Alpinetin promotes Bax translocation, induces apoptosis through the mitochondrial pathway and arrests human gastric cancer cells at the G2/M phase

Wang, Zhenran; Lü, Wenjing; Li, Yang; Tang, Bo

doi:10.3892/mmr.2012.1243

Cited by 51 publications

(30 citation statements)

References 34 publications

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“…1A) is a natural flavonoid primarily derived from the roots or seeds of Alpinia katsumadai Hayata that is known to exhibit antibacterial, anti-inflammatory and other important therapeutic properties (12)(13)(14)(15)(16)(17)(18). In previous studies, alpinetin was reported to inhibit proliferation of human tumor cells, including lung cancer and gastroenteric cancer cells (12)(13)(14)(15)(16)19), indicating the potential anticancer properties of this compound. However, the effects of alpinetin on ovarian cancer cells and its underlying mechanisms of action remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Alpinetin inhibits proliferation and migration of ovarian cancer cells via suppression of STAT3 signaling

et al. 2018

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Natural bioactive components are increasingly being applied in cancer research. Alpinetin is a type of natural flavonoid primarily derived from Alpinia katsumadai Hayata, which exhibits anti‑bacterial and anti‑inflammatory properties. Therefore, it may possess anticancer potential and be employed therapeutically for different diseases. The aim of the present study was to investigate the anticancer effects of alpinetin on the SKOV3 ovarian cancer cell line. The effect of alpinetin treatment on SKOV3 cell proliferation, apoptosis, spheroid and colony formation were measured using Cell Counting kit‑8, cell apoptosis, 3D spheroid and colony formation assays, respectively. Analysis of the cell cycle was performed using flow cytometry. Western blot analysis was used to determine the protein expression levels of B‑cell lymphoma (Bcl)‑2, Bcl‑2‑associated X protein, cleaved caspase‑3, cleaved poly (ADP‑ribose) polymerase (PARP), cyclin D1, cyclin‑dependent kinase (CDK) 4, CDK6, signal transducer and activator of transcription (STAT) 3, phosphorylated (p)‑STAT3, c‑myc, survivin, tissue inhibitor of metalloproteinase (TIMP)‑1, TIMP‑2, matrix metalloproteinase (MMP)‑2 and MMP‑9. In addition, a wound healing assay was used to determine cancer cell migration. The results revealed alpinetin suppressed cell viability and induced apoptosis of SKOV3 cells in a dose‑ and time‑dependent manner, and cells were arrested in the G1 phase. Alpinetin treatment upregulated protein expression levels of Bax, cleaved caspase‑3 and PARP, and downregulated protein expression levels of Bcl‑2, cyclin D1, CDK4 and CDK6. Alpinetin also inhibited cell migration, through increased protein expression levels of TIMP‑1 and TIMP‑2, and decreased protein expression levels of MMP‑2 and MMP‑9. Alpinetin also significantly suppressed colony and spheroid formation by SKOV3 cells. In addition, the STAT3 pathway was suppressed as demonstrated by downregulation of p‑STAT3 and reduced expression of downstream factors, including c‑myc and survivin. Overall, these results indicated that alpinetin may have anticancer effects on human ovarian cancer by inhibiting the STAT3 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Alpinetin inhibits proliferation and migration of ovarian cancer cells via suppression of STAT3 signaling

et al. 2018

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“…A number of genes and proteins can influence or instigate the progression of apoptosis along the mitochondrial pathway (10). The most important genes associated with apoptosis are proteins of the Bcl family and caspases (11,12).…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin exerts neuroprotective effects against glutamate-induced PC12 cellular cytotoxicity by inhibiting apoptosis

