Dietary flavonoid carvacrol triggers the apoptosis of human breast cancer MCF-7 cells via the p53/Bax/Bcl-2 axis

Moradipour, Ayat; Dariushnejad, Hassan; Ahmadizadeh, Changiz; Lashgarian, Hamed Esmaiil

doi:10.1007/s12032-022-01918-2

Cited by 11 publications

(6 citation statements)

References 25 publications

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“…These changes in apoptotic markers were in line with a rise in the number of cells that started early or late apoptosis after being exposed to SeNPs-CV, as shown in Figure 3. These results were in harmony with former studies [36,39], which stated that CV's anti-proliferative effects on metastatic BC cells were based on the typical apoptotic response, which includes a drop in mitochondrial membrane potential and a rise in cytochrome c discharge from mitochondria, a decline in the Bcl-2/Bax ratio, an elevation in caspase activity, PARP cleavage, and DNA fragmentation. In the same context, CV has also been observed to cause mitochondrial apoptosis in human oral squamous cell cancer [40], leukemia and lymphoma cells [13], and colon cancer cells [28] by disrupting matrix metalloproteinases (MMPs) and altering the expression rates of Bax/Bcl2 proteins.…”

Section: Discussionsupporting

confidence: 89%

The Potential Therapeutic Role of Green-Synthesized Selenium Nanoparticles Using Carvacrol in Human Breast Cancer MCF-7 Cells

et al. 2023

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The disadvantages and side effects of currently available breast cancer (BC) therapies have compelled researchers to seek new therapeutic strategies. This study was designed to investigate the effect of selenium nanoparticles biosynthesized with carvacrol (SeNPs-CV) on breast cancer (MCF-7) cell lines and to explore possible underlying pathways. Flow cytometry, MTT assays, and various biochemical techniques were used to evaluate the anti-proliferative effects of SeNPs-CV on MCF-7 cells. Cytotoxicity assays showed that treatment with SeNPs-CV could effectively reduce MCF-7 cell proliferation and viability in a dose-dependent manner. However, SeNPs-CV had no cytotoxic effect against Vero cells. Furthermore, SeNPs-CV showed better anticancer activity than metal nanoparticles of selenium evidenced by the lower IC50 obtained in MCF-7 cells (8.3 µg/mL versus 41.6 µg/mL, respectively). Treatment with SeNPs-CV directly targeted Bcl-2, Bax, and caspase-3, leading to the mitochondrial leakage of cytochrome C and subsequent activation of the apoptotic cascade in MCF-7 cells. In addition, MCF-7 cells treated with SeNPs-CV exhibited elevated levels of oxidative stress, as indicated by noticeable rises in 8-OHDG, ROS, NO, and LPO, paralleled by significant exhaustion in GSH levels and antioxidant enzymes activity. In addition, the administration of SeNPs-CV induced the inflammatory mediator IL-1β and downregulated the expression of cell-proliferating nuclear antigen (PCNA) in MCF-7 cells, which plays a critical role in apoptosis. Therefore, the ability of SeNPs-CV to fight BC may be due to its ability to induce oxidative stress, inflammation, and apoptosis in tumor cells. These findings demonstrate the therapeutic potential of Se nanoparticles conjugated with CV, which may provide a novel approach for combination chemotherapy in BC.

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Section: Discussionsupporting

confidence: 89%

The Potential Therapeutic Role of Green-Synthesized Selenium Nanoparticles Using Carvacrol in Human Breast Cancer MCF-7 Cells

et al. 2023

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“…Therefore, the Bax/Bcl-2 ratio is commonly used to assess the apoptotic status of cells. 42 In the present study, treatment with HCTMPPK resulted in a decrease in Bcl-2 and an increase in Bax expression, leading to apoptosis in A549 cells. This pro-apoptotic property may be attributed to the compound's ability to enhance cysteinase-3 activation while downregulate Bcl-2 and up-regulate Bax expression.…”

supporting

confidence: 47%

A Novel Tetramethylpyrazine Chalcone Hybrid- HCTMPPK, as a Potential Anti-Lung Cancer Agent by Downregulating MELK

