Comparison of local excision and total mesorectal excision for rectal cancer: Systematic review and meta-analysis of randomised controlled trial.

To report the first and largest systematic review and meta-analysis of radomised controlled trials (RCTs) to compare the efficacy and safety of transanal endoscopic microsurgery (TEM) and total mesorectal excision (TME) for rectal cancer for perioperative and oncological outcomes. Methods: We conducted a systematic literature retrieval via PubMed, Embase, Web of Science, and Cochrane until December 2022 for RCTs which evaluated the efficacy and/or safety between TEM and TME for rectal cancer. Outcomes included operative time, blood loss, transfusion rates, hospital stay, complication rates, recurrence rates, and mortality. Results: A total of 5 RCTs involving 545 patients (272 TEM versus 273 TME) were included for the meta-analysis. There were no significant differences between the two groups for age, gender, and distance from lower border of tumor to anal verge. Meta-analysis found that the TEM group was significantly favorable than the TME group for blood loss (WMD: 172.01; 95 % CI: 212.78, -131.24; P < 0.00001), hospital stay (WMD: 2.58; 95 % CI: 3.01, -2.16; P < 0.00001), operative time (WMD: 81.86; 95 % CI: 87.51, -76.21; P < 0.00001) and transfusion rates (RR: 0.05; 95 % CI: 0.01, 0.38; P = 0.004). The complication rates (RR: 0.60; 95 % CI: 0.32, 1.11; P = 0.10), recurrence rates (RR: 1.10; 95 % CI: 0.66, 1.83; P = 0.72), and mortality (RR: 1.23; 95 % CI: 0.67, 2.26; P = 0.51) were similar in the two groups. Conclusions: TEM was an effective and safe approach with advantages in perioperative outcomes compared with TME approach. Caution should be exercised in interpreting the differences in surgical complications between TEM and TME group due to significant heterogeneity and instability.

Unveiling the greenhouse gas emissions of drinking water treatment plant throughout the construction and operation stages based on life cycle assessment.

The carbon peaking and carbon neutrality targets proposed by the Chinese government have initiated a green transformation that is full of challenges and opportunities and endowed sustainable development strategy for combating global warming issue. It is essential to execute comprehensive identification and carbon reduction measures across all industries that produce greenhouse gas (GHG) emissions. Water supply system, as an energy-intensive sector, plays a crucial role in GHG reduction. This work conducted a life cycle assessment (LCA) to account the GHG emissions associated with the construction and operation phases of the drinking water treatment plant (DWTP). During the construction phase, the total GHG emissions were 19,525.762 t CO2-eq, with concrete work and rebar project being the dominant contributors (87.712%). The promotion of renewable or recyclable green building materials and low-carbon construction methods, such as the utilization of prefabricated components and on-site assembly, holds significant importance in reducing GHG emissions during the construction phase of DWTP. Regarding the operation stage, the DWTP possessed an average annual GHG emission of 37,660.160 t CO2-eq and an average GHG intensity of 0.202 kg CO2-eq/m3. Most emissions were attributed to electricity consumption (67.388%), chemicals utilization (12.893%), and heat consumption (10.414%). By increasing the use of clean energy and implementing strict control measures in the water supply pumps, energy consumption and GHG emissions can be effectively reduced. This study offers valuable insights into the mapping of GHG emissions in the DWTP, facilitating the identification of key areas for targeted implementation of energy-saving and carbon-reducing measures.

Black phosphorous nanomaterials as a new paradigm for postoperative tumor treatment regimens.

Surgery is currently a mainstream treatment modality for various solid tumor indications. However, aggressive resection of tumor tissues frequently causes postoperative complications, which severely undermine the well-being of patients. Moreover, the residue tumor cells may substantially increase the risk of local and distant tumor relapse. The recent development in black phosphorus (BP)-based nanomaterials offers a promising opportunity to address these clinical challenges. BP is an emerging nanomaterial with excellent biocompatibility and versatile functionality, which has already demonstrated great potential for a variety of biomedical applications including tumor therapy and tissue engineering. In this review, the recent advances in BP-based nanobiomaterials for the post-surgery treatment of solid tumor have been summarized, while specific emphasis was placed on their capability to continuously inhibit residue tumor growth at the surgery site as well as stimulating various healing mechanisms, aiming to preventing tumor relapse while promoting the healing of surgery-induced traumatic soft/hard tissue injuries. It is anticipated that the nanoengineered BP-based materials may open new avenues to tackle those clinical challenges in surgical treatment of solid tumors.

