High-Efficient Dust Trapping Performance of AES/Polyacrylamide Strengthen Foam Based on the Structure Stability and Dust Wettability.

The atmospheric dust has a great negative impact on the societal harmonious development that starves for an efficient dust suppressant. This paper proposes a novel AES/polyacrylamide strengthen foam (APSF) to improve the dust trapping effectiveness. The APSF structure property and dust suppression capacity are studied and evaluated through the molecular dynamics simulation and experimental tests. The results express that APSF exhibits the stronger structure stability, superior water retention, and slower drainage performance than the traditional water-based foam (WBF). APSF dynamic simulation is studied by the relative concentration, radial distribution function, head group orientation, and mean square displacement. Research shows that APSF introduces water to thicken the hydration layer. The interaction strength between water and surfactant head groups is enhanced by 22.62 and 31.37% in the first and second hydrated water shells. APSF improves the sodium fatty alcohol ether sulfate (AES) orientation and weakens the diffusion of water molecules, which favors the foam stability. APSF exerts a better wettability on the coal dust through the wet settlement and contact angle tests. The APSF liquid film thickness reduces to 58.05 from 64.80 µm that is 3.14 times of WBF according to the foam liquid film decay experiment. Fourier transform infrared (FTIR) spectroscopy analysis indicates that there is an evident reinforcement on the coal surface absorption peak intensity of hydroxyl- and oxygen-containing functional groups treated by APSF. FTIR results are further determined by energy-dispersion spectrum analysis.

Impact of Cold Ischemic Time and Freeze-Thaw Cycles on RNA, DNA and Protein Quality in Colorectal Cancer Tissues Biobanking.

Tissue-derived RNA, DNA and protein samples become more and more crucial for molecular detection in clinical research, personalized and targeted cancer therapy. This study evaluated how to biobanking colorectal tissues through examining the influences of cold ischemic time and freeze-thaw cycles on RNA, DNA and protein integrity. Here, 144 pairs of tumor and normal colorectal tissues were used to investigate the impact of cold ischemic times (0-48h) on RNA, DNA and protein integrity at on ice or room temperature conditions. Additionally, 45 pairs of tissues experienced 0-9 freeze-thaw cycles, and then the RNA, DNA and protein quality were analyzed. On ice, RNA, DNA and protein from colorectal tumor and normal tissues were all stable up to 48h after surgery. At room temperature, RNA in colorectal tumor and normal tissues began to degrade at 8h and 24h, respectively. Meanwhile, the tumor tissues DNA degradation occurred at 24h after surgery at room temperature. Similarly, the protein expression level of tumor and normal tissues began to change at 24h after the surgery at room temperature. Interestingly, tissue RNA and DNA remained stable even after 9 freeze-thaw cycles, whereas the proteins levels were remarkably changed after 7 freeze-thaw cycles. This study provided a useful evidence on how to store human colorectal tissues for biobanking. Preserving the surgical colorectal tissue on ice was an effective way to prevent RNA, DNA and protein degradation. Importantly, more than 7 repeated freeze-thaw cycles were not recommended for colorectal tissues.

KRAS G12V Mutation is an Adverse Prognostic Factor of Chinese Gastric Cancer Patients.

This study aims to investigate the molecular characteristics of Chinese gastric cancer patients. In our study, the KRAS, BRAF, and PIK3CA mutation status of 485 GC patients were analyzed by Sanger sequencing. Kaplan-Meier analysis was used to plot survival curves according to different genotypes. The results show that the frequency of KRAS, BRAF and PIK3CA mutations were 4.1%, 1.2% and 3.5%, respectively. BRAF mutations were significantly concentrated in stage III and IV gastric cancer (P=0.009). KRAS G12V mutation carriers have much shorter OS than other mutation carriers and wild-type group patients (P=0.013). In conclusion, only the KRAS G12V mutation has an adverse effect on patient survival.

Prognostic value of autophagy related proteins ULK1, Beclin 1, ATG3, ATG5, ATG7, ATG9, ATG10, ATG12, LC3B and p62/SQSTM1 in gastric cancer.

