasing the effect of the former drug or improving the microenvironment in which the drug acts, all may effectively increase clinical efficacy. The primary metabolites of the C. Rhizoma extract, known as natural deep eutectic solvents, improves the pharmacokinetics of orally administered berberine (Zhao J. et al, 2021).…”

Section: Synergistic Effectsmentioning

confidence: 99%

“…CD47 is a target for improving treatment efficacy, and the overexpression of CD47 is related to immune escape ( Casey et al, 2016 ; Takimoto et al, 2019 ; Eladl et al, 2020 ). Berberine, a suppressor of CD47, downregulates CD47 mRNA by suppressing c-Myc expression ( Ren et al, 2021 ). The suppression of CD47 enhances the phagocytosis of macrophages, which contributes to eliminate diffuse large B-cell lymphoma cells both in vitro and in vivo .…”

Section: Antitumor Effects and Corresponding Mechanismsmentioning

confidence: 99%

“…In addition, berberine can improve the efficiency of the anti-CD47 antibody and rituximab on cell phagocytosis ( Chao et al, 2010 ; Weiskopf et al, 2016 ; Schürch et al, 2019 ). Berberine is beneficial in immunochemotherapy based on rituximab in combination with anti-CD47 in diffuse large B-cell lymphoma ( Harris et al, 2020 ; Ren et al, 2021 ).…”

Section: Antitumor Effects and Corresponding Mechanismsmentioning

confidence: 99%

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Current Advances in Coptidis Rhizoma for Gastrointestinal and Other Cancers

Chen

Liang

et al. 2022

Front. Pharmacol.

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Cancer is a serious disease with an increasing number of reported cases and high mortality worldwide. Gastrointestinal cancer defines a group of cancers in the digestive system, e.g., liver cancer, colorectal cancer, and gastric cancer. Coptidis Rhizoma (C. Rhizoma; Huanglian, in Chinese) is a classical Chinese medicinal botanical drug for the treatment of gastrointestinal disorders and has been shown to have a wide variety of pharmacological activity, including antifungal, antivirus, anticancer, antidiabetic, hypoglycemic, and cardioprotective effects. Recent studies on C. Rhizoma present significant progress on its anticancer effects and the corresponding mechanisms as well as its clinical applications. Herein, keywords related to C. Rhizoma, cancer, gastrointestinal cancer, and omics were searched in PubMed and the Web of Science databases, and more than three hundred recent publications were reviewed and discussed. C. Rhizoma extract along with its main components, berberine, palmatine, coptisine, magnoflorine, jatrorrhizine, epiberberine, oxyepiberberine, oxyberberine, dihydroberberine, columbamine, limonin, and derivatives, are reviewed. We describe novel and classic anticancer mechanisms from various perspectives of pharmacology, pharmaceutical chemistry, and pharmaceutics. Researchers have transformed the chemical structures and drug delivery systems of these components to obtain better efficacy and bioavailability of C. Rhizoma. Furthermore, C. Rhizoma in combination with other drugs and their clinical application are also summarized. Taken together, C. Rhizoma has broad prospects as a potential adjuvant candidate against cancers, making it reasonable to conduct additional preclinical studies and clinical trials in gastrointestinal cancer in the future.

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“…Furthermore, myc overexpression is associated with early disease progression from myelodysplastic syndromes to AML ( 93 ). For these reasons, different treatment modalities targeting the myc/CD47 axis are tested for therapeutic usage ( 94 , 95 ). Myc has also been involved in the evasion from natural killer (NK) cell surveillance by reducing the expression of ligands for the NKG2D activating receptor ( 96 ).…”

Section: Oncogenic and Tsg Pathways In Tumors Influence The Frequency...mentioning

confidence: 99%

Modulation of Lymphocyte Functions in the Microenvironment by Tumor Oncogenic Pathways

Seliger

Massa

2022

Front. Immunol.

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Despite the broad application of different immunotherapeutic strategies for the treatment of solid as well as hematopoietic cancers, the efficacy of these therapies is still limited, with only a minority of patients having a long-term benefit resulting in an improved survival rate. In order to increase the response rates of patients to the currently available immunotherapies, a better understanding of the molecular mechanisms underlying the intrinsic and/or extrinsic resistance to treatment is required. There exist increasing evidences that activation of different oncogenic pathways as well as inactivation of tumor suppressor genes (TSG) in tumor cells inhibit the immune cell recognition and influegnce the composition of the tumor microenvironment (TME), thus leading to an impaired anti-tumoral immune response. A deeper understanding of the link between the tumor milieu and genomic alterations of TSGs and oncogenes is indispensable for the optimization of immunotherapies and to predict the patients’ response to these treatments. This review summarizes the role of different cancer-related, oncogene- and TSG-controlled pathways in the context of anti-tumoral immunity and response to different immunotherapies.

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Berberine exerts anti-tumor activity in diffuse large B-cell lymphoma by modulating c-myc/CD47 axis

Cited by 27 publications

References 54 publications

Target c-Myc to treat pancreatic cancer

Target c-Myc to treat pancreatic cancer

Current Advances in Coptidis Rhizoma for Gastrointestinal and Other Cancers

Modulation of Lymphocyte Functions in the Microenvironment by Tumor Oncogenic Pathways

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