Dose- and time-dependent effects of doxorubicin on cytotoxicity,cell cycle and apoptotic cell death in human colon cancer cells

The cytostatic drug doxorubicin is a well-known chemotherapeutic agent which is used in treatment of a wide variety of cancers. A key factor in the response of cancer cells to chemotherapeutic drugs is the activation of the apoptotic pathway, a pathway that is often impaired in chemoresistant colon cancer cells. The aim of the present study was to investigate the effects of doxorubicin in Hct-116 human colon carcinoma cells in order to clarify if a time/concentration range for optimal doxorubicin-induced apoptosis exists. We compared a treatment schedule were cells were bolus incubated for 3 h with doxorubicin followed by 24 h in drug-free medium, with a continuous doxorubicin treatment schedule for 24 h. Bolus incubation was carried out to determine effects of doxorubicin accumulated during the first 3 h, whereas continuous incubation allowed further (continuous) exposure to doxorubicin. We found that bolus (3 h) treatment with doxorubicin resulted in a dose-dependent decrease of viable cells and concomitant increase of apoptosis. Additionally, bolus (3 h) doxorubicin incubation led to phosphorylation of p53 at serine 392, induction of p21, G2 arrest and increase of proapoptotic protein Bax. In contrast, continuous (24 h) treatment with doxorubicin reduced the number of living cells with no parallel raise in the amount of dead cells. Continuous (24 h) treatment with 5 μM doxorubicin resulted in cell cycle arrest in G0/G1 phase that was neither accompanied by phosphorylation and activation of p53 nor enhanced expression of p21. These results suggest that doxorubicin is able to induce cell death by apoptosis only at particular dose and treatment conditions and imply a completely different cellular response following bolus or continuous exposure to doxorubicin.     

Chelerythrine and dihydrochelerythrine induce G1 phase arrest and bimodal cell death in human leukemia HL-60 cells

A quaternary benzo[c]phenanthridine alkaloid chelerythrine displays a wide range of biological activities including cytotoxicity to normal and cancer cells. In contrast, less is known about the biological activity of dihydrochelerythrine, a product of chelerythrine reduction. We examined the cytotoxicity of chelerythrine and dihydrochelerythrine in human promyelocytic leukemia HL-60 cells. After 4 h of treatment, chelerythrine induced a dose-dependent decrease in the cell viability with IC₅₀ of 2.6 μM as shown by MTT reduction assay. Dihydrochelerythrine appeared to be less cytotoxic since the viability of cells exposed to 20 μM dihydrochelerythrine for 24 h was reduced only to 53%. Decrease in the viability induced by both alkaloids was accompanied by apoptotic events including the dissipation of mitochondrial membrane potential, activation of caspase-9 and -3, and appearance of cells with sub-G1 DNA. Moreover, chelerythrine, but not dihydrochelerythrine, elevated the activity of caspase-8. A dose-dependent induction of apoptosis and necrosis by chelerythrine and dihydrochelerythrine was confirmed by annexin V/propidium iodide dual staining flow cytometry. Besides, both alkaloids were found to induce accumulation of HL-60 cells in G1 phase of the cell cycle. We conclude that both chelerythrine and dihydrochelerythrine affect cell cycle distribution, activate mitochondrial apoptotic pathway, and induce apoptosis and necrosis in HL-60 cells.     

Antiproliferative effects of quercetin through cell cycle arrest and apoptosis in human breast cancer MDA-MB-453 cells

To explore the anticancer effects of the flavonoid quercetin on human breast cancer MDA-MB-453 cells via cell cycle regulation and the induction of apoptosis, the antiproliferative effect of quercetin was first examined by MTT assay. When MDA-MB-453 cells were treated with quercetin for various periods of time (3–24 hrs) and at various doses (1–100 μM), cell growth decreased significantly in a time-and dose-dependent manner. To elucidate the mechanism underlying the antiproliferative effect of quercetin, cell cycle progression and the induction of apoptosis in MDA-MB-453 cells exposed to 100 μM quercetin for 24 hrs were investigated. Quercetin caused a remarkable increase in the number of sub-G1 phase cells, and an Annexin-V assay revealed that exposure to quercetin affected apoptosis. Moreover, treatment with quercetin increased Bax expression but decreased Bcl-2 expression. Cleaved caspase-3 and PARP expression was also increased by quercetin. Thus, quercetin has probable anticancer activity. Our results suggest the existence of multiple pathways for the induction of cell cycle arrest and apoptosis by quercetin.     

