Induction of apoptosis in human lung cancer cells by curcumin

Curcumin, a phenolic compound from the rhizome of the plant Curcuma longa has anti-inflammatory, antioxidant and anti-cancer activities. Although the precise mode of action of this compound is not yet elucidated, studies have shown that chemo-preventive action of curcumin might be due to its ability to induce apoptosis and to arrest cell cycle. This study investigated the cellular and molecular changes induced by curcumin leading to the induction of apoptosis in human lung cancer cell lines-A549 and H1299. A549 is p53 proficient and H1299 is p53 null mutant. The lung cancer cells were treated with curcumin (0-160 microM) for 12-72 h. Curcumin inhibited the growth of both the cell lines in a concentration dependent manner. Growth inhibition of H1299 cell lines was both time and concentration dependent. Curcumin induced apoptosis in both the lung cancer cell lines. A decrease in expression of p53, bcl-2, and bcl-X(L) was observed after 12 h exposure of 40 microM curcumin. Bak and Caspase genes remained unchanged up to 60 microM curcumin but showed decrease in expression levels at 80-160 microM. The data also suggest a p53 independent induction of apoptosis in lung cancer cells.     

ROS generation mediates the anti-cancer effects of WZ35 via activating JNK and ER stress apoptotic pathways in gastric cancer

Gastric cancer is one of the leading causes of cancer mortality in the world, and finding novel agents and strategies for the treatment of advanced gastric cancer is of urgent need. Curcumin is a well-known natural product with anti-cancer ability, but is limited by its poor chemical stability. In this study, an analog of curcumin with high chemical stability, WZ35, was designed and evaluated for its anti-cancer effects and underlying mechanisms against human gastric cancer. WZ35 showed much stronger anti-proliferative effects than curcumin, accompanied by dose-dependent induction of cell cycle arrest and apoptosis in gastric cancer cells. Mechanistically, our data showed that WZ35 induced reactive oxygen species (ROS) production, resulting in the activation of both JNK-mitochondrial and ER stress apoptotic pathways and eventually cell apoptosis in SGC-7901 cells. Blockage of ROS production totally reversed WZ35-induced JNK and ER stress activation as well as cancer cell apoptosis. In vivo, WZ35 showed a significant reduction in SGC-7901 xenograft tumor size in a dose-dependent manner. Taken together, this work provides a novel anticancer candidate for the treatment of gastric cancer, and importantly, reveals that increased ROS generation might be an effective strategy in human gastric cancer treatment.     

Enhancing Effects of Curcumin on Cytotoxicity of Paclitaxel,Methotrexate and Vincristine in Gastric Cancer Cells

Curcumin (Diferuloylmethane), a polyphenolic compound with antioxidant, anti-inflammatory and anticancer properties, has been found to increase chemotherapeutic agents-induced cytotoxicity in some resistant cancer cell lines. This investigation aimed to study the effects of curcumin on efficacy of some common anticancer agents in gastric cancer cells. AGS cells were cultured in RPMI-1640 medium under standard culture conditions (5% CO2 and 95% humidified air at 37°C). Curcumin was used at concentrations of 5, 15, 30 and 50 μM. Cells were treated with a combination of curcumin and paclitaxel (300 nm) or methotrexate (100 μm) or vincristine (5 nm). Cell viability, the percentage of live cells in the whole population, was evaluated by MTT assay after 48 hours. The results showed that cell viability was significantly decreased after incubation of AGS cells with curcumin. Combination with curcumin (15-50 μm) significantly increased cytotoxicity of all three agents (P<0.001). Regarding high anticancer potential and enhancement of chemotherapeutic agent-induced cytotoxicity, the combined use of curcumin with standard chemotherapy of gastric cancer is suggested as a strategy for better management of this fatal cancer.     