Omarigliptin alleviates cognitive dysfunction in Streptozotocin-induced diabetic mouse.

Increasing epidemiological evidence supports the strong association between diabetes mellitus (DM) and cognitive dysfunction. Omarigliptin is a long-acting dipeptidyl peptidase 4 (DPP-4) inhibitor for the treatment of diabetes. However, the effect of Omarigliptin in diabetes-associated cognitive dysfunction has not been reported. In this study, we established an in vivo diabetic mice model through streptozotocin (STZ) treatment and investigated the therapeutic effect of Omarigliptin in diabetic mice. The results show that administration with Omarigliptin reduced the food and water intake of STZ-induced diabetic mice, accompanied by decreased blood glucose levels and increased serum insulin levels. The Y-Maze test demonstrated that Omarigliptin ameliorated cognitive dysfunction in STZ-induced diabetic mice. Omarigliptin presented a protective role in the brain, as shown by the decreased reactive oxygen species (ROS) level, increased NAD+/NADH ratio, adenosine triphosphate (ATP) level, and ATP synthase activity in the hippocampus. Omarigliptin induced the increased expression level of mitochondrial inner membrane protein sirtuin 3 (SIRT3) and regulated its substrates, including forkhead box O3a (FOXO3a) and superoxide dismutase 2 (SOD2). Furthermore, knockdown of SIRT3 abolished the protective effects of Omarigliptin on mitochondrial dysfunction and cognitive dysfunction in STZ-induced diabetic mice. Taken together, these findings suggest that Omarigliptin improved insulin sensitivity and cognitive function in STZ-induced diabetic mice. Mechanistically, SIRT3 expression is required for the effect of Omarigliptin. This study provided preclinical evidence that Omarigliptin has the neuroprotective effect to improve diabetes-associated cognitive dysfunction.

Effects of various alcohol sacrificial agents on hydrogen evolution based on CoS2@SCN nanomaterials and its mechanism.

Visible light induced photocatalysis converted solar energy to chemical energy in the form of hydrogen. g-C3N4 modified by thermal oxidation etching, doped S, and nonprecious metal cocatalyst CoS2 (CoS2@SCN) were used for photocatalytic hydrogen production. And then the charge transfer behavior and mechanism of various alcohol sacrificial agents on hydrogen evolution was analyzed by optical characterization, impedance analysis, Mott-Schottky, and photocurrent tests. The relationship between the structure and catalytic performance was also explored using characterization methods. The results showed that CoS2 significantly improved the light absorption of g-C3N4, and carrier migration and separation. And when the sacrificial agent was triethanolamine, the nanocomposite CoS2@SCN exhibited best catalytic performance with the highest hydrogen activity of 223.6 µmol g-1 h-1, the minimum volume in-phase charge transfer resistance with 55.19 Ω and the maximum photocurrent and photocurrent density with 5.5 µA cm-2 and 0.63 mA cm-2. The more negatively charged surface of organic alcohols were, the easier they were to react with holes, thus enhanced charge transfer and hydrogen production efficiency. This report provides guidance for the selection of hydrogen producing sacrificial agents and preparation of highly charge-efficient catalysts. And it also provides a theoretical basis for hydrogen production from wastewater and environmental remediation.

[Down-regulation of HDAC6 Expression Can Influence KG1α Cell Proliferation by Inhibiting ERK Pathway].

OBJECTIVE: To study the inhibitory effect of HDAC6 on proliferation of human leukemia KG1α and to explore its mechanism by ERK signaling pathways. METHODS: .The siRNA interference technology was used to inhibit the HDAC6 gene expression; the expression of HDAC6 and prateins of ERK signal pathway was detected by Western blot; the cell proliferation ability was detected by colony forming experiment and trypan blue staining; cell cycle was detected by FCM; and the expression of Ki67 was detected by immunofluorescence. RESULTS: Western blot showed that HDAC6 expression was up-regulated in leukemia cell lines in comparison with the healthy volunteers and bone marrow stromal cells (P＜0.05). Knockdown of HDAC6 significantly inhibited the proliferation and colony formation ability of leukemia cells, promoted cell arrest at G0/G1 phase. The Western blot and immunefluorescence showed that knockdown of HDAC6 suppressed the expression level of Ki67, CDK4, Cyclin D1 and enhanced the expression level of p16, p21, p-ERK (P＜0.05). CONCLUSION: Knockdown of HDAC6 significantly inhibits the proliferation, arrest the cell cycle at G0/G1 phase, and its mechanism probably relates with the activation of ERK signaling pathway.