Chen

Wang

Zhang

et al. 2017

International Journal of Molecular Medicine

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Paeoniflorin (PF) is an active ingredient of Radix Paeoniae, which is known to exert neuroprotective effects. However, the mechanims behind the neuroprotective effects of PF are not yet fully understood. The apoptosis of neurons plays an important role in the cerebral ischemia-induced cascade response. This study aimed to investigate neuroprotective effects of PF against glutamate-induced PC12 cellular cytotoxicity and to determine whether these effects are mediated via the inhibition of apoptosis in vitro and the activity of mitochondrial apoptosis-associated proteins in PC12 cells. Exposure of the PC12 cells to glutamate induced cell morphological changes, significantly decreased cell viability and induced apoptosis, with similar results being observed from the Hoechst 33342 staining and Annexin V/PI staining experiments. Glutamate also increased the lactate dehydrogenase release by the PC12 cells. However, treatment with PF prevented these effects. Furthermore, PF inhibited Bax and Bad expression and increased Bcl-2 and Bcl-xL expression; it also decreased the levels of downstream protein (caspase-3 and caspase-9). Collectively, our results indicate that PF protects PC12 cells against glutamate-induced neurotoxicity possibly through the inhibition of the expression of mitochondrial apoptosis-associated proteins.

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“…Mitochondrial dysfunction has been shown to induce apoptosis and is suggested to be central to the apoptotic pathway (23,24). As a group of proteolytic enzymes at the end of the apoptotic signaling pathway, the caspase family plays an essential role in apoptosis.…”

Section: Discussionmentioning

confidence: 99%

15‑hydroxy‑6α,12‑epoxy‑7β,10αH,11βH‑spiroax‑4‑ene‑12‑one exerts anti‑tumor effects against osteosarcoma through apoptosis induction

Chen

et al. 2020

Exp Ther Med

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Osteosarcoma is the most common type of malignant bone tumor, which has an overall survival rate of only 15-30%. The present study aimed to investigate the effects of 15-hydroxy-6α,12-epoxy-7β,10αH,11βH-spiroax-4-ene-1 2-one (HESEO), a compound extracted from the endophytic fungus Penicillium sp. FJ-1 isolated from Avicennia marina, on the proliferation of osteosarcoma cells and to explore its underlying mechanisms of action. Cell number was counted to measure the cell proliferation. JC-1 reagent was used to measure mitochondrial membrane potential. ELISA was used to measure the cytochrome c level and caspase activities. Apoptosis was detected by Annexin V-Propidium Iodide staining. Gene and protein expression were measured by reverse-transcription-PCR and western blot analysis, respectively. Additionally, the anti-tumor effects of HESEO were explored within a syngeneic osteosarcoma tumor model. The results suggested that HESEO significantly inhibited the proliferation of osteosarcoma cells and induced apoptosis of MG-63 cells, evidenced by their decreased mitochondrial membrane potential, and increased cytochrome c release, caspase activities and percentage of apoptotic cells. In addition, HESEO increased the expression of pro-apoptotic genes and proteins compared with control cells. The results indicated that HESEO may act through increasing p53 upregulated modulator of apoptosis expression. Furthermore, HESEO treatment significantly increased the survival time and decreased the tumor burden of osteosarcoma tumor-bearing mice compared with vehicle treatment. Furthermore, combined treatment with HESEO enhanced the effects of the chemotherapeutic agent methotrexate on a lung metastasis osteosarcoma model. These data suggested that HESEO could be developed as a potential anti-tumor agent against osteosarcoma.

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Alpinetin promotes Bax translocation, induces apoptosis through the mitochondrial pathway and arrests human gastric cancer cells at the G2/M phase

Cited by 51 publications

References 34 publications

Alpinetin inhibits proliferation and migration of ovarian cancer cells via suppression of STAT3 signaling

Alpinetin inhibits proliferation and migration of ovarian cancer cells via suppression of STAT3 signaling

Paeoniflorin exerts neuroprotective effects against glutamate-induced PC12 cellular cytotoxicity by inhibiting apoptosis

15‑hydroxy‑6α,12‑epoxy‑7β,10αH,11βH‑spiroax‑4‑ene‑12‑one exerts anti‑tumor effects against osteosarcoma through apoptosis induction

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