Antitumor Activity of Copper (I)–Nicotinate Complex and Autophagy Modulation in HCC1806 Breast Cancer Cells

Abdel‐Mohsen, Mohamed A.; El‐Shafey, Eman Salah; Malak, Camelia A. Abdel; Abou-Yossef, Morsy M.

doi:10.2174/1871520617666170327144122

Cited by 17 publications

(22 citation statements)

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“…Microscopic examination showed alterations in the morphology of CNC-treated TNBC cells, which become more rounded, reflecting the antiproliferative activity CNC against the HCC-1806 cell line. These observations are in accordance with a previous study reported by Abdel-Mohsen et al 20 HCC-1806 cells treated with 1% or 10% of the IC 50 of CNC showed a significant increase in cell populations at early and late apoptotic phases, which reflects the machinery of cell death via apoptosis. However, at higher CNC concentration (ie, IC 50 ), the death mechanism involves cell necrosis rather than apoptosis, indicated by PI staining.…”

Section: Discussionsupporting

confidence: 93%

“…29 On the other hand, the anticancer activity of copper complexes including CNC has been previously suggested. 20,30 Therefore, throwing more light on the potential role of CNC as antitumor agent through affecting the apoptotic machinery was investigated in the TNBC cell line. Microscopic examination showed alterations in the morphology of CNC-treated TNBC cells, which become more rounded, reflecting the antiproliferative activity CNC against the HCC-1806 cell line.…”

Section: Discussionmentioning

confidence: 99%

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Oncostatic treatment effect of triple negative breast cancer cell line with copper (I)‐nicotinate complex

Abdel‐Mohsen

Toson

Helal

2018

J of Cellular Biochemistry

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The treatment of triple-negative breast cancer (TNBC) remains a major challenge. The present study aimed to throw more light on the role of copper (I)-nicotinate complex (CNC) as an antitumor as well as a proapoptotic agent. In this study, the HCC-1806 cell line was used as a model for TNBC. Cell cycle, apoptosis assay, and programmed cell death protein-1 were investigated by flowcytometry. Besides, the comet assay was performed using a fluorescence microscope. The enzyme-linked immunosorbent assay technique was used for the detection of phospho-Chk1 at ser 317 and caspase-3. Moreover, the gene expression of survivin was identified by real-time polymerase chain reaction.Finally, superoxide dismutase (SOD) was calorimetrically assayed. The viability of HCC-1806 cells treated with CNC was decreased in a dose-dependent manner. The tendency for apoptotic machinery was observed through the increase in the sub G0 peak, the percentage of early and late apoptotic phases, and the elevation in caspase-3 levels associated with a downregulation of the survivin gene expression. The antioxidant property of the complex, reflected by elevated SOD activity, may contribute to mediate the cell death pathways. Low concentrations of CNC were found to favor the apoptotis-mediated mechanism. However, one cannot neglect the abundance of cell necrosis-mediated death of cells via CNC, especially at higher concentrations.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Oncostatic treatment effect of triple negative breast cancer cell line with copper (I)‐nicotinate complex

Abdel‐Mohsen

Toson

Helal

2018

J of Cellular Biochemistry

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“…For example, Gambogic acid (GA), an anti-tumor drug and ROS inducer, cleaves and inactivates both p62 and Nbr1, among others, through ROS-mediated caspase activation (Ishaq et al, 2014 ). Furthermore, testing for possible anti-tumor effects of copper (I) nicotinate complex (CNC) on squamous cell cancer revealed that the drug could decrease general autophagy levels and elevate Nbr1 expression through yet unknown mechanisms (Abdel-Mohsen et al, 2017 ).…”

Section: Selective Autophagy Components In Cancermentioning

confidence: 99%

Hypoxia and Selective Autophagy in Cancer Development and Therapy

Daskalaki

Gkikas

Tavernarakis

2018

Front. Cell Dev. Biol.

