Fangchinoline Induces G1 Arrest in Breast Cancer Cells Through Cell‐Cycle Regulation

Xing, Zhibo; Zhang, Youxue; Zhang, Xianyu; Yang, Yanmei; Ma, Yuyan; Pang, Da

doi:10.1002/ptr.4936

Cited by 48 publications

(35 citation statements)

References 25 publications

(27 reference statements)

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“…Wogonin inhibited β-catenin-mediated transcription by interfering in the transcriptional activity of TCF/LEF, and repressing the kinase activity of CDK8, an oncogene involved in the development of colorectal cancers [98]. Lycoris is aurea agglutinin, which triggers the cell cycle arrest in G2/M phase via upregulating CDKN1A (p21) expression, as well as downregulating CDK1/cyclin A signaling pathway in human lung adenocarcinoma A549 cells [99]. …”

Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

et al. 2017

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Natural compounds from various plants, microorganisms and marine species play an important role in the discovery novel components that can be successfully used in numerous biomedical applications, including anticancer therapeutics. Since uncontrolled and rapid cell division is a hallmark of cancer, unraveling the molecular mechanisms underlying mitosis is key to understanding how various natural compounds might function as inhibitors of cell cycle progression. A number of natural compounds that inhibit the cell cycle arrest have proven effective for killing cancer cells in vitro, in vivo and in clinical settings. Significant advances that have been recently made in the understanding of molecular mechanisms underlying the cell cycle regulation using the chemotherapeutic agents is of great importance for improving the efficacy of targeted therapeutics and overcoming resistance to anticancer drugs, especially of natural origin, which inhibit the activities of cyclins and cyclin-dependent kinases, as well as other proteins and enzymes involved in proper regulation of cell cycle leading to controlled cell proliferation.

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Section: Cell Cycle Regulation By Natural Compounds Affecting Cyclinsmentioning

confidence: 99%

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

et al. 2017

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“…Fcn is a potent antioxidant, showing protective effects in oxidative cell injury [10]. This compound was also found to inhibit the growth of several cancers, such as lung cancer, breast cancer and prostate cancer, through proliferation inhibition and/or apoptosis [11][12][13][14] and induces autophagic cell death in hepatocellular cancer cells [15]. More recently, Fcn was found to block the well-known P-glycoprotein, indicating that Fcn may enhance the effects of chemotherapy drugs and prevents multidrug resistance [16].…”

Section: Introductionmentioning

confidence: 99%

Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

Fan¹,

Zhang²,

Ma³

et al. 2017

Cell Physiol Biochem

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Key Words Bladder cancer • Fangchinoline • Autophagy • Apoptosis • ProliferationAbatract Background/Aims: Tetrandrine and Fangchinoline (Fcn) are two natural products that are found in Stephania tetrandra. Tetrandrine is a known anti-bladder cancer compound, but the effects of Fcn on bladder cancer have been previously unclear. In the present study, we focused on the anti-tumor effects of Fcn on bladder cancer. Methods and Results: We treated T24 and 5637 bladder cancer cell lines with Fcn in vitro. We observed that Fcn inhibited the viability of bladder cancer cells in a concentration-dependent manner. The expression of PCNA, a biomarker of proliferation, was down-regulated. Fcn treatment induced both apoptosis and autophagy in bladder cancer cells, as shown by the increased cleavage of caspase-3, an upregulated LC3-II/LC3-I ratio and the down-regulated p62 level. Blocking autophagy with 3-MA (3-Methyladenine) enhanced Fcn-induced apoptosis, indicating that Fcn-induced autophagy was adaptive. Additionally, we observed that Fcn treatment inhibited mTOR and reduced the intracellular ATP levels. The exogenous addition of methyl pyruvate (MP) to compensate metabolic substrates alleviated Fcn-induced apoptosis and autophagy. Conclusions: Our data indicated that Fcn caused an impairment in energy generation, which led to apoptosis and adaptive autophagy in bladder cancer. These results demonstrated that Fcn may be a potential candidate for use in the prevention and treatment of bladder cancer.

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“…Cell cycle regulation plays a key role in controlling cell function and changing cell proliferation status. Abnormal cell cycle checkpoint could lead to genetic change, and may result in the malignant cell transformation (Xing et al, 2013). Differentially expressed gene PSMA7 has been demonstrated to interact with some important proteins involved in cell cycle transition and even tumor initiation and progression by previous study (Du et al, 2009).…”

Section: Age-related Differentially Expressed Genes Analysismentioning

confidence: 98%

Analysis of Different Activation Statuses of Human Mammary Epithelial Cells from Young and Old Groups

Feng

Chen²,

Chen³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Human mammary epithelial cells have different proliferative statuses and demonstrate a close relationship with age and cell proliferation. Research on this topic could help understand the occurrence, progression and prognosis of breast cancer. In this article, using significance analysis of a microarray algorithm, we analyzed gene expression profiles of human mammary epithelial cells of different proliferative statuses and different age groups. The results showed there were significant differences in gene expression in the same proliferation status between elderly and young groups. Three common differentially expressed genes were found to dynamically change with the proliferation status and to be closely related to tumorigenesis. We also found elderly group had less status-related differential genes from actively proliferating status to intermediate status and more statusrelated differential genes from intermediate status than the young group. Finally, functional enrichment analyses allowed evaluation of the detailed roles of these differentially-expressed genes in tumor progression.

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Fangchinoline Induces G1 Arrest in Breast Cancer Cells Through Cell‐Cycle Regulation

Cited by 48 publications

References 25 publications

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies

Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

Analysis of Different Activation Statuses of Human Mammary Epithelial Cells from Young and Old Groups

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