Autophagy-related (ATG) genes contributed to tumorigenesis and cancer progression. This study aims to investigate the expression of ATG proteins and their clinicopathological significance in gastric cancer. Nine well-known ATG proteins, (ULK1, Beclin 1, ATG3, ATG5, ATG7, ATG9, ATG10, ATG12 and LC3B) and p62/SQSTM1, which represented key regulators that participated in whole autophagosomes stepwise processes, were detected in a large cohort of 352 primary gastric cancer patients. Among these 352 patients, 117 cases were randomly assigned to the training set to detect the clinicopathological value of ATG proteins, and another 235 patients were used as the testing set for further validation. Except for Beclin 1, ATG9 and ATG10, another six ATG proteins and p62/SQSTM1 were closely correlated with histological types for gastric cancer. Moreover, low expression of ULK1, Beclin 1 and ATG10 were associated with lymph node metastasis. In addition, down-regulation of ULK1, Beclin 1, ATG7 and ATG10, up-regulation of ATG12 correlated with advanced TNM stage. Importantly, multivariate cox analysis identified ULK1, Beclin 1, ATG3 and ATG10 as favorable independent prognostic factors for overall survival. Combination analysis of ULK1, Beclin 1, ATG3, ATG10 revealed the improved prognostic accuracy for gastric cancer. Our study showed that ATG proteins might serve as novel prognostic biomarkers in gastric cancer, and supply a new valuable insight into cancer treatment targeting autophagy for patients.

Phosphorylated p38, a negative prognostic biomarker, complements TNM staging prognostication in colorectal cancer.

Phosphorylated p38 (p-p38) played a pivotal role in the regulation of disease progression and correlated with tumor prognosis. Here, we characterized the prognostic effect of p-p38 in colorectal cancer (CRC). Three hundred and sixteen CRC patients in stages I-III were recruited in this study. P-p38 expression was semi-quantitatively evaluated using tissue microarrays and immunohistochemistry staining. Overall survival (OS), disease-free survival (DFS), local failure-free survival (LFFS), and distant metastasis-free survival (DMFS) of patient subgroups, segregated by p-p38 expression level and clinical stage, were compared using Kaplan-Meier analysis. We found that p-p38 was overexpressed in 48.1 % (152/316) CRC tissues, whereas low or deficiently expressed in normal adjacent epithelia. Overexpression of p-p38 predicted poor OS (P < 0.001), DFS (P = 0.002), LFFS (P = 0.016), and DMFS (P = 0.025) in CRC. Importantly, patient subgroups in the early stage (stages I + II) and with low p-p38 had similar OS, PFS, LFFS, and DMFS probabilities to that of stage I, whereas those with high p-p38 were similar to stage III disease. In addition, for stage III disease, the subgroup with low p-p38 had a similar survival probability to that of stage I, whereas the subgroup with high p-p38 had the worst survival. Multivariate Cox analysis confirmed that p-p38 was indeed a significantly independent factor for death, recurrence, and distant metastases in CRC. Our results demonstrated that p-p38 was a negative independent prognostic factor for CRC. Complementing TNM staging with p-p38 might refine the risk definition more accurately for a subset of patients.

Snail promotes lymph node metastasis and Twist enhances tumor deposit formation through epithelial-mesenchymal transition in colorectal cancer.

Snail and Twist, transcriptional repressors of E-cadherin as well as inducers of epithelial-mesenchymal transition, play pivotal roles in tumor invasion and metastasis. We investigated the expression of Snail, Twist, and E-cadherin by immunohistochemistry in 193 colorectal cancers, including 79 with positive lymph nodes, 36 with tumor deposits, 39 with both, and 39 with no metastases. Snail was expressed to a greater extent in the group with positive lymph nodes (68.4%), whereas Twist was overexpressed in patients with other metastases (75.0%). Ectopic expression of Snail and Twist correlated with reduced membranous expression of E-cadherin. Importantly, Snail overexpression correlated significantly with lymph node metastasis (P < .0001), whereas Twist up-regulation correlated strongly with other metastases (P < .0001). Multivariate logistic regression analysis showed that Snail was an independent predictor of lymph node metastasis (odds ratio, 4.445; 95% confidence interval, 2.250-8.781; P < .0001), whereas Twist displayed predictive value for metastasis formation (odds ratio, 5.606; 95% confidence interval, 2.829-11.111; P < .0001), suggesting that lymph node and other metastases may follow different signaling pathways. In conclusion, ectopic expression of Snail and Twist contributed to lymph node and disseminated metastasis, respectively, by reducing E-cadherin expression, providing a novel role for Snail and Twist in the progression of colorectal cancer.