Ma,

Cui,

Zhu

et al. 2024

DDDT

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Lung adenocarcinoma currently ranks the leading causes of cancer-related mortality worldwide. Many anti-inflammation herbs, like tetramethylpyrazine, have shown their anti-tumor potentials. Here, we evaluated the role of a novel chalcone derivative of tetramethylpyrazine ((E) -1-(E) -1-(2-hydroxy-5-chlorophenyl) -3-(3,5,6-trimethylpyrazin-2-yl) -2-propen-1, HCTMPPK) in lung adenocarcinoma. Methods: The effects of HCTMPPK on cell proliferation, apoptosis, and invasion were investigated by in-vitro assays, including CCK-8, colony formation assay, flow cytometry, transwell assay, and wound-healing assay. The therapeutic potential of HCTMPPK in vivo was evaluated in xenograft mice. To figure out the target molecules of HCTMPPK, a network pharmacology approach and molecular docking studies were employed, and subsequent experiments were conducted to confirm these candidate molecules. Results: HCTMPPK effectively suppressed the proliferative activity and migration, as well as enhanced the apoptosis of A549 cells in a concentration-dependent manner. Consistent with this, tumor growth was inhibited by HCTMPPK significantly in vivo. Regarding the mechanisms, HCTMPPK down-regulated Bcl-2 and MMP-9 and up-regulating Bax and cleaved-caspase-3. Subsequently, we identified 601 overlapping DEGs from LUAD patients in TCGA and GEO database. Then, 15 hub genes were identified by PPI network and CytoHubba. Finally, MELK was verified to be the HCTMPPK targeted site, through the molecular docking studies and validation experiments. Conclusion: Overall, our study indicates HCTMPPK as a potential MELK inhibitor and may be a promising candidate for the therapy of lung cancer.

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“…Of note, a number of studies have revealed that PTGS2, AKT, and ESR1 are key proteins involved in cancer cell proliferation, migration, and invasion, 42 − 44 while p53 and its downstream genes Bcl-2 and Bax play crucial roles in the apoptosis of tumor cells. 45 − 47 Importantly, we found that Cur markedly decreases AKT phosphorylation and subsequently inhibits PTGS2 and ESR1 expression, reducing the proliferation, migration, and invasion of colorectal cancer cells. In contrast, Cur induces cancer cell apoptosis by increasing P53 expression and decreasing the Bax/Bcl-2 ratio.…”

Section: Discussionmentioning

confidence: 73%

Exploration of the Molecular Mechanism of Curcuma aromatica Salisb’s Anticolorectal Cancer Activity via the Integrative Approach of Network Pharmacology and Experimental Validation

Yin,

Tan,

Jiang

2024

ACS Omega

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Curcuma aromatica Salisb (Cur), a well-known herbal medicine, has a wide spectrum of anti-inflammatory, anticarcinogenic, and antioxidant activities. However, the roles of its active compounds and potential mechanisms in colorectal cancer remain unknown. This research utilized network pharmacology and experimental validation to explore the possible mechanisms by which Cur protects against colorectal cancer. The active compounds of Cur and related genes for colorectal cancer were obtained from public databases. The DrugBank database was used to search for anticolorectal cancer drugs licensed through the FDA and their targets, and a "drug-component-target" relationship network was created using the Cytoscape program. The String database produced the PPI network. The ability of these active ingredients to bind to core targets was confirmed by molecular docking using AutoDock Vina. Cell and animal experiments were then carried out. A total of 274 targets were obtained from Cur, 49 of which were potential therapeutic targets. Four key targets, PTGS2, AKT1, TP53, and estrogen receptor 1 (ESR1), were screened via the PPI network and the FDA drug-target network. Molecular docking results revealed that Cur had strong binding abilities to these targets. In vivo and in vitro experiments demonstrated that Cur suppressed the development of colorectal cancer by regulating its targets (PTGS2, AKT1, TP53, and ESR1), which play crucial roles in promoting apoptosis and suppressing cell proliferation, migration, and invasion. Collectively, Cur protects against colorectal cancer by regulating the AKT1/PTGS2/ESR1 and P53 pathways, which lays the groundwork for further research and clinical applications of Cur in colorectal cancer therapy.

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Dietary flavonoid carvacrol triggers the apoptosis of human breast cancer MCF-7 cells via the p53/Bax/Bcl-2 axis

Cited by 11 publications

References 25 publications

The Potential Therapeutic Role of Green-Synthesized Selenium Nanoparticles Using Carvacrol in Human Breast Cancer MCF-7 Cells

The Potential Therapeutic Role of Green-Synthesized Selenium Nanoparticles Using Carvacrol in Human Breast Cancer MCF-7 Cells

A Novel Tetramethylpyrazine Chalcone Hybrid- HCTMPPK, as a Potential Anti-Lung Cancer Agent by Downregulating MELK

Exploration of the Molecular Mechanism of Curcuma aromatica Salisb’s Anticolorectal Cancer Activity via the Integrative Approach of Network Pharmacology and Experimental Validation

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