Breast cancer: Small molecules targeting apoptosis, a prospective approach to safe scientific success

Choene, Mpho; Mthembu, Nonkululeko; Dlamini, Zodwa; Mokgotho, M. P.; Wachira, James; Motadi, Lesetja Raymond

doi:10.4236/abb.2012.37104

Cited by 2 publications

(3 citation statements)

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“…BRCA1 tumor suppressor gene induces apoptosis through both intrinsic and extrinsic pathways. However, BRCA1 acts through both P53-dependent and P53-independent pathways and JNK signaling pathway and GADD45 are involved in P53-independent pathway (Fabbro et al, 2004;Ostrakhovitch and Cherian, 2005;Choene et al, 2012;Kim, 2017). The result of the present study showed that the expression of BRCA1 and GADD45 increased following treatment with myricetin.…”

Section: Discussionsupporting

confidence: 43%

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Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach

Soleimani

Sajedi

2020

Asian Pac J Cancer Prev

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Objective: Using nutraceuticals in cancer therapy is a strategy contributing with other approaches to promote apoptosis in cancer cells. Myricetin is a polyphenol flavonoid that forms main ingredients of various type of foods and beverages. The inducing properties of myricetin in apoptosis is reported by several investigations. The present study aimed to assess apoptotic effects of myricetin on T47D breast cancer cells and to evaluate part of the mechanisms of action. Materials and Methods: T47D breast cancer cells were assigned into five groups: control (cells in normal condition), myricetin (cells treated with myricetin IC50 concentration) in two different incubation times (24, 48 and 72 hours). MTT assay, annexin v assay, flow cytometry, caspase-3 assay and Real-time PCR were used to evaluate apoptosis in breast cancer cells. Results: The expression rate of apoptotic genes caspase-3, caspase-8, caspase-9 , the ratio of BAX /Bcl-2 as well as the expression of P53, BRCA1, GADD45 genes were increased significantly after treatment of T47D breast cancer cells with myricetin. Annexin v assay confirmed significant expression of annexin as were displyed by flow cytometry. Conclusion: Myricetin enhances apoptosis in T47D breast cancer cells by evoking both extrinsic and intrinsic apoptotic pathways. myricetin may practices its apoptotic properties on T47D cells through inducing BRCA1- GADD45 pathway.

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Section: Discussionsupporting

confidence: 43%

“…BRCA1 induces cell apoptosis in both TP53-dependent and TP53-independent pathways. In TP53-independent pathway, c-Jun N-terminal kinase (JNK) signaling pathway and the GADD45 gene are involved (Fabbro et al, 2004;Ostrakhovitch and Cherian, 2005;Choene et al, 2012;Kim, 2017).…”

Section: Introductionmentioning

confidence: 99%

Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach

Soleimani

Sajedi

2020

Asian Pac J Cancer Prev

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“…Indeed, deposition of β-catenin transferred from cytoplasm to the nucleus and activated the transcription genes mediated by T-cell factor/lymphoid enhancer factor (TCF/LEF) related to the formation of breast tumor [20,21]. However, as the downstream gene of the Wnt/β-catenin signaling pathway, c-Myc affects the tumor cell cycle by inhibiting growth suppression gene transcription and was significantly increased in Tun + Li group compared with Tun treatment (Figure 3(c)), which could lead to poor survival and continuous growing of MDA-MB-231 cells [22]. Recently, Xu et al also found similar experiment results and investigated the possibility that Schisandrin A could suppress the cell cycle and introduce apoptosis of cells in TNBC though the Wnt/ER stress signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Tunicamycin-Induced Endoplasmic Reticulum Stress Promotes Breast Cancer Cell MDA-MB-231 Apoptosis through Inhibiting Wnt/β-Catenin Signaling Pathway

You

Yan

2021

Journal of Healthcare Engineering

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Triple negative breast cancer (TNBC) has significantly threatened human health. Many aspects of TNBC are closely related to Wnt/β-catenin pathway, and cell apoptosis induced by endoplasmic reticulum stress (ER stress) in TNBC may act as a potential target of non-chemotherapy treatment. However, how ER stress interacts with this pathway in TNBC has not yet been understood. Here, the tunicamycin and LiCl have been applied to MDA-MB-231. The related proteins’ expression was measured by western blotting. Moreover, acridine orange/ethidium bromide (AO/EB) staining was applied to test the apoptosis degree of the cells, and cell viability was tested by MTT experiment. Then, we found the ER stress and apoptosis degree of MDA-MB-231 were induced after treatment with tunicamycin. Besides, tunicamycin dose dependently inhibited both Wnt/β-catenin pathway and cells viability. Licl, an activator of Wnt/β-catenin signaling pathway, could significantly inhibit cell apoptosis. In conclusion, our study found that the activation of ER stress could promote the MDA-MB-231 apoptosis by repressing Wnt/β-catenin pathway, which provides some promising prospects and basic mechanism to the further research.

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Breast cancer: Small molecules targeting apoptosis, a prospective approach to safe scientific success

Cited by 2 publications

References 62 publications

Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach

Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach

Tunicamycin-Induced Endoplasmic Reticulum Stress Promotes Breast Cancer Cell MDA-MB-231 Apoptosis through Inhibiting Wnt/β-Catenin Signaling Pathway

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