Expression of sonic hedgehog signaling components in hepatocellular carcinoma and cyclopamine-induced apoptosis through Bcl-2 downregulation in vitro.

BACKGROUND AND AIMS: Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Aberrant activation of sonic hedgehog (Shh) signaling pathway plays important roles in tumorigenesis and progression of several tumors. Cyclopamine, an important inhibitor of Shh signaling pathway, can induce cell apoptosis. However, the mechanisms underlying cyclopamine-induced apoptosis are not well understood. The aim of this study is to determine the expression of the Shh signaling pathway components in HCC and to investigate the mechanisms underlying cyclopamine-induced apoptosis in HCC cells. METHODS: Shh signaling components (Shh, Ptch, Smo and Gli-1) expression levels were evaluated by immunohistochemistry on tissue microarrays containing 98 HCCs with paired adjacent noncancerous liver tissues. The relationships between sonic hedgehog signal pathway and clinicopathological factors were analyzed in HCC. Cell viability was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Apoptosis was detected by flow cytometry. mRNA and protein levels were analyzed by RT-PCR and Western blot, respectively. RESULTS: Shh, Ptch, Smo and Gli-1 were overexpressed in HCC tissues compared with paired adjacent noncancerous liver tissue. Activated Shh signaling pathway was associated with tumor size, capsular invasion and vascular invasion in HCC. Cyclopamine remarkably decreased cell viability, induced apoptosis and downregulated Bcl-2 expression in HCC cells. CONCLUSIONS: Shh signaling pathway plays an important role in HCC tumorigenesis and progression, indicating that Shh signaling pathway is a potential therapeutic target for HCC. Cyclopamine induces apoptosis through downregulating Bcl-2 in HCC.

FAK is involved in invasion and metastasis of hepatocellular carcinoma.

Studies have shown that focal adhesion kinase (FAK) is overexpressed in several human tumors and plays an important role in tumor progression. However, the role and underlying mechanisms of FAK in hepatocellular carcinoma (HCC) progression remains to be elucidated. In this study, we examined FAK and phosphorylated FAK Tyr397 expression in a large series of HCCs. We found that both FAK and phosphorylated FAK Tyr397 were overexpressed in HCC samples and HCC cell lines. Increased FAK and phosphorylated FAK Tyr397 expressions were correlated with tumor stage, vascular invasion and intrahepatic metastasis in HCC. Furthermore, HCC cell adhesion, migration and invasion were substantially impaired by siRNA-mediated knockdown of FAK expression, whereas cell growth, apoptosis and cell cycle distribution were not affected. In addition, depletion of FAK induced a significant reduction in expressions and activities of both MMP-2 and MMP-9. Taken together, FAK contributes to invasion and metastasis of HCC partly through regulating expressions and activations of both MMP-2 and MMP-9, suggesting FAK could be a promising therapeutic target for HCC.

MicroRNA-9 reduces cell invasion and E-cadherin secretion in SK-Hep-1 cell.

MicroRNAs (miRNAs) are an abundant class of short noncoding RNAs that can posttranscriptionally regulate gene expression in animals. They are also involved in cancer initiation and progression, and their expression profiles serve as phenotypic signatures of different cancers. The roles played by microRNAs specifically in "micromanagement of metastasis" has been addressed only recently. The molecular mechanisms of hepatocellular carcinoma (HCC) metastasis are still poorly understood. Recent evidence implies genetic determinants of cancer metastasis. Because gene expression signature significantly differs between primary metastasis-free HCC and primary HCC with intrahepatic metastases, miRNA expression in those primary HCC may change correspondingly. The 28 up-regulated miRNAs, part of the reported miRNA profiles of HCC, were compared in primary HCC with or without metastases. Only eight miRNAs were found to be significantly up-regulated in primary HCC with metastases while miR-9 had the highest hold change. miR-9 was highly expressed in SK-Hep-1 cell when compared with other hepatoma cell lines and downregulation of miR-9 reduced SK-Hep-1 cell invasion. E-cadherin, a tumor invasion suppressor in HCC, was found to be a putative gene target of miR-9. E-cadherin was up-regulated by miR-9 inhibitor. The findings suggest miR-9 could be involved in HCC metastasis.

Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-fluorouracil antitumor activity through activation of the PPARgamma signaling pathway.

AIM: Resistance to 5-fluorouracil (5-FU) is a major cause of chemotherapy failure in advanced hepatocellular carcinoma (HCC). Rosiglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, has a crucial role in growth inhibition and induction of apoptosis in several carcinoma cell lines. In this study, we examine rosiglitazone-induced sensitization of HCC cell lines (BEL-7402 and Huh-7 cells) to 5-FU. METHODS: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to evaluate cell viability. Western blotting analysis was performed to detect the protein expression (PPARgamma, PTEN, and COX-2) in BEL-7402 cells. Immunohistochemistry staining was used to examine the expression of PTEN in 100 advanced HCC tissues and paracancerous tissues. In addition, small interfering RNA was used to suppress PPARgamma, PTEN, and COX-2 expression. RESULTS: Rosiglitazone facilitates the anti-tumor effect of 5-FU in HCC cell lines, which is mediated by the PPARgamma signaling pathway. Activation of PPARgamma by rosiglitazone increases PTEN expression and decreases COX-2 expression. Since distribution of PTEN in HCC tissues is significantly decreased compared with the paracancerous tissue, over-expression of PTEN by rosiglitazone enhances 5-FU-inhibited cell growth of HCC. Moreover, down-regulation of COX-2 is implicated in the synergistic effect of 5-FU. CONCLUSION: Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-FU antitumor activity through the activation of PPARgamma. The results suggest potential novel therapies for the treatment of advanced liver cancer.

Bead-based microarray analysis of microRNA expression in hepatocellular carcinoma: miR-338 is downregulated.

AIM: Recent studies have underlined causative links between microRNA (miRNA) deregulation and cancer development. However, the relevance of abnormally expressed miRNA to tumor biology has not been well understood in hepatocellular carcinoma (HCC). METHODS: A bead-based miRNA expression profiling method was performed on 20 pairs of surgically removed HCC and adjacent non-tumorous tissue (NT). Special miR-338 downregulations and miR-338 associated with clinical characteristics was validated in an extended samples set of 36 paired HCC and adjacent non-tumorous liver tissues by real-time reverse transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: Out of our bead-based microarray data, 12 upregulated and 19 downregulated miRNA were found to be associated with HCC. Further characterization of miRNA-338, in which 20 pairs of the samples were clustered clearly into two groups according to expression of miR-338, revealed that the level of miR-338 expression can be associated with clinical aggressiveness, such as, tumor size, tumor-node-metastasis stage, vascular invasion and intrahepatic metastasis. These results were validated by real-time RT-PCR analysis. CONCLUSION: Our study suggests that miRNA expression could have relevance to the clinical behavior of HCC and that the bead-based miRNA expression profiling method might be a suitable system to assay miRNA expression in large-scale diagnostic trails.

Involvement of PI3K/PTEN/AKT/mTOR pathway in invasion and metastasis in hepatocellular carcinoma: Association with MMP-9.

AIM: To investigate the status of Phosphatidylinositol 3-kinase (PI3K)/PTEN/AKT/mammalian target of rapamycin (mTOR) pathway and its correlation with clinicopathological features and matrix metalloproteinase-2, -9 (MMP-2, 9) in human hepatocellular carcinoma (HCC). METHODS: PTEN, Phosphorylated AKT (p-AKT), Phosphorylated mTOR (p-mTOR), MMP-2, MMP-9 and Ki-67 expression levels were evaluated by immunohistochemistry on tissue microarrays containing 200 HCCs with paired adjacent non-cancerous liver tissues. PTEN, MMP-2 and MMP-9 mRNA levels were determined by real-time RT-PCR in 36 HCCs. The relationships between PI3K/PTEN/AKT/mTOR pathway and clinicopathological factors and MMP-2, 9 were analyzed in HCC. RESULTS: In HCC, PTEN loss and overexpression of p-AKT and p-mTOR were associated with tumor grade, intrahepatic metastasis, vascular invasion, TNM stage and high Ki-67 labeling index (P < 0.05). PTEN loss was correlated with p-AKT, p-mTOR and MMP-9 overexpression. Furthermore, PTEN and MMP-2, 9 mRNA levels were down-regulated and up-regulated in HCC compared with paired non-cancerous liver tissues, respectively (P < 0.01). PTEN, MMP-2 and MMP-9 mRNA levels were correlated with tumor stage and metastasis. There was an inverse correlation between PTEN and MMP-9 mRNA expression. However, PI3K/PTEN/AKT/mTOR pathway was not correlated with MMP-2. CONCLUSIONS: PI3K/PTEN/AKT/mTOR pathway, which is activated in HCC, is involved in invasion and metastasis through up-regulating MMP-9 in HCC.

