Anticancer effect of 2,7-dihydroxy-3-methylanthraquinone on human gastric cancer SGC-7901 cellsin vitroandin vivo

Zhu, Hai‐Tao; Zheng, Zhichao; Zhang, Jianjun; Li, Xiaoping; Liu, Yang; Yang, Wei; Liu, Yong; Zhang, Tao; Zhao, Yan; Liu, Yanqing; Su, Xiaohui; Gu, Xiaohu

doi:10.3109/13880209.2015.1033563

Cited by 10 publications

(7 citation statements)

References 28 publications

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“…26 Likewise, these findings are consistent with previous studies showing that chemotherapeutic sensitivity is enhanced by both rubimaillin and puerarin, which inhibit the expression of the mdr1 gene in breast cancer via the AMPK pathway. 30,31 Analogously, APS promotes glucose uptake in L6 myotubes through AMPK activation and, consequently, AS160/TBC1D4 phosphorylation. 24 However, it remains unclear whether APS regulates chemotherapeutic sensitivity of GC to adriamycin via the AMPK pathway.…”

Section: Discussionmentioning

confidence: 99%

Astragalus Polysaccharide Promotes Adriamycin-Induced Apoptosis in Gastric Cancer Cells

Song¹,

Chen²,

He³

et al. 2020

CMAR

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Astragalus polysaccharide (APS), a common Chinese herbal compound extracted from Astragalus membranaceus, has been proposed to increase the tumour response of and stabilize chemotherapy drugs while reducing their toxicity. Here, we examined the effects of APS on apoptosis in gastric cancer (GC) cells in the presence or absence of adriamycin (0.1 µg/mL). Methods: GC cells cultured in the presence or absence of adriamycin (0.1 µg/mL) were administered APS (50-200 µg/mL) for 24-72 h and subjected to an MTT assay to examine cell viability. Active caspase-3 expression and DNA fragmentation were assessed to evaluate apoptosis, and real-time PCR was used to analyse the expression levels of multidrug resistance (MDR1) genes and tumour suppressor genes. Western blot analysis was applied to detect cleaved caspase-3 and phosphorylated AMPK (p-AMPK). Results: Cellular viability was profoundly reduced by APS, and GC cell apoptosis was strongly increased by APS in a time-and dose-dependent manner; these changes may be linked to an increase in p-AMPK levels because the AMPK inhibitor compound C blocked the effects of APS. Similarly, adriamycin-induced decreases in cellular viability and apoptosis of GC cells were enhanced by APS administration. The expression of tumour suppressor genes (SEMA3F, P21 WAF1/CIP1 , FBXW7), but not of MDR1, was increased by APS compared to the control, and p-AMPK levels were lower in adriamycin-resistant GC cells than in either adriamycin-sensitive GC cells or an immortalized human gastric epithelial cell line. Conclusion: APS induces apoptosis independently and strengthens the proapoptotic effect of adriamycin on GC cells, suggesting that APS may act as a chemotherapeutic sensitizer.

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Section: Discussionmentioning

confidence: 99%

Astragalus Polysaccharide Promotes Adriamycin-Induced Apoptosis in Gastric Cancer Cells

Song¹,

Chen²,

He³

et al. 2020

CMAR

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“…Xenograft is an accepted model for investigating the effects of anti-carcinogenic agents, as well as their underlying mechanisms [15,16]. The results obtained in the xenograft assay revealed that DHF exerted significant inhibition on the growth of tumor tissue induced by HepG2 cells by reductions in levels of Survivin and Bcl-2, upregulation of Bax, c-caspase-9 and c-caspase-3 expressions, and increases in cytoplasmic levels of Smac and cytochrome c ( Figures 6 -8).…”

Section: Discussionmentioning

confidence: 99%

“…At the end of the treatment duration, the animals were sacrificed and the tumor tissues were excised and subjected to western blot assay. Tumor volume (TV) was estimated as in Eq 2 [16].…”

Section: Xenograft Studiesmentioning

confidence: 99%

Apoptosis-inducing effect of 6,7-dimethoxy-4'-hydroxy-8- formylflavon from Nicotiana tabacum L leaf in human hepatoma HepG2 cells via activation of mitochondriamediated apoptotic pathway