姜黄素抑制结肠癌SW480细胞的增殖及其机制

目的:研究姜黄素对人结肠癌SW480细胞增殖以及survivin、caspase-3和p-Akt表达的影响。方法:用不同浓度姜黄素(5～40μmol/L)作用SW480细胞24、48和72 h,MTT法检测姜黄素对SW480细胞生长的抑制作用,Western blotting法检测SW480细胞中survivin、caspase-3和p-Akt蛋白的表达。结果:姜黄素以剂量(5～40μmol/L)和时间(24～72 h)依赖的方式抑制SW480细胞的增殖(P<0.01),40μmol/L姜黄素作用72 h对SW480细胞生长的抑制率可达(75.86±3.93)%。姜黄素抑制SW480细胞中p-Akt、survivin蛋白的表达、促进caspase-3蛋白的表达,均呈时间和剂量依赖性;40μmol/L姜黄素作用SW480细胞48 h后p-Akt和survivin蛋白表达显著减少[(0.204±0.025)vs(0.367±0.035),P<0.01;(0.208±0.014)vs(0.385±0.034),P<0.01],caspase-3蛋白表达显著增加[(0.371±0.028)vs(0.127±0.023),P<0.01]。结论:姜黄素抑制SW480细胞增殖,其机制可能与抑制Akt磷酸化、下调survivin和上调caspase-3蛋白的表达有关。     

姜黄素对人胃腺癌细胞株BGC-823生长抑制及诱导凋亡的作用

目的 探讨姜黄素对人胃腺癌细胞BGC-823的生长抑制及诱导凋亡作用。方法MTT法检测不同浓度姜黄素对人胃腺癌BGC-823细胞的生长抑制作用,计算半数抑制浓度（IC₅₀）;将1.2μmol／L姜黄素作用于BGC-823细胞24、48、72h,用DAPI染色检测细胞凋亡;用RT-PCR、Western blotting法分别检测姜黄素对Bax、Bcl-2基因以及Bax、Bcl-2、caspase-3蛋白的影响。结果 不同浓度的姜黄素作用于BGC-823细胞0～72h后,细胞呈不同程度的抑制作用,随着药物浓度的增加,抑制率明显上升,作用48h的IC₅₀为1.2μmol／L。DAPI染色可见典型的凋亡细胞形态学特征。RT-PCR、Western blotting结果显示1.2μmol/L姜黄素可以增加Bax表达、减少Bcl-2表达和激活caspase-3。结论 姜黄素对人胃腺癌BGC-823细胞有生长抑制和诱导凋亡的作用,这可能与增加Bax表达、减少Bcl-2表达、激活caspase-3有关。     

Antiproliferative Effects of Curcumin Different Types of Breast Cancer

Objective: Breast cancer is one of the most frequently diagnosed malignancy among women. Turmeric is isolated from Curcuma longa. Curcumin is main curcuminoid of the turmeric which is a member of Zingiberaceae. In this current study antiproliferative effects of curcumin were investigated in luminal A breast cancer cell line MCF-7 and triple negative breast cancer cell line MDA-MB-231. Methods: For this purpose cell viability, cell index values by xCELLigence Real-Time Cell Analysis DP instrument, mitotic index and apoptotic index analysis were used. Results: Cell viability and cell index values showed that 75 µM concentration of curcumin was IC50 concentration. When IC50 concentration was applied to both cell lines, a significant decrease was observed in the mitotic index values, while a significant increase was observed in the apoptotic index values (p<0.05). Conclusion: Curcumin, which has antiproliferative effects on breast cancer cells, is thought to be effective in cancer treatment.     

姜黄素联合5-FU对胃癌MGC-803细胞生长的抑制作用

目的:探讨姜黄素联合低剂量5-FU对胃癌MGC-803细胞生长抑制作用是否达到或优于高剂量5-FU单用以及两药联合应用的效果。为临床上联合应用姜黄素和氟尿嘧啶治疗胃癌提供理论和实验依据。方法:用MTT检测姜黄素（20μmol/L）和不同剂量的5-FU（2、6、20、60μmol/L）联合或5-FU（10、100μmol/L）单独作用于体外培养的胃癌MGC-803细胞12h、24h、36h而产生的增殖抑制效应,并对实验数据进行方差分析和析因分析。结果:两种药物单用及联用时,均对体外培养人胃癌MGC-803细胞增殖有显著抑制作用（P<0.05）,且呈剂量时间依赖效应。姜黄素联合低剂量5-FU对胃癌MGC-803细胞的抑制作用优于高剂量5-FU单用（P<0.05）;两药有很好的协同作用（P<0.05）。结论:姜黄素联合低剂量5-FU对胃癌MGC-803生长的抑制作用优于高剂量5-FU单用;姜黄素与5-FU的联合用药对胃癌细胞的抑制呈协同作用。     

Specific inhibition of cyclooxygenase-2 (COX-2) expression by dietary curcumin in HT-29 human colon cancer cells