[Down-regulation of HDAC6 Expression Promotes Apoptosis of Human Leukemia K562 Cells].

OBJECTIVE: To study the promoting-apoptosis effect of HDAC6 on the human leukemia cells and its mechanism. METHODS: The siRNA interference technology was used to inhibit the expression of HDAC6 gene, the RT-PCR and Western blot were used to detect the expression of HDAC6 and related signal pathway proteins respectively, the flow cytometry and Hoechest staining were used to detect the apoptosis and morphology changes of K562 cells. RESULTS: Compared with the periphal blood monocyte and bone marrow stromal cells of healthy volunteers, the expression level of HDAC6 in leukemia cell lines was up-regulated significantly(P<0.05); the flow cytometry and Hoechest staining showed that after interference of HDAC6 gene, the apoptosis of K562 cells increased, moreover the cell morphology was changed; the Western blot detection showed that the interfering HDAC6 increased BAX/BCL-2 ratio and cleaved caspase 3 expression, and activated the MAPK, ATK, ERK signaling pathway. CONCLUSION: The interferance of HDAC6 can promote the K562 cell apoptosis, its mechanism may relate with activation of MAPK signaling pathway.

[Ginsenoside Rh2 induces apoptosis and autophagy of K562 cells by activating p38].

To study the effect of ginseng saponin Rh2 in inducing apoptosis of human leukemia K562 cells, and explore its mechanism from the aspect of autophagy pathway. CCK-8 assay was used to examine the growth inhibition of human leukemia cell lines K562 treated with ginsenoside Rh2; flow cytometry (FCM) was used to detect cell apoptosis; Hoechst staining was used to observe the changes of cell morphological apoptosis; Acridine and MDC staining were used to detect the effects of the Rh2 on autophagy; Western blot and RT-PCR were used to detect the expression levels of the proteins closely associated with autophagy and apoptosis. In order to study the effect of autophagy in proliferation and apoptosis, we used the autophagy inhibitor (3-MA).CCK-8 indicated that Rh2 at low concentration could effectively inhibit the proliferation of leukemia cellsin dose- and time-dependent manners in K562 cells; FCM indicated that Rh2 induced apoptosis; Hoechest staining showed that K562 cells had typical apoptotic morphological changes by treated Rh2; Acridine and MDC staining showed that Rh2 enhanced the green fluorescence and a large number of acidic autophagy vesicles were present; Western blot and RT-PCR results showed that Rh2 increased the expression levels of Beclin-1, LC3A, LC3B, activated Caspase-3 and p-p38 in K562 cells; application of autophagy inhibitors(3-MA) could weaken the inhibition effect of Rh2 on proliferation and induction effect on apoptosis in K562 cells. Ginsenoside Rh2 inhibited the proliferation and induced apoptosis probably through activating p-p38, and inducing cell autophagy signaling pathway in K562 cells.

Protective effects of astragaloside IV against ovalbumin-induced allergic rhinitis are mediated by T-box protein expressed in T cells/GATA-3 and forkhead box protein 3/retinoic acid-related orphan nuclear receptor γt.

3-O-ß-D-xylopyranosyl-6-O-ß-D-glucopyranosyl-cycloastragenol, or Astragaloside IV (AST), is one of the major active ingredients isolated from Astragalus membranaceous with distinct pharmacological effects, and possesses anti-inflammatory, immunoregulatory and antifibrotic properties. However, the effects of AST on allergic rhinitis remain to be elucidated. The present study aimed to examine the effects of AST on immunoglobulin (Ig) E­mediated allergic reactions in vivo, by using a mouse model of allergic rhinitis established via repetitive sensitization and intranasal challenge with ovalbumin (OVA). Intragastric administration of AST (25 mg/kg or 50 mg/kg) or dexamethasone (DEX; 3 mg/kg) significantly alleviated the inflammatory response, nasal symptoms and mucosa remodeling, and decreased the serum levels of OVA­specific IgE in allergic mice. Furthermore, treatment with AST or DEX significantly suppressed the mRNA and protein expression levels of the transcription factor GATA­3 and retinoic acid receptor­related orphan nuclear receptor (ROR)γt in tissue samples isolated from the spleen and nasal mucosa of mice with allergic rhinitis. Conversely, mRNA and protein expression levels of T­box protein expressed in T cells (T­bet) and forkhead box protein 3 (Foxp3) were upregulated in the spleen and nasal mucosa of mice with allergic rhinitis following treatment with AST or DEX, and spleen protein levels of signal transducer and activator of transcription 3 followed a similar trend. In addition, treatment with AST was associated with fewer adverse events compared with treatment with DEX. The present results suggested that treatment with AST may attenuate OVA­induced allergic rhinitis via regulating the expression of the transcription factors GATA­3, RORγt, T­bet and Foxp3, which commit T helper cells to the Th1 phenotype. Therefore, AST may represent an alternative therapeutic approach for the treatment of patients with allergic rhinitis.