Arctigenin induces cell cycle arrest by blocking the phosphorylation of Rb via the modulation of cell cycle regulatory proteins in human gastric cancer cells

Gastric cancer is a leading cause of cancer-related deaths, worldwide being second only to lung cancer as a cause of death. Arctigenin, a representative dibenzylbutyrolactone lignan, occurs in a variety of plants. However, the molecular mechanisms of arctigenin for anti-tumor effect on gastric cancer have not been examined. This study examined the biological effects of arctigenin on the human gastric cancer cell line SNU-1 and AGS. Cell proliferation was determined by MTT assay. In MTT assay, the proliferation of SNU-1 and AGS cells was significantly inhibited by arctigenin in a time and dose dependent manner, as compared with SNU-1 and AGS cells cultured in the absence of arctigenin. Inhibition of cell proliferation by arctigenin was in part associated with apoptotic cell death, as shown by changes in the expression ratio of Bcl-2 to Bax by arctigenin. Also, arctigenin blocked cell cycle arrest from G₁ to S phase by regulating the expression of cell cycle regulatory proteins such as Rb, cyclin D1, cyclin E, CDK4, CDK2, p21Waf1/Cip1 and p15 INK4b. The antiproliferative effect of arctigenin on SNU-1 and AGS gastric cancer cells revealed in this study suggests that arctigenin has intriguing potential as a chemopreventive or chemotherapeutic agent.     

Tebufenozide induces G1/S cell cycle arrest and apoptosis in human cells

Tebufenozide is a non-steroidal insect growth regulator and is extensively used to control pests, although it is considered to be safe for mammals and environmentally friendly. However, previous studies have found that tebufenozide is cytotoxic to man, although the exact mechanism remains elusive. This study will investigate the apoptotic molecular mechanisms which result from tebufenozide-induced DNA damage in HeLa cells. Our results demonstrate that tebufenozide could trigger arrest in G1/S phase related to a downregulation of cyclin E and cyclin-dependent kinase (CDK) 2 protein. In addition, Western blotting showed apoptosis was associated with the upregulation of p53, Bax and cleaved-PARP, as well as downregulation of Bcl-2 and PARP. Tebufenozide also regulated changes in mitochondrial permeability and reduced mitochondrial number and intracellular ATP production. Briefly, these results suggest that tebufenozide- induces cell cycle arrest and apoptosis through activating p53 protein in a Bax- and Bcl-2-triggered mitochondrial pathway. This work provides some scientific context for the safe use of tebufenozide in agriculture.     

Luteolin induced G2 phase cell cycle arrest and apoptosis on non-small cell lung cancer cells

In this study, we investigated the underlying molecular mechanism for the potent cell cycle inhibition and pro-apoptotic effect of luteolin (2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4-chromenone) on human non-small-cell lung carcinoma cell line A549. MTT assay showed that luteolin had obvious cytotoxicity on A549 with IC₅₀ of 40.2 μM at 48 h. Pro-apoptotic effect of luteolin on A549 cells was demonstrated by Hoechst 33258 staining assay and annexin V-FITC/PI double staining analysis. A great quantity of apoptotic cells and increasing G2 phase cells were observed by flow cytometry. Western blotting assay revealed that luteolin activated JNK, increased Bax, promoted procaspase-9 cleavage and activated caspase-3 at last. Assay using TNFα, an active agent of NF-κB, showed that pretreatment of A549 cells with luteolin could inhibit TNFα induced trans-nuclear of NF-κB. In summary, luteolin displayed a significant cytotoxic effect through cell cycle arrest and apoptosis induction in A549 cells. Pro-apoptotic effect was implemented via activating JNK and inhibiting translocation of NF-κB (p65). These results suggested that luteolin might have therapeutic potential against NSCLC.     