Curcumin, a major yellow pigment and active component of turmeric, has been shown to possess anti-inflammatory and anti-cancer activities. Cyclooxygenase (COX)-2 plays an important role in colon carcinogenesis. To investigate the effect of curcumin on COX-2 expression, we treated HT-29 human colon cancer cells with various concentrations of curcumin. Curcumin inhibited the cell growth of HT-29 cells in a concentration- and time-dependent manner. Curcumin markedly inhibited the mRNA and protein expression of COX-2, but not COX-1. These data suggest that a non-toxic concentration of curcumin has a significant effect on the in vitro growth of HT-29 cells, specifically inhibits COX-2 expression, and may have value as a safe chemopreventive agent for colon cancer.     

Helicobacter pylori seropositivity and subsite-specific gastric cancer risks in Linxian, China

BACKGROUND: Helicobacter pylori carriage (i.e., persistent exposure to the organism without gastric epithelial cell invasion) is an established risk factor for noncardia gastric cancer. However, its association with the risk of cancer of the gastric cardia is controversial. Consequently, we designed this prospective, nested case-control study to further explore the subsite-specific gastric cancer risks associated with H. pylori seropositivity (a surrogate marker for persistent exposure). METHODS: A total of 99 patients with gastric cardia cancer, 82 patients with noncardia gastric cancer, and 192 cancer-free subjects were selected from among the participants (n = 29 584) of a nutrition intervention trial previously conducted in Linxian, China. H. pylori seropositivity was determined by assaying for the presence of H. pylori whole cell and CagA antibodies in baseline serum samples from all subjects. Seropositivity was defined as one or both serum assays being positive. Odds ratios (ORs) for subsite-specific gastric cancer were estimated by multivariate logistic regression analyses. All statistical comparisons were two-sided (alpha =.05). RESULTS: H. pylori seropositivity rates for subjects with gastric cardia cancer, noncardia gastric cancer, and gastric cardia and noncardia cancers combined were 70% (P =.02), 72% (P: =.01), and 71% (P =.003) compared with 56% for cancer-free control subjects. OR estimates for H. pylori seropositivity were 1.87 (95% confidence interval [CI] = 1.10 to 3.17) for gastric cardia cancer, 2.29 (95% CI = 1.26 to 4.14) for noncardia gastric cancer, and 2.04 (95% CI = 1.31 to 3.18) for gastric cardia and noncardia cancers combined. CONCLUSIONS: H. pylori seropositivity was associated with increased risks for both gastric cardia cancer and noncardia gastric cancer in this well-characterized cohort. Thus, H. pylori carriage may increase the risk of cancer throughout the stomach.     

Development of PEGylated PLGA Nanoparticles Co-Loaded with Bioactive Compounds: Potential Anticancer Effect on Breast Cancer Cell Lines

Objective: The incidence of breast cancer continues to rise despite decades of laboratory, epidemiological and clinical research. Breast cancer is still the leading cause of cancer death in women. Cyclin D1 is one of the most important oncoproteins associated with cancer cell proliferation and is overexpressed in more than 50% of cases. Curcumin and chrysin are plant-derived components that are believed to assist in inhibiting the viability of breast cancer cells. These agents are involved in cancer cells’ growth and reducing cyclin D1 expression. In this study, the hypothesis of combining curcumin and chrysin is applied to analyze the potential synergistic effect in inhibiting cancer cell proliferation and down-regulation of cyclin D1. Furthermore, applying PLGA-PEG NPs could improve the bioavailability of free curcumin and chrysin components and at the same time increases the anti-cancer potential of this compound. Methods: PLGA-PEG NPs were synthesized via the ring-opening polymerization technique and characterized with FT-IR and FE-SEM for chemical structure and morphological characteristics, respectively. Next, curcumin and chrysin were loaded in PLGA-PEG NPs and MTT assay was performed to assess the cytotoxic effect of these agents. T-47D cells were treated with appropriate concentrations of these agents and cyclin D1 expression level was evaluated by real-time PCR. Results: The obtained results from FT-IR and FE-SEM techniques illustrated that curcumin and chrysin were efficiently encapsulated into PLGA-PEG NPs. Curcumin, chrysin, and curcumin-chrysin in free and nano-encapsulated forms exhibited an anti-cancer effect on T-47D cells in a time- and dose-dependent manner, especially in a combination of free and encapsulated forms demonstrated synergistic anti-cancer effects. Compared to free form, Nano-curcumin, Nano-chrysin, and Nano-combination remarkably down-regulated cyclin D1 gene expression. (p-value < 0.05). Conclusion: Our results revealed that the curcumin-chrysin combination has a synergistic effect and the encapsulated form of this nano-component has more inhibition on cyclin D1 expression.     