Zhang¹,

Qiu²,

Cui³

et al. 2018

Trop. J. Pharm Res

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Purpose: To study the anti-proliferative and apoptotic influences of 6,7-dimethoxy-4'-hydroxy-8formylflavon (DHF) from the leaves of Nicotiana tabacum L. in human hepatoma HepG2 cells, and the underlying mechanisms. Methods: The anti-proliferative effect of DHF (10-50 μg/mL) on HepG2 cells was assessed by CCK-8 assay. The pro-apoptotic effect of DHF (10, 20 and 30 μg/mL) on HepG2 cells was investigated via flow cytometry, while the mechanisms involved were studied using western blot. Xenograft assay was employed for determination of the in vivo effect of DHF (40 mg/kg/day) on HepG2 cell-induced tumor. Results: The proliferation of HepG2 cells was inhibited by DHF (IC50 = 25.87 μg/mL) due to apoptosis. In addition, xenograft assay revealed that HepG2 cell-induced tumor growth was significantly suppressed by DHF (p < 0.05 or 0.01) without any effects on mice body weights. The expressions of Survivin and Bcl-2 proteins were significantly decreased, while those of Bax, c-caspase-9, and ccaspase-3 proteins were significantly increased by DHF (p < 0.05 or 0.01), leading to increase in cytoplasmic levels of Smac and cytochrome c proteins. Conclusion: The underlying mechanism DHF-mediated apoptotic changes in HepG2 cells in vitro and in vivo involves induction of the mitochondrial pathway of apoptosis. Thus, DHF is a good drug candidate for the development of an effective therapy for liver cancer.

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“…2, 7dihydroxy-3-methylanthraquinone (DDMN), a flavone isolated from Hedyotis diffusa Willd. Herba, induced caspase-dependent apoptosis of SGC-7901 gastric cancer cells [48]. 6, 7, 30-trimethoxy-3, 5, 40-trihydroxy flavone (TTF), extracted from Chrysosplenium nudicaule Ledeb.…”

Section: Apoptosis-inducing Natural Molecules In Gastric Cancermentioning

confidence: 99%

“…Wu et al revealed that phenolic alkaloids of Menispermum dauricum induced apoptosis and suppressed gastric tumor growth by inducing apoptosis and inhibiting oncogenic Kirsten Rat sarcoma viral oncogene homolog (K-RAS) expression [42]. Xenograft mice treated with trifolirhizin, DDMN or arsenic trioxide developed smaller tumors compared to the control group [44,48,69]. When BALB/C mice grafted with MFC mouse gas-tric cancer cells were treated curcumin solution every day for 60 days, expressions of interferon gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), granzyme B, and perforin were upregulated while differentiated embryonic chondrocyte gene 1 (DEC1), hypoxiainducible factor-1 alpha (HIF-1α), STAT3 and VEGF expressions were downregulated in the experimental group [71].…”

Section: Apoptosis-inducing Natural Molecules In Gastric Cancermentioning

confidence: 99%

Emerging Potential of Naturally Occurring Molecules against Gastric Cancer: Insights Molecular Mechanism and Therapeutic Targets

Kang¹,

Hwang²,

Shin³

et al. 2021

Preprint

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Gastric cancer, also known as stomach cancer, is a cancer which develops from the lining of the stomach. Accumulated evidences and epidemiological studies have been indicated that natural products play an important role in gastric cancer prevention and treatment, although its mechanism of action did not elucidate yet. Particularly, experimental studies have been showed that natural products displayed a protective effect against gastric cancer via numerous molecular mechanisms such as suppression of cell metastasis, anti-angiogenesis, inhibition of cell proliferation, induction of apoptosis, and modulation of autophagy. Although chemotherapy remains the standard treatment for advanced gastric cancer along with surgery, radiation therapy, hormone therapy and immunotherapy, but its adverse side effects including neutropenia, stomatitis, mucositis, diarrhea, nausea, and emesis are well documented. Additionally, intake of naturally occurring phytochemicals could increase the efficacy of gastric chemotherapy and chemotherapeutics resistance. However, natural product structural stability and powerful bioactivity are important to develop novel treatments for gastric cancer that may minimize such adverse effects. Therefore, the purpose of this review is to summarize the potential therapeutic effects of natural products on prevention and treatment of gastric cancer with intensive molecular mechanisms of action, bioavailability, and safety efficacy.

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Anticancer effect of 2,7-dihydroxy-3-methylanthraquinone on human gastric cancer SGC-7901 cellsin vitroandin vivo

Cited by 10 publications

References 28 publications

<p>Astragalus Polysaccharide Promotes Adriamycin-Induced Apoptosis in Gastric Cancer Cells</p>

<p>Astragalus Polysaccharide Promotes Adriamycin-Induced Apoptosis in Gastric Cancer Cells</p>

Apoptosis-inducing effect of 6,7-dimethoxy-4'-hydroxy-8- formylflavon from <i>Nicotiana tabacum</i> L leaf in human hepatoma HepG2 cells via activation of mitochondriamediated apoptotic pathway

Emerging Potential of Naturally Occurring Molecules against Gastric Cancer: Insights Molecular Mechanism and Therapeutic Targets

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