三氧化二砷对雄激素非依赖性前列腺癌PC-3细胞株细胞增殖及细胞周期的影响

目的　了解三氧化二砷对雄激素非依赖性前列腺癌PC 3细胞株细胞增殖及细胞周期的影响。方法　以不同浓度的三氧化二砷作用于PC 3细胞 ,采用四甲基偶氮唑蓝 (MTT)法、流式细胞仪、相差显微镜和透射电镜观察细胞增殖状况、细胞周期变化以及细胞形态学的变化。结果　各浓度的三氧化二砷均可抑制PC 3细胞的增殖 ,具有剂量和时间累积效应 (P <0 0 1 )。三氧化二砷可使PC 3细胞生长停滞于G1 期。G1 期细胞数目随三氧化二砷的作用浓度增高而增多。其中3μmol/L、6 μmol/L、1 0 μmol/L的三氧化二砷作用 4 8小时后 ,可见PC 3细胞凋亡 ,分别为 1 1 8%,1 2 7%,2 9 6 %。透射电镜检查 3μmol/L三氧化二砷作用 4 8小时后的PC 3细胞 ,可见明显的凋亡小体。结论　三氧化二砷可抑制PC 3细胞的增殖 ,并具有剂量和时间依赖性 ;抑制细胞增殖与细胞周期阻滞于G1 期有关 ;三氧化二砷并可诱导PC 3细胞凋亡。     

紫草素促进食管癌细胞凋亡及细胞周期阻滞的作用机制研究

目的研究紫草素促进食管癌细胞凋亡及细胞周期阻滞的作用及机制。方法 2019年 1月至 2020年 6月期间开展细胞实验,培养食管癌 Eca109细胞,分为不含药物杜氏改良 Eagle培养基( DMEM)处理的对照组,含不同剂量紫草素 DMEM处理的紫草素组,含 2.0 μmol/L紫草素和 10 μg/L胰岛素样生长因子 -1(IGF-1)DMEM处理的 2.0 μmol/L紫草素 +10μg/L IGF-1组。检测细胞凋亡率、细胞周期及凋亡基因活化的胱天蛋白酶 -3(cleaved caspase-3)、细胞周期蛋白 D1(cyclin D1)、磷酸化磷酸肌醇 3激酶( PI3K)、蛋白激酶 B(AKT)的表达量。结果 0.5 μmol/L紫草素组、 1.0 μmol/L紫草素组、 2.0 μmol/L紫草素组的细胞凋亡率、细胞周期 G1期比例、 cleaved caspase-3的表达量［ 0.5 μmol/L紫草素组( 0.64±0.14)、 1.0 μmol/L紫草素组( 0.81±0.19)、2.0 μmol/L紫草素组( 1.02±0.24)］高于对照组 0.41±0.07,细胞周期 S期、 G2期比例及 cyclin D1［0.5 μmol/L紫草素组( 0.80±0.16)、 1.0 μmol/L紫草素组( 0.68±0.13)、 2.0 μmol/L紫草素组( 0.45±0.09)］、 p-PI3K、p-AKT表达量低于对照组［ cyclin D1表达量(0.91±0.18)］(P<0.05); 2.0 μmol/L紫草素 +10 μg/L IGF-1组的细胞凋亡率、细胞周期 G1期比例、 cleaved caspase-3的表达量低于 2.0 μmol/L紫草素组,细胞周期 G2期比例及 cyclin D1、p-PI3K、p-AKT表达量高于 2.0 μmol/L紫草素组( P<0.05)。结论紫草素具有促进食管癌细胞凋亡及细胞周期阻滞的作用,该作用与抑制 PI3K/AKT通路激活有关。     

Ciprofloxacin-mediated induction of S-phase cell cycle arrest and apoptosis in COLO829 melanoma cells

Background

Low effectiveness of anti-melanoma therapies makes it necessary to search for new drugs that could improve or replace the standard chemotherapy. Fluoroquinolones are a group of synthetic antibiotics, used in the treatment of wide range of bacterial infections. Moreover, this class of antibiotics has shown promising anti-tumor activity in several cancer cell lines. The aim of this study was to examine the effect of ciprofloxacin on cell viability, apoptosis and cell cycle distribution in COLO829 melanoma cells.

Induction of cell cycle arrest in human MCF-7 breast cancer cells by cis-stilbene derivatives related to VIOXX

In our present study, 12 new cis-stilbene derivatives (CRI-1–CRI-13) related to VIOXX^® were synthesized and studied for their inhibitory effects on cell cycle progression and anti-estrogenicity in human adenoma breast cancer MCF-7 cells. Based on the different substituents in the cis-stilbene molecule, we studied a possible structure activity relationship (SAR) for the inhibition of the cell cycle, cytotoxicity and (anti-) estrogenicity. The results showed that some cis-stilbenes have a pronounced effect on cell cycle distribution. CRI-5, 7, 10 and 12 caused an arrest of G2/M phase and reduction of G1/S phase in all tested doses (1–50 μM). In addition, some of these cis-stilbenes, have a moderate anti-estrogenic effect around 10 μM. Based on these results a preliminary SAR for cis-stilbene derivatives is suggested in which the presence and position of methoxy or thiomethoxy groups play an essential role in this cell cycle arrest. For this substitution on the para position of the left aromatic ring appears to be a prerequisite. However, the SAR for anti-estrogenicity appears to be different, but experimental information was too limited to define a possible SAR. In conclusion, our study shows that some synthetic cis-stilbene related to VIOXX^® might have chemopreventive properties that can effectively interfere with the cell cycle distribution of breast tumor cells.     