Research on the effect of ginseng polysaccharide on apoptosis and cell cycle of human leukemia cell line K562 and its molecular mechanisms.

Ginseng polysaccharide (GPS), a polymer of glucose and the primary constituent extracted from panax ginseng, has been documented to exert various pharmacological properties, including anti-tumor properties. To provide further insights into the anti-tumor functions of GPS, the present study was designed to investigate the effect of GPS on apoptosis and the cell cycle of human leukemia cell line K562 cells, and its underlying mechanisms. The results demonstrated that GPS could inhibit K562 cell proliferation and induce apoptosis in vitro in a concentration- and time-dependent manner. The transcription of P38 and c-Jun NH2-terminal kinase (JNK) mRNA were significantly augmented, while the transcription of extracellular signal-regulated kinase (ERK) mRNA were significantly reduced following treatment with GPS compared with the control group (all P<0.05). In addition, GPS treatment markedly suppressed the expression of phosphorylated (p)-ERK, nuclear factor (NF)-κB p65 and cyclin D1, and increased the synthesis of p-P38 and p-JNK protein expression, as evidenced by immunofluorescence and western blotting analyses. In conclusion, the results indicate that the GPS-mediated MAPK/NF-κB/cyclin D1 signaling pathway serves a crucial role in cell cycle arrest and apoptosis of K562 cells.

20(S)-ginsenoside Rh2 inhibits the proliferation and induces the apoptosis of KG-1a cells through the Wnt/ß-catenin signaling pathway.

Previous research has shown that total saponins of Panax ginseng (TSPG) and other ginsenoside monomers inhibit the proliferation of leukemia cells. However, the effect has not been compared among them. Cell viability was determined by Cell Counting Kit-8 assay, and ultra-structural characteristics were observed under transmission electron microscopy. Cell cycle distribution and apoptosis were determined by flow cytometry (FCM). Real-time fluorescence quantitative­PCR, western blotting and immunofluorescence were used to measure the expression of ß-catenin, TCF4, cyclin D1 and NF-κBp65. ß-catenin/TCF4 target gene transcription were observed by ChIP-PCR assay. We found that 20(S)-ginsenoside Rh2 [(S)Rh2] inhibited the proliferation of KG-1a cells more efficiently than the other monomers. Moreover, (S)Rh2 arrested KG-1a cells in the G0/G1 phase and induced apoptosis. In addition, the levels of ß-catenin, TCF4, cyclin D1 mRNA and protein were decreased. The ChIP-PCR showed that (S)Rh2 downregulated the transcription of ß-catenin/TCF4 target genes, such as cyclin D1 and c-myc. These results indicated that (S)Rh2 induced cell cycle arrest and apoptosis through the Wnt/ß-catenin signaling pathway, demonstrating its potential as a chemotherapeutic agent for leukemia therapy.

[Ginsenoside Rh2-induced inhibition of histone deacetylase 6 promotes K562 cells autophagy and apoptosis in vivo].