[Epigallocatechin-3-gallate induces apoptosis in human hepatocellular carcinoma cells].

OBJECTIVE: To investigate the effects of epigallocatechin-3-gallate (EGCG) on human hepatocellular carcinoma (HCC) cells and mechanism thereof. METHOD: Human HCC cells of the lines HepG2 and SMMC-7721 were cultured and treated with of EGCG of the concentrations of 6.25, 12.5, 25, 50, 100, 200, and 400 microg/ml respectively for 24 h and 48 h. The cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Trypan blue staining was used to count the cells. Flow cytometry was conducted to detect the cell apoptosis. The protein levels of Bcl-2, an anti-apoptosis factor, and cyclooxygenase-2 (COX-2), an up-regulator of Bcl-2. The activities of caspase-9 and caspase-3 hat promote the apoptosis of HCC cells, were measured using colorimetric method. RT-PCR was used to detect the mRNA expression of COX-2 and Bcl-2 family. RESULTS: The viabilities of the HepG2 and SMMC-7721 cells treated with EGCG of the concentrations of 50 - 400 microg/ml for 48 h reduced to 93.8% +/- 2.8%, 62.3% +/- 5.4%, 33.9% +/- 2.5%, and 17.6% +/- 3.2% respectively, all significantly lower than that of the control group [(100.0% +/- 2.8%), all P < 0.05]; and the viabilities of the SMMC-772 cells treated with EGCG of the concentrations of 50 - 400 microg/ml for 48 h reduced to 49.6% +/- 3.5%, 30.3% +/- 3.8%, 17.7% +/- 2.2%, and 13.0% +/- 2.5% respectively, all significantly lower than that of the control group [(100.0% +/- 0.8%), all P < 0.05]. After treatment with 100 microg/ml EGCG for 24 h, 48 h, 72 h, and 96 h, the live HepG2 cell numbers were (8.0 +/- 1.5), (22.0 +/- 3.1), (37.0 +/- 5.4), and (61.0 +/- 8.7) 10(4) respectively, all significantly lower than those of the control cells [(15.0 +/- 2.5), (45.0 +/- 5.3), (86.0 +/- 11.0), and (210.0 +/- 23.0) 10(4) respectively, all P < 0.05]; and the live SMMC-7721 cell numbers were (7.0 +/- 2.2), (13.0 +/- 2.5), (20.0 +/- 3.7), and (31.0 +/- 4.0) 10(4) respectively, all significantly lower than those of the control cells [(15.0 +/- 2.5), (45.0 +/- 5.3), (86.0 +/- 11.0), and (210.0 +/- 23.0) 10(4) respectively, all P < 0.05]. The apoptotic rates of HepG2 cells treated with EGCG of the concentrations of 50, 100, and 200 microg/ml for 12 h were 8.7% +/- 0.4%, 18.1% +/- 1.1%, and 22.1% +/- 1.8% respectively, all significantly higher than that of the control group (3.3% +/- 0.3%, P < 0.05); and the apoptotic rates of SMMC-7721 cells were 5.9% +/- 0.3%, 7.8% +/- 0.6%, and 12.2% +/- 0.8% respectively, all significantly higher than that of the control group (3.7% +/- 0.4%, P < 0.05). After treatment with EGCG of the concentrations of 100 and 200 microg/ml for 12 h, the caspase-9 activities of the HepG2 cells increased to (1.8 +/- 0.4) and (2.5 +/- 0.4) respectively, both significantly higher than that of the control group (1.0 +/- 0.1, both P < 0.05); and the caspase-3 activities of the HepG2 cells increased to (2.0 +/- 0.4) and (2.8 +/- 0.5) respectively, both significantly higher than that of the control group (1.0 +/- 0.2, P < 0.05) ; and the caspase-9 activities of the SMMC-7721 cells increased to (1.7 +/- 0.4) and (2.5 +/- 0.4), both significantly higher than that of the control group (1.0 +/- 0.1, both P < 0.05), and the caspase-3 activities of the SMMC-7721 cells increased to (1.9 +/- 0.4) and (2.6 +/- 0.3) respectively, both significantly higher than that of the control group [ (1.0 +/- 0.2), both P < 0.05]. When the concentration of EGCG was over 200microg/ml, it down-regulated the expression of COX-2 and Bcl-2 in both cell lines, however, EGCG resulted in no significant changes of Bcl-xl, Bax, Bad, and Bid. CONCLUSION: EGCG induces apoptosis in HCC cells through down-regulation of COX-2 and Bcl-2 and consequently activating caspase-9 and caspase-3.