分解前后白术挥发油对细胞凋亡及细胞周期影响的研究

目的研究分解前、后白术挥发油对人类卵巢癌细胞SKOV-3细胞形态、生长抑制率、细胞凋亡及细胞周期的影响。方法使用倒置显微镜及采用四甲基偶氮唑蓝(MTT)法和流式细胞术,观察不同浓度分解前、后白术挥发油作用SKOV-3细胞不同时间后,对细胞形态、生长抑制率、细胞凋亡及细胞周期的影响。结果镜下可见凋亡小体。分解前、后白术挥发油各浓度样品作用细胞时间72h,或100,200mg/L作用细胞24,48h时,对细胞增殖均有显著影响(P<0.01)。浓度12.5,25,50mg/L分解后白术挥发油作用细胞24,48h时,对细胞增殖有显著影响(P<0.05)。浓度25,50mg/L分解前白术挥发油作用细胞24,48,72h时的细胞增殖抑制率明显高于分解后挥发油的抑制率,差异有统计学意义。随着分解前、后挥发油作用浓度的增加,分解前白术挥发油早期细胞凋亡率增高,晚期凋亡率减少;分解后白术挥发油早期细胞凋亡率、晚期细胞凋亡率增加;分解前挥发油G0/G1期和S期的细胞比例降低,G2/M期的细胞比例升高;分解后挥发油G0/G1期和G2/M期的细胞比例降低,S期的升高。结论分解前、后白术挥发油对SKOV-3细胞均具有杀伤抑制作用,其作用与时间和剂量呈正相关。在一定浓度范围,分解前白术挥发油对SKOV-3细胞增殖影响明显大于分解后。分解前、后白术挥发油均具有诱导细胞凋亡作用。分解前白术挥发油主要在凋亡早期发挥作用,分解后的挥发油在凋亡早期、晚期均发挥作用;分解前挥发油可将细胞阻滞在G2/M期,分解后可将细胞阻滞在S期。     

2'-chloro-4'-aminoflavone derivatives selectively targeting hepatocarcinoma cells: convenient synthetic process, G(2)/M cell cycle arrest and apoptosis triggers

A series of 2'-chloro-4'-nitroflavone and 2'-chloro-4'-aminoflavone derivatives were synthesized by a convenient synthetic process. The in vitro anti-proliferation ability of these compounds was evaluated against hepatocarcinoma cells (HepG2), breast adenocarcinoma cells (MCF-7), and human chronic myelogenous leukemia cells (K562). Most of synthetic compounds possessed notable anti-proliferation activity against HepG2 cells and little activity against MCF-7 cells and K562 cells. In particular, compounds 4c and 4e exhibited high anti-proliferation activity against HepG2 cells with IC(50) at about 2.0 μM. Further toxicity screening toward normal human hepatocytes indicated that some compounds had low toxicity against normal liver cells, among which 4e displayed very weak effects on QSG7701 and HL7702 cells, with IC(50) values >100 and 50 μM, respectively. Compound 4c, with the best anti-proliferation activity in amino-substituted flavones (IC(50) = 2.0 μM), was selected for further evaluation of its effects on apoptosis and the cell cycle. HepG2 cells were exposed to this compound at 10 μM, which induced nuclear disassembly and DNA fragmentation. Flow cytometry analysis suggested that the population of apoptotic cells greatly increased in the 4c-treated HepG2 cells, and the cell cycle was arrested at the G(2)/M phase.     