Curcumin Inhibits MHCC97H Liver Cancer Cells by Activating ROS/TLR-4/Caspase Signaling Pathway

Curcumin can inhibit proliferation of liver cancer cells by inducing apoptosis, but the specific signalingpathways involved are not completely clear. Here, we report that curcumin inhibited proliferation of MHCC97Hliver cancer cells by induction of apoptosis in a concentration dependent manner via stimulating intracellularreactive oxygen species (ROS) generation. Also, we showed that increased intracellular ROS formation activatedthe TLR-4/MyD-88 signaling pathway, resulting in activation of caspase-8 and caspase-3, which eventually ledto apoptosis in MHCC97H cells. These results showed that as an prooxidant, curcumin exerts anti-cancer effectsby inducing apoptosis via the TLR-4/MyD-88 signaling pathway.     

ABO blood type, Lewis and Secretor genotypes, and chronic atrophic gastritis: a cross-sectional study in Japan.

BACKGROUND: the H type I structure, synthesized by the secretor (Se) enzyme in gastric foveolar cells, and its metabolite, Lewis b (le(b)) antigen, mediate the adhesion of Helicobacter pylori ( H. Pylori) to the gastric epithelium, whereas H. Pylori does not bind to modified forms of Le(b) specific for blood types A and B. Such host factors as Le and Se genotypes and ABO blood type may affect the establishment of H. Pylori infection and, once infected, the risk of chronic atrophic gastritis. METHODS: we investigated the cross-sectional relation of abo blood type and Le and Le genotypes to gastric atrophy, assessed by serum pepsinogen levels, in japanese residents from two sources. RESULTS: among the 151 h. Pylori-positive participants of the h. Pylori eradication program, odds ratios (ors) for gastric atrophy, adjusted for age, sex, and smoking, were elevated for blood types a (or = 5.35; 95% confidence interval (ci), 2.11-13.58) and b (or = 4.79; 95% ci, 1.77-12.93) relative to type o. Ors for blood types a and b were also elevated in h. Pylori-negative subjects. These associations were not observed among 250 h. Pylori-positive health check-up examinees. The le genotype was not associated with gastric atrophy in either study population. The se/ se genotype was associated with statistically nonsignificant elevation of gastric atrophy risk in both populations. CONCLUSIONS: the present data showed a strong association of blood types a and b with gastric atrophy in one, but not the other, study population. Discrepant results between the two populations warrant further investigation. Background: the h type i structure, synthesized by the secretor (se) enzyme in gastric foveolar cells, and its metabolite, lewis b (le(b)) antigen, mediate the adhesion of helicobacter pylori ( h. Pylori) to the gastric epithelium, whereas h. Pylori does not bind to modified forms of le(b) specific for blood types a and b. Such host factors as le and se genotypes and abo blood type may affect the establishment of h. Pylori infection and, once infected, the risk of chronic atrophic gastritis. Methods: we investigated the cross-sectional relation of abo blood type and le and se genotypes to gastric atrophy, assessed by serum pepsinogen levels, in japanese residents from two sources. Results: among the 151 h. Pylori-positive participants of the h. Pylori eradication program, odds ratios (ors) for gastric atrophy, adjusted for age, sex, and smoking, were elevated for blood types a (or = 5.35; 95% confidence interval (ci), 2.11-13.58) and b (or = 4.79; 95% ci, 1.77-12.93) relative to type o. Ors for blood types a and b were also elevated in h. Pylori-negative subjects. These associations were not observed among 250 h. Pylori-positive health check-up examinees. The le genotype was not associated with gastric atrophy in either study population. The se/ se genotype was associated with statistically nonsignificant elevation of gastric atrophy risk in both populations. Conclusions: the present data showed a strong association of blood types a and b with gastric atrophy in one, but not the other, study population. Discrepant results between the two populations warrant further investigation.     

