A natural flavonoid, apigenin isolated from Clerodendrum viscosum leaves, induces G2/M phase cell cycle arrest and apoptosis in MCF-7 cells through the regulation of p53 and caspase-cascade pathway

Shendge, Anil Khushalrao; Chaudhuri, Dipankar; Basu, Tapasree; Mandal, Nripendranath

doi:10.1007/s12094-020-02461-0

Cited by 37 publications

(30 citation statements)

References 40 publications

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“…Our results were consistent with the results of other previous studies, in which Api was shown to induce apoptosis in different cancer cells, such as BC [24][25][26][27][28]35], ovarian cancer [45], and lung cancer [46]. Api exerts apoptotic effects through increases in the expression of p53 and the ratio of Bax/Bcl2, activation of caspases and cleavage of PARP [44][45][46]. Since the cell number is the result of cell proliferation, survival and cell death, the apoptotic effects of Api, accompanied by our results regarding the cell cycle, can explain the anti-proliferative effects of Api observed in our cell proliferation assays.…”

Section: Discussionsupporting

confidence: 93%

“…In that study, Ziegler et al showed that NB-73 decreased the expression of FOXM1 and simultaneously increased the accumulation of cells in the G2/M phases. Furthermore, the induction of G2/M phase cell cycle arrest by Api in MCF-7 cells was also recently documented by Shendge et al [44]. According to those authors, this effect of Api is due to its induction of intracellular ROS production.…”

Section: Discussionmentioning

confidence: 55%

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Apigenin, a Partial Antagonist of the Estrogen Receptor (ER), Inhibits ER-Positive Breast Cancer Cell Proliferation through Akt/FOXM1 Signaling

Pham

Page

Percevault

et al. 2021

IJMS

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Approximately 80% of breast cancer (BC) cases express the estrogen receptor (ER), and 30–40% of these cases acquire resistance to endocrine therapies over time. Hyperactivation of Akt is one of the mechanisms by which endocrine resistance is acquired. Apigenin (Api), a flavone found in several plant foods, has shown beneficial effects in cancer and chronic diseases. Here, we studied the therapeutic potential of Api in the treatment of ER-positive, endocrine therapy-resistant BC. To achieve this objective, we stably overexpressed the constitutively active form of the Akt protein in MCF-7 cells (named the MCF-7/Akt clone). The proliferation of MCF-7/Akt cells is partially independent of estradiol (E2) and exhibits an incomplete response to the anti-estrogen agent 4-hydroxytamoxifen, demonstrating the resistance of these cells to hormone therapy. Api exerts an antiproliferative effect on the MCF-7/Akt clone. Api inhibits the proliferative effect of E2 by inducing G2/M phase cell cycle arrest and apoptosis. Importantly, Api inhibits the Akt/FOXM1 signaling pathway by decreasing the expression of FOXM1, a key transcription factor involved in the cell cycle. Api also alters the expression of genes regulated by FOXM1, including cell cycle-related genes, particularly in the MCF-7/Akt clone. Together, our results strengthen the therapeutic potential of Api for the treatment of endocrine-resistant BC.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 55%

Apigenin, a Partial Antagonist of the Estrogen Receptor (ER), Inhibits ER-Positive Breast Cancer Cell Proliferation through Akt/FOXM1 Signaling

Pham

Page

Percevault

et al. 2021

IJMS

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“…Previous observations support our current results; these studies showed that cancer cell proliferation inhibition and apoptosis induction are mediated by oxidative stress induction [ 42 ]. Importantly, the induction of oxidative stress by metal-based drugs is believed to mediate the activation of autophagy-associated cell death pathway markers [ 43 ]. PtMet2 and PtMet2–PAMAM treatment also triggered autophagy, as evidenced by the resulted autophagosomes and the accumulations of LC3A/B and Beclin-1, which are commonly known as methods for monitoring autophagy.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Anticancer Action of Novel Imidazole Platinum(II) Complex Conjugated with G2 PAMAM-OH Dendrimer in Breast Cancer Cells

Czarnomysy

Muszyńska

Rok

et al. 2021

IJMS

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Transition metal coordination compounds play an important role in the treatment of neoplastic diseases. However, due to their low selectivity and bioavailability, as well as the frequently occurring phenomenon of drug resistance, new chemical compounds that could overcome these phenomena are still being sought. The solution seems to be the synthesis of new metal complexes conjugated with drug carriers, e.g., dendrimers. Numerous literature data have shown that dendrimers improve the bioavailability of the obtained metal complexes, solving the problem of their poor solubility and stability in an aqueous environment and also breaking down inborn and acquired drug resistance. Therefore, the aim of this study was to synthesize a novel imidazole platinum(II) complex conjugated with and without the second-generation PAMAM dendrimer (PtMet2–PAMAM and PtMet2, respectively) and to evaluate its antitumor activity. Cell viability studies indicated that PtMet2–PAMAM exhibited higher cytotoxic activity than PtMet2 in MCF-7 and MDA-MB-231 breast cancer cells at relatively low concentrations. Moreover, our results indicated that PtMet2–PAMAM exerted antiproliferative effects in a zebrafish embryo model. Treatment with PtMet2–PAMAM substantially increased apoptosis in a dose-dependent manner via caspase-9 (intrinsic pathway) and caspase-8 (extrinsic pathway) activation along with pro-apoptotic protein expression modulation. Additionally, we showed that apoptosis can be induced by activating POX, which induces ROS production. Furthermore, our results also clearly showed that the tested compounds trigger autophagy through p38 pathway activation and increase Beclin-1, LC3, AMPK, and mTOR inhibition. The high pro-apoptotic activity and the ability to activate autophagy by the imidazole platinum(II) complex conjugated with a dendrimer may be due to its demonstrated ability to reverse multidrug resistance (MDR) and thereby increase cellular accumulation in breast cancer cells.

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“…Moreover, Shendge et al . have previously isolated the ellagic acid[ 33 ] and apigenin[ 34 ] from the leaves of C. viscosum . In the present study, we have performed HPLC analysis and Figure 6 shows the presence of various phytocompounds such as catechin, tannic acid, reserpine, and rutin in the CVLME extract.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of anticancer activity of Clerodendrum viscosum leaves against breast carcinoma

2021

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A natural flavonoid, apigenin isolated from Clerodendrum viscosum leaves, induces G2/M phase cell cycle arrest and apoptosis in MCF-7 cells through the regulation of p53 and caspase-cascade pathway

Cited by 37 publications

References 40 publications

Apigenin, a Partial Antagonist of the Estrogen Receptor (ER), Inhibits ER-Positive Breast Cancer Cell Proliferation through Akt/FOXM1 Signaling

Apigenin, a Partial Antagonist of the Estrogen Receptor (ER), Inhibits ER-Positive Breast Cancer Cell Proliferation through Akt/FOXM1 Signaling

Mechanism of Anticancer Action of Novel Imidazole Platinum(II) Complex Conjugated with G2 PAMAM-OH Dendrimer in Breast Cancer Cells

Evaluation of anticancer activity of Clerodendrum viscosum leaves against breast carcinoma

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