Gli-1 siRNA induced apoptosis in Huh7 cells.

AIM: To investigate the effects of Gli-1 small interference RNA (siRNA) on Huh7 cells, and the change of Bcl-2 expression in Huh7 cells. METHODS: Human hepatocellular carcinoma cells Huh7 were used. Cell viability was analyzed by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. The expressions of Gli-1 and Bcl-2 family members were detected by RT-PCR and Western blot. Apoptosis was detected by Flow cytometry using propidium iodide, measured by Hoechst 33258 staining using Advanced Fluorescence Microscopy and caspase-3 enzymatic assay. Cell growth was analyzed after treatment with Gli-1 siRNA and 5-fluorouracil (5-Fu). RESULTS: Inhibition of Gli-1 mRNA in Huh7 cells through Gli-1 siRNA reduced cell viability. Gli-1 siRNA treatment also induced apoptosis by three criteria, increase in the sub-G1 cell cycle fraction, nuclear condensation, a morphologic change typical of apoptosis, and activation of caspase-3. Gli-1 siRNA was also able to down-regulate Bcl-2. However, Gli-1 siRNA resulted in no significant changes in Bcl-xl, Bax, Bad, and Bid. Furthermore, Gli-1 siRNA increased the cytotoxic effect of 5-Fu on Huh7 cell. CONCLUSION: Down-regulation of Bcl-2 plays an important role in apoptosis induced by Gli-1 siRNA in HCC cells. Combination Gli-1 siRNA with chemotherapeutic drug could represent a more promising strategy against HCC. The effects of the strategies need further investigation in vivo and may have potential clinical application.

[15-deoxy-Delta(12,14)-prostaglandin J(2) induces anoikis of hepatocellular carcinoma cells: an in vitro experiment].

OBJECTIVE: To investigate the effect of 15-deoxy-Delta(12,14)-prostaglandin J(2) (15-d-PGJ(2)) on the anoikis of hepatocellular carcinoma (HC) cells and mechanisms thereof. METHODS: Fibronectin or polyhydroxyethyl methacrylate (poly-HEMA) were coated onto tissue culture plates, cell growth status and morphological changes were detected by optical microscope. DNA fragmentation analysis and Flow cytometry were used to measure cell apoptotic activity. Western blotting analysis was performed to detect the levels of focal adhesion kinase (FAK) and phosphorylated FAK(p-FAK). Furthermore, small interfering RNA (siRNA) was used to suppress FAK expression. RESULTS: The adhesion rate of the BEL-7402 cells treated with 15-d-PGJ(2) began to decrease 12 h after the treatment, time- and dose-dependently compared with the HC cell control group (all P < 0.05); when the concentration of 15-d-PGJ2 was 20 micromol/L, the adherent cells ratio at 24 h and 48 h later were (66.0 +/- 3.6)% and (35.0 +/- 5.0)% respectively. Anoikis of BEL-7402 cells was observed by flow cytometry and DNA fragmentation analysis. Western blotting showed that the p-FAK level of the BEL-7402 cells treated with 15-d-PGJ2 for 24 h decreased dose-dependently, however, the total FAK protein did not change. CONCLUSION: 15-d-PGJ(2) induces anoikis and decreases the phosphorylated FAK expression of the hepatocellular carcinoma cells.