姜黄素诱导NSCLC细胞凋亡机制探讨

目的 肺癌位居我国居民癌症发病率和死亡率的首位,其中非小细胞癌(non-small cell lung cancer,NSCLC)约占80%,筛选高效低毒的抗癌药物尤为迫切.本研究拟探讨姜黄素对NSCLC细胞的可能作用机制.方法 用不同浓度的姜黄素(0、10、20、30 μmol/L)或活性氧清除剂(CAT和NAC)加姜黄素处理肺癌细胞A549和SPC-A1,采用流式细胞术检测细胞周期、细胞凋亡率、活性氧(reactive oxygen species,ROS)水平和线粒体膜电位的变化,蛋白质印迹法检测自噬相关蛋白LC3、P62和细胞凋亡相关蛋白PARP、Caspase-3和Caspase-9的表达变化.结果 姜黄素抑制非小细胞肺癌细胞株A549和SPC-A1增殖及克隆形成,主要将细胞阻滞在G2/M期,0、10、20和30 μmol/L姜黄素处理的A549细胞G2/M期细胞百分比分别为(12.67±2.52)%、(22.67±2.52)%、(27.00±2.01)%和(42.33±4.04)%,SPC-A1细胞G2/M期细胞百分比分别为(9.33±2.52)%、(18.33±1.53)%、(20.67±2.52)%和(30.67±1.53)%.0、10、20和30 μmol/L姜黄素处理A549细胞凋亡率分别为(4.40±1.02)%、(7.31±1.52)%、(9.32±1.08)%和(13.97±1.98)%,P<0.05;SPC-A1细胞凋亡率分别为(4.38±1.22)%、(5.98±0.75)%、(9.42±1.25)%和(16.13±3.09)%,P<0.05.姜黄素导致ROS水平增高、线粒体膜电位降低和线粒体自噬的发生,并且呈剂量依赖性,而应用ROS清除剂可以减弱以上药物作用.相关信号转导通路蛋白表达与以上细胞生物行为改变表现一致.结论 姜黄素通过ROS途径诱导NSCLC细胞发生线粒体自噬,是一种有潜力的抗癌药物.     

Anti-Tumor Effect of Curcumin on Human Cervical Carcinoma HeLa Cells In Vitro and In Vivo

Objective: To investigate the anti-tumor effect of curcumin on human cervical carcinoma HeLa cells in vitro and in vivo. Methods: (1) Human cervical carcinoma cell line HeLa was cultured in vitro. HeLa cells were treated with 5-50 μmol/L curcumin for 24. 48, 72 h and the growth inhibition rates of HeLa cells were measured by MTT method. Cell apoptosis was inspected by electron microscopy and flow cytometry (FCM). (2) A transplanted tumor model by injecting HeLa cells into subcutaneous tissue of BABL/C mice was established and its growth curve was measured. 30 BABL/C mice with tumors were divided into 2 groups at random and 0.2 ml saline or 0.2 ml 250 μmol/L curcumin was injected into abdominal cavity respectively once everyday and lasted for ten days. The changes of tumor volume were measured continuously and tumor inhibition rate was calculated. At last the expressions of caspase-3 and bax protein in transplanted tumors were detected by immunohistochemistry. Results: (1) Curcumin inhibited the proliferation of Lela cells on a dose-depending manner. Apoptosis of cells could be observed by FCM. Partial cells presented the characteristic morphological changes of apoptosis under electron microseope. (2) When 1×107 HeLa cells were inoculated for each mouse, 100% of the mice developed growing tumors after seven days. An inhibition effect was observed in treatment group, and the inhibition rate of curcumin was 74.33%. The expressions of caspase-3 and bax in the transplanted tumors were increased in curcumin group. Conclusion: Curcumin is effective as an anti-cancer drug not only in vitro but also in vivo.     

A phase I/II study of gemcitabine-based chemotherapy plus curcumin for patients with gemcitabine-resistant pancreatic cancer

Purpose

Curcumin, a plant-derived natural polyphenol, could be a promising anti-cancer drug and shows synergic effects with cytotoxic agents. We evaluated the safety and feasibility of combination therapy using curcumin with gemcitabine-based chemotherapy.

Methods

Gemcitabine-resistant patients with pancreatic cancer received 8?g oral curcumin daily in combination with gemcitabine-based chemotherapy. The primary endpoint was safety for phase I and feasibility of oral curcumin for phase II study.

