Berberine inhibits the chemotherapy‐induced repopulation by suppressing the arachidonic acid metabolic pathway and phosphorylation of <scp>FAK</scp> in ovarian cancer

Zhao, Yawei; Cui, Lianzhi; Pan, Yue; Shao, Dan; Zheng, Xiao; Zhang, Fan; Zhang, Hansi; He, Kan; Chen, Li

doi:10.1111/cpr.12393

Cited by 45 publications

(40 citation statements)

References 35 publications

(83 reference statements)

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“…Previous studies demonstrated that berberine possesses various pharmacological activities and may treat different diseases, such as sepsis, inflammation, diabetes and cancer, by multiple mechanisms, e.g., halting cell cycle progression and triggering apoptosis (Chen et al, 2017;Hou et al, 2017;Zou et al, 2017). In cancer cells, berberine could induce apoptosis and inhibit the chemotherapyinduced repopulation by suppressing the arachidonic acid metabolic pathway Zhao et al, 2017), enhance chemosensitivity through dose-orchestrated AMPK signaling , and reverses hypoxia-induced chemoresistance through the inhibition of AMPK-HIF-1a , In addition, berberine also plays a role in the regulation of immune response, oxidant stress, tissue fibrosis, and autophagy with low side effects and good resistance, suggesting its clinical and research values (Yang et al, 2019). In this study, berberine alone or in combination with doxorubicin maintained the N1 neutrophil phenotype to prevent carcinogenesis and chemotherapeutic resistance.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Berberine Maintains the Neutrophil N1 Phenotype to Reverse Cancer Cell Resistance to Doxorubicin

et al. 2020

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This study explores the contributions of neutrophils to chemotherapeutic resistance and berberine-regulated cancer cell sensitivity to doxorubicin (DOX). In vitro experiments, continuous DOX treatment led to the shift of HL-60 cells to N2 neutrophils and thus induced chemotherapeutic resistance. The combination treatment with DOX and 2 µM berberine resulted in the differentiation of HL-60 cells toward N1 and therefore stimulated HL-60 cell immune clearance. Berberine increased reactive oxygen species (ROS) and decreased autophagy and therefore induced apoptosis in HL-60-N2 cells with morphological changes, but had no effect on cell viability in HL-60-N1 cells. The neutrophil-regulating efficacy of berberine was confirmed in the urethane-induced lung carcinogenic model and H22 liver cancer allograft model. Furthermore, we found that DOX-derived neutrophils had high levels of CD133 and CD309 surface expression, which prevented both chemotherapeutic sensitivity and immune rejection by self-expression of PD-L1 and surface expression of PD-1 receptor on T cells, whereas berberine could downregulate CD133 and CD309 surface expression. Finally, berberine-relevant targets and pathways were evaluated. This study first suggests an important role of berberine in regulating neutrophil phenotypes to maintain cancer cell sensitivity to DOX.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Berberine Maintains the Neutrophil N1 Phenotype to Reverse Cancer Cell Resistance to Doxorubicin

et al. 2020

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“…Ovarian cancer is the most lethal gynecological malignancy and the fifth leading cause of cancer-associated deathin women (1,2). Ovarian cancers are responsible for more than half of the female genital tract cancers caused deaths, with more than 2 million new cases being diagnosed every year (1,3,4). Despite significant advances in surgery and chemotherapy, the long-term survival rate of patients with ovarian cancers is still very low (3).…”

Section: Introductionmentioning

confidence: 99%

SPARCL1 suppresses the proliferation and migration of human ovarian cancer cells via the MEK/ERK signaling