To study the in vivo inhibition effect of ginsenoside Rh2 on humanleukemia cells, and explore its mechanism from autophagy and apoptosis aspects, human leukemia K562 cells allograft tumor models were applied, and after administration of ginsenosides Rh2 by gavage, the tumor diameter, volume and inhibitory rate were measured, and the anti-tumor activity of ginsenosides Rh2 was observed. The levels of HAT and HDAC in tumor tissues were detected by chemical colorimetry assay, and expressions of HDAC1, HDAC2, HDAC3, HDAC4, HDAC5 and HDAC6 were detected by Western blotting assay. The expression levels of vital genes closely associated with autophagy and mRNA expressions of HDAC6 and Hsp90 were detected by Real time-PCR. HE staining was used to observe apoptosis, and immunohistochemistry was used to detect the protein expressions of HDAC6, Hsp90 and activated caspases 3. The results showed that ginsenoside Rh2 could inhibit the growth of k562 cells allograft tumor, with a tumor inhibition rate up to 53.10%. Ginsenoside Rh2 could significantly decrease HDAC activity and decrease the expressions of HDAC1, HDAC2 and HDAC6, and inhibit the expressions of HDAC6 and HSP90, increase the expressions of vital autophagy genes (beclin-1, LC3A and LC3B). Histopathological results showed that ginsenosides Rh2 could significantly increase the tumor apoptosis. Therefore, ginsenoside Rh2 had good anti-tumor effect in vivo, and the mechanism maybe associated with regulating autophagy and apoptosis through HDAC6 and Hsp90 pathways and inhibiting the in vivo proliferation of tumor cells.

Ginsenoside 20(s)-Rh2 as potent natural histone deacetylase inhibitors suppressing the growth of human leukemia cells.

BACKGROUND AND OBJECTIVE: Activation and abnormal expression of histone deacetylase (HDAC) which is important target for cancer therapeutics are related to the occurrence of human leukemia. 20(s)-Ginsenoside Rh2 (20(s)-Rh2) may be a potential HDAC inhibitor (HDACi) of leukemia, but the mechanism has not been reported. METHODS: The cell proliferation and apoptosis was assessed in cultured K562 and KG-1α cells. The protein expression was measured with immunoblotting. The activities of HDAC and histone acetyltransferase (HAT) were measured with BCA. In vivo experiments were performed on naked mice carrying K562 cells for assessment of tumor growth, apoptosis, protein expression, and HDAC/HAT activities. RESULTS: 20(s)-Rh2 effectively induced cell cycle arrest at G0/G1 phase and apoptosis in K562 and KG1-α cells, decreased the levels of proteins associated with cell proliferation (Cyclin D1, Bcl-2, ERK, p-ERK) and activated pro-apoptotic proteins (Bax, cleaved Caspase-3, p38, p-p38, JNK, p-JNK). 20(s)-Rh2 down-regulated HDAC1, HDAC2, HDAC6, increased histone H3 acetylation and HAT activity. Moreover, 20(s)-Rh2 inhibited the growth of human leukemia xenograft tumors in vivo. CONCLUSION: 20(s)-Rh2 inhibited the proliferation of K562 and KG1-α cell by reducing the expression and activity of HDACs, increasing histone acetylation, and regulating key proteins in the downstream signaling pathways. Therefore, 20(s)-Rh2 could become a potential natural HDACi for chemotherapy of leukemia.

[Regulatory effect of ginsenoside Rh2 on HDAC1/2 activity and cyclin in human erythroleukemia K562 cells].

OBJECTIVE: To investigate the effects of the 20(S)-ginsenoside Rh2 [Rh2(S)]on cell proliferation, histone deacetylase 1 (HDAC1) and HDAC2 activity, and expression of cyclin in human erythroleukemia K562 cells. METHODS: The K562 cells were treated with Rh2(S) at various concentrations (10-80 µmol/L). Cell proliferation activity was detected by CCK-8 assay. Flow cytometry (FCM) was used to detect cell cycle and apoptotic changes. The HDAC activity of cells was measured by chemical colorimetry. The protein expressions of HDAC1, HDAC2, cyclin D1, CDK4, p16INK4A and p21 after 48 hour-treatment of Rh2 (S) (10, 20, 40, 60 µmol/L) were examined by Western blotting. RESULTS: The proliferation of K562 cells was inhibited by Rh2 (S) (20-80 µmol/L) in dose-and time-dependent manner. FCM analyses revealed that the number of the K562 cells treated with 60 µmol/L Rh2(S) was arrested in G0/G1 phase. The apoptosis rates of K562 cells were respectively (8.09±0.86)%, (9.44±0.53)% and (22.80±2.16)% after induced by 20, 40, 60 µmol/L Rh2(S), which showed statistically significant difference (P<0.05) compared with the control group (2.63±0.14)%. HDAC activity of the cells treated with Rh2(S) (40, 60 µmol/L) was reduced. Western blotting showed that the expressions of HDAC1, HDAC2, cyclin D1 and CDK4 decreased after induced by Rh2(S), and p16INK4A, p21 proteins were enhanced significantly. CONCLUSION: The Rh2(S) can inhibit the proliferation of K562 cells and induce its cycle arrest and apoptosis through inhibiting HDAC1 and HDAC2 activity, down-regulating the expression of cyclin D1 and activating p16INK4A and p21.

