Chemosensitizing Effect of Astragalus Polysaccharides on Nasopharyngeal Carcinoma Cells by Inducing Apoptosis and Modulating Expression of Bax/Bcl-2 Ratio and Caspases

Zhou, Zhen; Meng, Minhua; Ni, Haifeng

doi:10.12659/msm.903170

Cited by 38 publications

(29 citation statements)

References 39 publications

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“…For example, APS treatment suppressed the tumor growth in mice model of lung cancer [7]. APS inhibited the growth of nasopharyngeal carcinoma (NPC) cells and enhanced the therapeutic effect when combined with cisplatin in the xenograft model [8]. A clinical study has indicated the beneficial roles of APS combined with chemotherapy in advanced non-small-cell lung cancer (NSCLC) patients [9], with few associated side effects; however, the role and mechanisms of APS in OC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Astragalus polysaccharides inhibit ovarian cancer cell growth via microRNA-27a/FBXW7 signaling pathway

et al. 2020

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Astragalus polysaccharide (APS), a natural antioxidant found in Astragalus membranaceus emerging as a novel anticancer agent, exerts antiproliferative and pro-apoptotic activity in various cancer cell types, but its effect on ovarian cancer (OC) remains unknown. In the present study, we tried to elucidate the role and mechanism of APS in OC cells. Our results showed that APS treatment suppressed the proliferation and induced apoptosis in OC cells. Afterward, the microRNA (miRNA) profiles in APS-treated cells were determined by a microarray assay, and whether APS affected OV-90 cells through regulation of miRNA was determined. Among these aberrant miRNAs, miR-27a was selected for further study as its oncogenic roles in various human cancers. Moreover, we found overexpression of miR-27a reversed the antiproliferation and pro-apoptotic effects of APS on OC cells. F-box and WD-40 domain protein 7 (FBXW7), a classical tumor suppressor, was found directly targeted by miR-27a and its translation was suppressed by miR-27a in OC cells. Finally, it was also observed that knockdown of FBXW7 by si-FBXW7 reversed the tumor suppressive activity of APS in OC cells, which is similar to the effects of miR-27a overexpression. Our findings demonstrate that APS can suppress OC cell growth in vitro via miR-27a/FBXW7 axis, and this observation reveals the therapeutic potential of APS for treatment of OC.

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Section: Introductionmentioning

confidence: 99%

Astragalus polysaccharides inhibit ovarian cancer cell growth via microRNA-27a/FBXW7 signaling pathway

et al. 2020

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“…e proapoptosis gene Bax and the antiapoptosis gene Bcl-2 belong to the Bcl-2 family and play opposing roles in apoptosis regulation. Studies have confirmed that a shift in the Bax/Bcl-2 ratio is an important factor contributing to the low apoptosis rate of tumor cells and that this ratio is targeted by various antitumor drugs [27]. Our western blot results showed that isoimperatorin can inhibit the PCNA, XIAP, and survivin expression, upregulate the Bax expression, downregulate the Bcl-2 expression, and increase the Bax/Bcl-2 ratio, indicating that isoimperatorin-mediated inhibition of CNE2 cell proliferation is closely related to inhibition of DNA synthesis and induction of apoptosis-related protein expression.…”

Section: Discussionmentioning

confidence: 95%

Isoimperatorin Induces Apoptosis of Nasopharyngeal Carcinoma Cells via the MAPK/ERK1/2 Signaling Pathway

Liu

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Objective. To investigate the effect of isoimperatorin on nasopharyngeal carcinoma CNE2 cell apoptosis and the role of the MAPK/ERK1/2 signaling pathway in inducing apoptosis. Methods. Real-time cellular analysis technology (RTCA) and MTT were used to detect cell proliferation; Annexin V-FITC/PI dual-fluorescence flow cytometry analysis, Hoechst 33342 staining, and mitochondrial membrane potential detection kit were used to detect cell apoptosis; western blot was used to detect protein expression. Results. Different concentrations of isoimperatorin (10 μM, 20 μM, 30 μM, and 40 μM) significantly inhibited the nasopharyngeal carcinoma CNE2 cell proliferation, and 48 h later, the inhibitory effect of the 40 μM treatment was significantly higher than that of 10 μM and 20 μM. Treatment for 48 h significantly induced nasopharyngeal carcinoma cell apoptosis and resulted in nuclear pyknosis and fragmentation. At the same timepoint, the expression levels of proliferation-related protein PCNA as well as antiapoptosis proteins XIAP, survivin, and Bcl-2 were decreased by drug treatment, the expression level of proapoptosis protein Bax was increased, and the expression of the key MAPK/ERK1/2 signaling pathway proteins p-c-Raf, p-MEK, and p-ERK1/2 of were decreased. After activation of the MAPK/ERK1/2 signaling pathway by isoprenaline hydrochloride (ISO), the efficacy of isoimperatorin to downregulate p-c-Raf, p-MEK, and p-ERK1/2 expressions in the MAPK/ERK1/2 signaling pathway and proliferation-related protein PCNA as well as antiapoptosis proteins XIAP, surviving, and Bcl-2 was reduced compared with that of isoimperatorin alone, the effect of upregulating the proapoptotic protein Bax was reduced, and the apoptosis rate was also decreased. Conclusion. Isoimperatorin can induce nasopharyngeal carcinoma CNE2 cell apoptosis through the MAPK/ERK1/2 signaling pathway.