Effect of zeranol on expression of apoptotic and cell cycle proteins in murine placentae

Mycotoxins are chemicals produced by fungus and many of them are toxic to humans. Zeranol is a mycotoxin used to promote growth in cattle in North America; yet such a practice draws concern about the residual compound in meat in European countries. In the present study, the toxicity of zeranol was tested in a mouse model for reproduction. Pregnant ICR mice were given p.o. daily doses of zeranol at 0, 1, 10, 100 mg/kg for 4 days (from E13.5 to E16.5). Increased rates of fetal resorption at late gestation (E17.5) and preterm birth (<E18.5) were observed in mice treated with zeranol. The apparent factors causing these perinatal conditions were subsequently investigated. Perturbation of cell death or proliferation-related proteins might deter the growth and maintenance of the placentae, and the subsequent fetal resorption and preterm birth. Placental tissue isolated from pregnant mice at E17.5 showed that the expressions of Cdk2 and 4, Cyclin D1 and Bcl-xL were reduced in zeranol-treatment groups. The downregulations might signify growth or maintenance failure in the placentae. Furthermore, reduction in the signaling proteins Erk-1/2 in the placentae could trigger the decrease in the cell cycle/apoptosis proteins. In addition, relaxin is associated with preterm labor. An increase in placental Relaxin-1 expression could also contribute to early delivery in this study. Result of the current study suggested that exposure to zeranol might introduce adverse effect in pregnancy.     

Supercritical carbon dioxide extract of Physalis peruviana induced cell cycle arrest and apoptosis in human lung cancer H661 cells

Physalis peruviana L. (PP) is a popular folk medicine used for treating cancer, leukemia, hepatitis, rheumatism and other diseases. In this study, our objectives were to examine the total flavonoid and phenol content of different PP extracts (aqueous: HWEPP; ethanolic: EEPP; supercritical carbon dioxide: SCEPP-0, SCEPP-4 and SCEPP-5) and their antiproliferative effects in human lung cancer H661 cells. Among all the extracts tested, results showed that SCEPP-5 possessed the highest total flavonoid (226.19 ± 4.15 mg/g) and phenol (100.82 ± 6.25 mg/g) contents. SCEPP-5 also demonstrated the most potent inhibitory effect on H661 cell proliferation. Using DNA ladder and flow cytometry analysis, SCEPP-5 effectively induced H661 cell apoptosis as demonstrated by the accumulation of Sub-G1 peak and fragmentation of DNA. SCEPP-5 not only induced cell cycle arrest at S phase, it also up-regulated the expression of pro-apoptotic protein (Bax) and down-regulated the inhibitor of apoptosis protein (IAP). Furthermore, the apoptotic induction in H661 cells was found to associate with an elevated p53 protein expression, cytochrome c release, caspase-3 activation and PARP cleavage. Taken together, these results conclude that SCEPP-5 induced cell cycle arrest at S phase, and its apoptotic induction could be mediated through the p53-dependent pathway and modification of Bax and XIAP proteins expression. The results have also provided important pharmacological backgrounds for the potential use of PP supercritical fluid extract as products for cancer prevention.     

Involvement of apoptotic cell death and cell cycle perturbation in retinoic acid-induced cleft palate in mice

Retinoic acid (RA), a metabolite of vitamin A, plays a key role in a variety of biological processes and is essential for normal embryonic development. On the other hand, exogenous RA could cause cleft palate in offspring when it is given to pregnant animals at either the early or late phases of palatogenesis, but the pathogenetic mechanism of cleft palate caused by excess RA remains not fully elucidated. The aim of the present study was to investigate the effects of excess of RA on early palatogenesis in mouse fetuses and analyze the teratogenic mechanism, especially at the stage prior to palatal shelf elevation. We gave all-trans RA (100 mg/kg) orally to E11.5 ICR pregnant mice and observed the changes occurring in the palatal shelves of their fetuses. It was found that apoptotic cell death increased not only in the epithelium of the palatal shelves but also in the tongue primordium, which might affect tongue withdrawal movement during palatogenesis and impair the horizontal elevation of palatal shelves. In addition, RA was found to prevent the G(1)/S progression of palatal mesenchymal cells through upregulation of p21(Cip1), leading to Rb hypophospholylation. Thus, RA appears to cause G(1) arrest in palatal mesenchymal cells in a similar manner as in various cancer and embryonic cells. It is likely that apoptotic cell death and cell cycle disruption are involved in cleft palate formation induced by RA.     