135

103

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Low oxygen availability, a condition known as hypoxia, is a common feature of various pathologies including stroke, ischemic heart disease, and cancer. Hypoxia adaptation requires coordination of intricate pathways and mechanisms such as hypoxia-inducible factors (HIFs), the unfolded protein response (UPR), mTOR, and autophagy. Recently, great effort has been invested toward elucidating the interplay between hypoxia-induced autophagy and cancer cell metabolism. Although novel types of selective autophagy have been identified, including mitophagy, pexophagy, lipophagy, ERphagy and nucleophagy among others, their potential interface with hypoxia response mechanisms remains poorly understood. Autophagy activation facilitates the removal of damaged cellular compartments and recycles components, thus promoting cell survival. Importantly, tumor cells rely on autophagy to support self-proliferation and metastasis; characteristics related to poor disease prognosis. Therefore, a deeper understanding of the molecular crosstalk between hypoxia response mechanisms and autophagy could provide important insights with relevance to cancer and hypoxia-related pathologies. Here, we survey recent findings implicating selective autophagy in hypoxic responses, and discuss emerging links between these pathways and cancer pathophysiology.

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“…If the drug-induced autophagy, the expression of LC3-II would be further increased. 33 Therefore, after CQ or BafA1 pretreatment, JHC-4 further dramatically enhanced the expression of LC3-II compared with CQ or BafA1 alone (Figure 3). In brief, these data indicated that JHC-4 induced autophagy in gastric cancer cells.…”

Section: Discussionmentioning

confidence: 86%

<p><em>Camellia nitidissima</em> Chi Extract Potentiates the Sensitivity of Gastric Cancer Cells to Paclitaxel via the Induction of Autophagy and Apoptosis</p>

Xu¹,

Li²,

Zhan³

et al. 2019

OTT

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Background: Camellia nitidissima Chi (CNC) has been applied as a traditional folk medicine for the effective treatment of various diseases. However, there is little research regarding the mechanism of CNC on pharmaceutical function including anticancer effect. Materials and methods: JHC-4 is a n-butanol extract from CNC. The anti-proliferation effect was evaluated by MTT assays. Monodansylcadaverine (MDC) staining, Western blotting and autophagy inhibitors (CQ and BafA1) were applied to determine whether JHC-4 induced autophagy. The synergistic anticancer effect was evaluated by MTT assays, flow cytometry, Western blotting and autophagy inhibitors. Western blotting was used to explore the influence of PI3K/Akt/mTOR signaling pathway induced by drug treatment. Results: JHC-4 caused significant growth inhibition and induced autophagy in human gastric cancer cells. Moreover, JHC-4 as an autophagy agonist synergistically potentiated the sensitivity of gastric cancer cells to paclitaxel. Meanwhile, JHC-4 could significantly enhance the growth inhibition effect of paclitaxel by the induction of autophagy and apoptosis. Finally, we demonstrated that the PI3K/Akt/mTOR signaling pathway was involved in the synergistic anti-proliferation effect of JHC-4 and paclitaxel. Conclusion: All these data indicated that JHC-4 was a novel autophagy inducer when combination with paclitaxel for gastric cancer, which provided the scientific evidence for the use of this Chinese traditional medicine against cancer.

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Antitumor Activity of Copper (I)–Nicotinate Complex and Autophagy Modulation in HCC1806 Breast Cancer Cells

Abstract: CNC, as an autophagy inhibitor and pro-apoptotic agent, could be a promising anti-cancer agent either alone or in combination with other therapeutic drugs.

Cited by 17 publications

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Oncostatic treatment effect of triple negative breast cancer cell line with copper (I)‐nicotinate complex

Oncostatic treatment effect of triple negative breast cancer cell line with copper (I)‐nicotinate complex

Hypoxia and Selective Autophagy in Cancer Development and Therapy

<p><em>Camellia nitidissima</em> Chi Extract Potentiates the Sensitivity of Gastric Cancer Cells to Paclitaxel via the Induction of Autophagy and Apoptosis</p>

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