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“…Although chemotherapy and targeted therapy are effective methods for cancer patients, these therapeutic processes have drawbacks of systemic toxicity and drug resistance . To overcome these problems, studies on combined therapy have focused on identifying phytotherapeutic agents with known action mechanisms that can augment the therapeutic index of chemotherapeutic agents, such as Lentinan combined with oxaliplatin in hepatocellular carcinoma, baicalein combined with docetaxel in thyroid cancer cells, curcumin combined with platinum in ovarian cancer cells, and Astragalus polysaccharides combined with cisplatin in nasopharyngeal carcinoma cells . Early reports have indicated that licochalcone A has biological activities, including antiallergic, anti‐inflammation, antimycobacterial, and anticancer .…”

Section: Discussionmentioning

confidence: 99%

“…28,29 To overcome these problems, studies on combined therapy have focused on identifying phytotherapeutic agents with known action mechanisms that can augment the therapeutic index of chemotherapeutic agents, such as Lentinan combined with oxaliplatin in hepatocellular carcinoma, 30 baicalein combined with docetaxel in thyroid cancer cells, 31 curcumin combined with platinum in ovarian cancer cells, 32 and Astragalus polysaccharides combined with cisplatin in nasopharyngeal carcinoma cells. 33 Early reports have indicated that licochalcone A has biological activities, including antiallergic, antiinflammation, antimycobacterial, and anticancer. [6][7][8][9][10]34,35 Our present data provide evidence that licochalcone A can induce apoptotic cell fragmentation, apoptotic body formation, and caspase activation.…”

Section: Discussionmentioning

confidence: 99%

Licochalcone A induces apoptotic cell death via JNK/p38 activation in human nasopharyngeal carcinoma cells

Chuang

Tang

et al. 2019

Environmental Toxicology

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Licochalcone A is widely studied in different fields and possesses antiasthmatic, antibacterial, anti‐inflammatory, antioxidative, and anticancer properties. Its antimalignancy activity on renal, liver, lung, and oral cancer has been explored. However, limited studies have been conducted on the inhibitory effects of licochalcone A in human nasopharyngeal carcinoma cells. We determined cell viability using MTT assay. Cell cycle distribution and apoptotic cell death were measured via flow cytometry. Caspase activation and mitogen‐activated protein kinase‐related proteins in nasopharyngeal cancer cells in response to licochalcone A were identified by Western blot analysis. Results indicated that licochalcone A reduces cell viability and induces apoptosis, as evidenced by the upregulation of caspase‐8 and caspase‐9, caspase‐3 activation, and cleaved‐poly ADP‐ribose polymerase expression. Treatment with licochalcone A significantly increases ERK1/2, p38, and JNK1/2 activation. Co‐administration of a JNK inhibitor (JNK‐IN‐8) or p38 inhibitor (SB203580) abolishes the activation of caspase‐9, caspase‐8, and caspase‐3 protein expression during licochalcone A treatment. These findings indicate that licochalcone A exerts a cytostatic effect through apoptosis by targeting the JNK/p38 pathway in human nasopharyngeal carcinoma cells. Therefore, licochalcone A is a promising therapeutic agent for the treatment of human nasopharyngeal cancer cells.

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Chemosensitizing Effect of Astragalus Polysaccharides on Nasopharyngeal Carcinoma Cells by Inducing Apoptosis and Modulating Expression of Bax/Bcl-2 Ratio and Caspases

Cited by 38 publications

References 39 publications

Astragalus polysaccharides inhibit ovarian cancer cell growth via microRNA-27a/FBXW7 signaling pathway

Astragalus polysaccharides inhibit ovarian cancer cell growth via microRNA-27a/FBXW7 signaling pathway

Isoimperatorin Induces Apoptosis of Nasopharyngeal Carcinoma Cells via the MAPK/ERK1/2 Signaling Pathway

Licochalcone A induces apoptotic cell death via JNK/p38 activation in human nasopharyngeal carcinoma cells

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