Piperine inhibits the proliferation of human prostate cancer cells via induction of cell cycle arrest and autophagy

Piperine, an alkaloid from black and long peppers (Piper nigrum Linn & Piper longum Linn), has been reported to exhibit antitumor activities in vitro and in vivo. To further understand the antitumor mechanism of piperine, we investigated the growth inhibitory effects of piperine on human prostate cancer DU145, PC-3 and LNCaP cells. Piperine treatment resulted in a dose-dependent inhibition of the proliferation of these cell lines. Cell cycle arrest at G₀/G₁ was induced and cyclin D1 and cyclin A were downregulated upon piperine treatment. Notably, the level of p21^Cip1 and p27^Kip1 was increased dose-dependently by piperine treatment in both LNCaP and DU145 but not in PC-3 cells, in line with more robust cell cycle arrest in the former two cell lines than the latter one. Although piperine induced low levels of apoptosis, it promoted autophagy as evidenced by the increased level of LC3B-II and the formation of LC3B puncta in LNCaP and PC-3 cells. The piperine-induced autophagic flux was further confirmed by assaying LC3-II accumulation and LC3B puncta formation in the presence of chloroquine, a well-known autophagy inhibitor. Taken together, these results indicated that piperine exhibited anti-proliferative effect in human prostate cancer cells by inducing cell cycle arrest and autophagy.     

Artesunate enhances radiosensitivity of human non-small cell lung cancer A549 cells via increasing NO production to induce cell cycle arrest at G2/M phase

The resistance of non-small cell lung cancer (NSCLC) to radiation is the major reason for radiotherapy failure of this kind cancer. Currently, there is no effective radiosensitizer in clinical use. Artemisinin and its derivates enhance radiotherapeutic effect in some kinds of tumors; however, whether artemisinin and its derivates can enhance the radiosensitivity of NSCLC remains unknown. Therefore, in the present experiments, artemisinin and its derivatives were firstly screened for their radiosensitization on NSCLC A549 (A549) cells and then the possible mechanisms were investigated. Our results showed that artesunate enhance radiosensitivity of A549 cells in vitro among artemisinin and its derivatives, and artesunate combined with local radiotherapy retarded the tumor growth in nude tumor xenografts; the inhibition produced by 30 mg/kg of artesunate was 74.6%. The results on the possible mechanisms showed artesunate increased the NO level within irradiated A549 cells. Artesunate didn't induce apoptosis of irradiated cells but induced G₂/M arrest. The induced G₂/M arrest was related to down-regulated cyclin B1 mRNA expression. Taken together, artesunate exhibited potent radiosensitivity against human A549 cells in vitro and in vivo, probably via NO signal transduction pathway to induce cell cycle arrest at G₂/M phase. Therefore, artesunate should be further investigated as a radiosensitizer in clinical application.     

UNBS1450, a steroid cardiac glycoside inducing apoptotic cell death in human leukemia cells

Cardiac steroids are used to treat various diseases including congestive heart failure and cancer. The aim of this study was to investigate the anti-leukemic activity of UNBS1450, a hemi-synthetic cardenolide belonging to the cardiac steroid glycoside family. Here, we report that, at low nanomolar concentrations, UNBS1450 induces apoptotic cell death. Subsequently, we have investigated the molecular mechanisms leading to apoptosis activation. Our results show that UNBS1450 inhibits NF-κB transactivation and triggers apoptosis by cleavage of pro-caspases 8, 9 and 3/7, by decreasing expression of anti-apoptotic Mcl-1 and by recruitment of pro-apoptotic Bak and Bax protein eventually resulting in cell death.     

Effect of active fraction of Eriocaulon sieboldianum on human leukemia K562 cells via proliferation inhibition,cell cycle arrest and apoptosis induction

Eriocaulon sieboldianum (Sieb. & Zucc. ex Steud.), a genus of Eriocaulon in the Eriocaulaceae family, is an edible and medicinal plant used in traditional Chinese medicine. It was processed into healthcare beverages for expelling wind-heat, protecting eyes, and reducing blood fat. Also, it has been used with other herbs as Traditional Chinese herbal compound to treat cancer as adjuvants in tumor therapy in China. However, the active fractions and precise cellular mechanisms of E. sieboldianum extract remain to be illustrated. The goal of this study was to investigate the effects of the active fraction of E. sieboldianum on the growth of K562 cells and understand the possible mechanisms of its action. Our findings suggested that the fraction E3 of E. sieboldianum could effectively inhibit the activity of Aurora kinase and induce apoptosis via blocking cell cycle, up-regulating the expression of proapoptotic proteins including p53 and Bax and reducing the expression of Bcl-2. The levels of Cytochrome C, cleaved caspase-9, cleaved caspase-3 and cleaved PARP were also found to be increased after treatment with fraction E3 of E. sieboldianum.This study could improve the development of E. sieboldianum and raise its application value in cancer adjuvant therapy. Considering it is both a dietary supplement and a traditional Chinese herbal medicine which exhibits anticancer activities, it can be developed into functional food.