2018

Exp Ther Med

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Ovarian cancer is the most lethal gynecological malignancy worldwide and is one of the five leading causes of cancer-associated mortality in women. There is an urgent requirement to obtain a greater understanding of the molecular mechanism underlying ovarian cancer progression in order to identify novel drug targets and biomarkers. Secreted protein acidic and rich in cysteine-like protein 1 (SPARCL1) has been suggested as a candidate tumor suppressor in various types of human cancers. However, the potential role of SPARCL1 for ovarian cancer has not yet been clearly established. In the present study, lower protein expression levels of SPARCL1 were detected in ovarian cancer tissues when compared with adjacent normal tissues. Overexpression of SPARCL1 significantly suppressed the proliferation and migration of cells from the ovarian cancer cell line SKOV-3, whereas knockdown of SPARCL1 significantly increased cell growth and migration. Furthermore, the results revealed that SPARCL1 overexpression significantly suppressed the activation of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway. Collectively, these results indicated that SPARCL1 may suppress the proliferation and migration of ovarian cancer cells by downregulating signaling via the MEK/ERK pathway.

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“…Berberine (BBR) is an isoquinoline alkaloid extracted from the rhizomes of Coptis, which displays multiple biochemical functions and anti‐microbial and anti‐inflammatory activities . BBR also exhibits anti‐cancer activities through suppressing cell proliferation and inducing tumour cell apoptosis . BBR reportedly directly binds with DNA, radio‐sensitizes lung and oesophageal cancer cells and sensitizes ovarian cancer cells to cisplatin and PARP inhibitors .…”

Section: Introductionmentioning

confidence: 99%

“…14,15 BBR also exhibits anti-cancer activities through suppressing cell proliferation and inducing tumour cell apoptosis. [16][17][18][19][20][21][22] BBR reportedly directly binds with DNA, radio-sensitizes lung and oesophageal cancer cells and sensitizes ovarian cancer cells to cisplatin and PARP inhibitors. 23,24 Consequently, BBR may interfere with cellular DNA repair and would be a promising adjuvant agent to sensitize breast cancer cells to chemotherapeutic drugs.…”

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confidence: 99%

Berberine attenuates XRCC1‐mediated base excision repair and sensitizes breast cancer cells to the chemotherapeutic drugs

Gao

Wang

et al. 2019

J Cellular Molecular Medi

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Berberine (BBR) is a natural isoquinoline alkaloid, which is used in traditional medicine for its anti‐microbial, anti‐protozoal, anti‐diarrhoeal activities. Berberine interacts with DNA and displays anti‐cancer activities, yet its effects on cellular DNA repair and on synthetic treatments with chemotherapeutic drugs remain unclear. In this study, we investigated the effects of BBR on DNA repair and on sensitization of breast cancer cells to different types of DNA damage anti‐tumoural drugs. We found BBR arrested cells in the cell cycle S phase and induced DNA breaks. Cell growth analysis showed BBR sensitized MDA‐MB‐231 cells to cisplatin, camptothecin and methyl methanesulfonate; however, BBR had no synergistic effects with hydroxurea and olaparib. These results suggest BBR only affects specific DNA repair pathways. Western blot showed BBR down‐regulated XRCC1 expressions, and the rescued XRCC1 recovered the resistance of cancer cells to BBR. Therefore, we conclude that BBR interferes with XRCC1‐mediated base excision repair to sensitize cancer cells to chemotherapeutic drugs. These finding can contribute to understanding the effects of BBR on cellular DNA repair and the clinical employment of BBR in treatment of breast cancer.

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Berberine inhibits the chemotherapy‐induced repopulation by suppressing the arachidonic acid metabolic pathway and phosphorylation of FAK in ovarian cancer

Cited by 45 publications

References 35 publications

RETRACTED: Berberine Maintains the Neutrophil N1 Phenotype to Reverse Cancer Cell Resistance to Doxorubicin

RETRACTED: Berberine Maintains the Neutrophil N1 Phenotype to Reverse Cancer Cell Resistance to Doxorubicin

SPARCL1 suppresses the proliferation and migration of human ovarian cancer cells via the MEK/ERK signaling

Berberine attenuates XRCC1‐mediated base excision repair and sensitizes breast cancer cells to the chemotherapeutic drugs

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