An adolescent presenting with malignant fibrous histiocytoma of the testis: a case report.

INTRODUCTION: Malignant fibrous histiocytoma is a very common subtype of soft-tissue sarcoma in middle and late adulthood. However, malignant fibrous histiocytoma of the testis is very rare in adolescents. CASE PRESENTATION: We report here the case of a 14-year-old Han Chinese boy, who presented with left scrotal mass lasting for 20 days along with distending pain for 5 days. A physical examination revealed a chicken egg-sized, firm, well-defined mass and unclear epididymis. A B-scan ultrasonography of the left scrotum displayed a 9.0×5.2×4.5cm medium- or low-echoic lobulated mass, which suggested a left testicular neoplasm. A fine needle aspiration cytology examination revealed that the cells obtained from the patient's testicular neoplasm were composed of myxoid spindle, and ovoid cells with nuclear atypia and mitotic activity, and arranged in a whirlpool or storiform pattern. Under histological examination, the tumor cells were arranged in a storiform pattern, which displayed mucoid matrix degeneration, and grew invasively. Consequently, a histopathological diagnosis suggested myxofibrosarcoma (or myxoid malignant fibrous histiocytoma). CONCLUSIONS: An ultrasonic examination combined with fine needle aspiration cytology should be helpful for the initial differential diagnosis of testicular malignant fibrous histiocytoma. However, the final confirmation relies on histopathological examination. To the best of our knowledge, this is the first reported case of malignant fibrous histiocytoma of the testis in an adolescent.

[Effect of ginseng polysaccharide-induced wnt/beta-catenin signal transduction pathway on apoptosis of human nasopharyngeal cancer cells CNE-2].

OBJECTIVE: To observe the effect of ginseng polysaccharide (GPS) on the proliferation and apoptosis of human nasopharyngeal cancer cells CNE-2, and discuss the possible mechanism. METHOD: The effect of GPS on the growth of CNE-2 cells was observed by CCK8 assay. CNE-2 cells in the logarithmic phase were collected and processed respectively with different concentrations (0, 0. 1, 0. 2, 0. 3. 0. 4 g L-1) of GPS for 48 h. The flow cytometry was used to detect its induction effect on CNE-2 cell apoptosis. Hoechst-33258 cell staining and electron microscope were used to observe the morphological changes of cells. The beta-catenin mRNA expression was detected by Real-time PCR. The protein localizations and expressions of beta-catenin and TCF4 were tested by the immunofluorescence staining. The expressions of beta-catenin, Bcl-2 and Bax proteins were detected by Western blot. RESULT: CCK8 assay results showed that GPS could remarkably inhibit the proliferation of CNE-2 cells, with dose-time dependence. IC50 of cells induced with GPS for 48 h was 0. 39 g L-1. After being processed with GPS with concentrations of 0.1, 0. 2, 0. 3, 0. 4 g L-1 for 48 h, the cell apoptosis rates of human nasopharyngeal cancer cells CNE-2 were (5. 69 +/- 0. 29)% , (10. 3 +/- 0. 63)% , (15. 4 +/- 0. 74 ) % and (35. 7 +/- 1. 86)% , respectively. Significant difference was observed compared with the control group (2. 08 +/- 0. 11) % (P <0. 05). The results of Hoechst-33258 staining showed the characteristics of cell apoptosis. Under the electron microscope, apoptosis bodies could be observed among CNE-2 cells induced with GPS with the concentration of 0. 4 g L -1 for 48 h. The results of Real-time PCR showed a significant reduction in beta-catenin mRNA expression. The results of laser confocal microscopy revealed notable decrease of beta-catenin and TCF4 expression in nucleus and transfer from nucleus to cell membranes in beta-catenin expression areas after being processed with GPS for 48 h. Western blot showed significant decrease in the expressions of beta-catenin and anti-apoptosis protein Bcl-2, with an increasing expression in apoptosis-promoting protein Bax (P <0. 05). CONCLUSION: GPS could significantly inhibit the proliferation of CNE-2 cells and promote thier apoptosis. The obstruction of Wnt/beta-catenin signaling pathway may be an important mechanism for GPS to induce the apoptosis of human nasopharyngeal cancer cells CNE-2.