Results

Twenty-one patients were enrolled. No dose-limiting toxicities were observed in the phase I study and oral curcumin 8?g/day was selected as the recommended dose for the phase II study. No patients were withdrawn from this study because of the intolerability of curcumin, which met the primary endpoint of the phase II study, and the median compliance rate of oral curcumin was 100% (Range 79?C100%). Median survival time after initiation of curcumin was 161?days (95% confidence interval 109?C223?days) and 1-year survival rate was 19% (4.4?C41.4%). Plasma curcumin levels ranged from 29 to 412?ng/ml in five patients tested.

Conclusions

Combination therapy using 8?g oral curcumin daily with gemcitabine-based chemotherapy was safe and feasible in patients with pancreatic cancer and warrants further investigation into its efficacy.     

Introduction

The effects of helicobacter pylori infection on gastric disorders have been proven by many epidemiological and experimental studies. To explore the relationships between h. Pylori infection and gastric carcinogenesis, many factors, including host responses, environmental status, and the virulence factors of the bacteria should be taken into account. Mongolian gerbils ( meriones unguiculatus) can be easily infected with h. Pylori, and provide an excellent in-vivo experimental model to clarify the role of h. Pylori in active gastritis, peptic ulcers, intestinal metaplasia, and gastric carcinoma. Studies have revealed that h. Pylori infection markedly enhances all histological types of gastric cancers in gerbils treated with a chemical carcinogen. Eradication reduced the enhancing effect of h. Pylori on gastric carcinogenesis, whereas a high-salt diet synergistically enhanced the effect of h. Pylori. Various factors involving inflammation, cell proliferation, and cell differentiation could be examined with this experimental model to help elucidate this mechanisms of gastric carcinogenesis.     

Curcumin induces apoptosis in human leukemic cell lines through an IFIT2-dependent pathway

Curcumin, the primary bioactive component isolated from turmeric, has been shown to possess variety of biologic functions including anti-cancer activity. However, molecular mechanisms in different cancer cells are various. In the present study, we demonstrated that curcumin induced G2/M cell cycle arrest and apoptosis by increasing the expression levels of cleaved caspase-3, cleaved PARP and decreasing the expression of BCL^?2 in U937 human leukemic cells but not in K562 cells. We found some interferon induced genes, especially interferon-induced protein with tetratricopeptide repeats 2 (IFIT2), were significantly upregulated when treated with curcumin in U937 cells by gene expression chip array, and further confirmed that the expression of IFIT2 was obviously higher in U937 than that in K562 cells by Western blot assay. In addition, inhibiting the expression of IFIT2 by shRNA in U937 rescued curcumin-induced apoptosis and exogenous overexpression of IFIT2 by lentiviral transduction or treating with IFNγ in K562 cells enhanced anti-cancer activity of curcumin. These results indicated for the first time that curcumin induced leukemic cell apoptosis via an IFIT2-dependent signaling pathways. The present study identified a novel mechanism underlying the antitumor effects of curcumin, and may provide a theoretical basis for curcumin combined with interferon in the cancer therapeutics.     

Curcumin Induces Apoptosis in SGC-7901 Gastric Adenocarcinoma Cells via Regulation of Mitochondrial Signaling Pathways

Curcumin, a polyphenol compound derived from the rhizome of the plant Curcuma longa L. has been verifiedas an anticancer compound against several types of cancer. However, understanding of the molecular mechanismsby which it induces apoptosis is limited. In this study, the anticancer efficacy of curcumin was investigated inhuman gastric adenocarcinoma SGC-7901 cells. The results demonstrated that curcumin induced morphologicalchanges and decreased cell viability. Apoptosis triggered by curcumin was visualized using Annexin V-FITC/7-AAD staining. Curcumin-induced apoptosis of SGC-7901 cells was associated with the dissipation of mitochondrialmembrane potential (MMP) and the release of cytochrome c into the cytosol. Furthermore, the down-regulationof Bcl-2 and up-regulation of Bax that led to the cleavage of caspase-3 and increased cleaved PARP was observedin SGC-7901 cells treated with curcumin. Therefore, curcumin-induced apoptosis of SGC-7901 cells might bemediated through the mitochondria pathway, which gives the rationale for in vivo studies on the utilization ofcurcumin as a potential cancer therapeutic compound.