Potential Mechanism of Taraxaci Herba Against Bladder Cancer： A Review / 中国实验方剂学杂志

Bladder cancer （BCa） is the most common malignant tumor of the urinary system， and its incidence is increasing year by year. At present， for all patients with resectable non-metastatic muscle-invasive BCa， radical cystectomy + bilateral pelvic lymph node dissection is strongly recommended， but they still face the risk of recurrence， metastasis and death. In recent years， the proportion of patients with advanced and metastatic BCa is increasing among patients with newly diagnosed BCa. Although current treatment models are diverse， they often struggle to achieve significant efficacy due to their low effectiveness and adverse effects， resulting in low survival rates for patients with advanced and metastatic BCa. Therefore， the treatment of BCa still faces great challenges， and there is an urgent need to discover an effective new antitumor drug. With the improvement of medical standards， traditional Chinese medicine has shown great advantages in the treatment of BCa. Traditional Chinese medicine is mild and easy to accept， and can inhibit tumor progression through a multi-pathway， multi-way and multi-target manner， so as to exert its anticancer effect. Taraxaci Herba is a medicinal and food homologous plant， which has many biological activities， such as antibacterial， anti-inflammatory， anti-oxidation， anti-tumor， protecting liver and gallbladder， reducing blood sugar and enhancing immunity， and it has shown a clear anticancer effect in breast cancer， liver cancer， gastric cancer， tongue cancer and lung cancer. By reviewing previous studies worldwide， this article summarizes the mechanism of Taraxaci Herba extract in inducing autophagy and apoptosis， inhibiting cell migration and invasion， regulating cell cycle and proliferation， regulating cell metabolism， inhibiting tumor angiogenesis， combining the effects of chemotherapeutic drugs， and regulating the transduction of related signal pathways. On this basis， this study systematically elaborates on the potential mechanism of Taraxaci Herba against BCa， in order to provide a theoretical basis for the research and treatment of BCa.

Chinese Medicine Monomers Regulate Autophagy of Cervical Cancer Cells： A Review / 中国实验方剂学杂志

Autophagy is a lysosome-mediated catabolic process that captures and degrades dysfunctional organelles and useless proteins during cellular stress process， which plays a dual role in cervical cancer. In the early stage of cervical cancer， autophagy inhibits the occurrence and development of cervical cancer by prohibiting the accumulation of oncogenic p62 protein. In the advanced stage of cervical cancer， inhibition of autophagy of cancer cells enhances the sensitivity of cancer cells to chemotherapeutic drugs， thus inhibiting their proliferation. In recent years， the research on Chinese medicine monomers regulating autophagy in the treatment of cervical cancer has attracted extensive attention from scholars at home and abroad. Chinese medicine monomers regulate the autophagy of cervical cancer cells through multiple pathways and multiple targets， so as to increase the apoptosis rate and reduce the resistance of cancer cells to chemotherapeutic drugs. Therefore， this paper reviewed the mechanism of Chinese medicine monomers in inhibiting cervical cancer through autophagy， expecting to find new breakthroughs in the discovery and development of preventive and therapeutic drugs for cervical cancer. By reviewing the literature， it was found that in the early stage of cervical cancer， Chinese medicine monomers activated autophagy to promote apoptosis of cancer cells， and the main mechanism was to increase lysosomal membrane permeability and chemotherapeutic sensitivity and activate intact autophagy flow. In the advanced stage of cervical cancer， inhibition of autophagy reduced the sensitivity of cancer cells to chemotherapy drugs by inhibiting the formation of autophagosomes and autolysosomes. The treatment of cervical cancer by Chinese medicine monomers regulating autophagy has achieved certain effect， but there are few clinical experimental studies and lack of reliable clinical theoretical basis. Therefore， it is essential to carry out more clinical experimental studies on Chinese medicine monomers regulating autophagy to treat cervical cancer， thus finding more reliable theoretical basis for the treatment of tumors.

Chinese Medicine Monomers Regulate Autophagy of Cervical Cancer Cells： A Review / 中国实验方剂学杂志

Autophagy is a lysosome-mediated catabolic process that captures and degrades dysfunctional organelles and useless proteins during cellular stress process， which plays a dual role in cervical cancer. In the early stage of cervical cancer， autophagy inhibits the occurrence and development of cervical cancer by prohibiting the accumulation of oncogenic p62 protein. In the advanced stage of cervical cancer， inhibition of autophagy of cancer cells enhances the sensitivity of cancer cells to chemotherapeutic drugs， thus inhibiting their proliferation. In recent years， the research on Chinese medicine monomers regulating autophagy in the treatment of cervical cancer has attracted extensive attention from scholars at home and abroad. Chinese medicine monomers regulate the autophagy of cervical cancer cells through multiple pathways and multiple targets， so as to increase the apoptosis rate and reduce the resistance of cancer cells to chemotherapeutic drugs. Therefore， this paper reviewed the mechanism of Chinese medicine monomers in inhibiting cervical cancer through autophagy， expecting to find new breakthroughs in the discovery and development of preventive and therapeutic drugs for cervical cancer. By reviewing the literature， it was found that in the early stage of cervical cancer， Chinese medicine monomers activated autophagy to promote apoptosis of cancer cells， and the main mechanism was to increase lysosomal membrane permeability and chemotherapeutic sensitivity and activate intact autophagy flow. In the advanced stage of cervical cancer， inhibition of autophagy reduced the sensitivity of cancer cells to chemotherapy drugs by inhibiting the formation of autophagosomes and autolysosomes. The treatment of cervical cancer by Chinese medicine monomers regulating autophagy has achieved certain effect， but there are few clinical experimental studies and lack of reliable clinical theoretical basis. Therefore， it is essential to carry out more clinical experimental studies on Chinese medicine monomers regulating autophagy to treat cervical cancer， thus finding more reliable theoretical basis for the treatment of tumors.

Bioactive constituents of animal-derived traditional Chinese medicinal materials for breast cancer: opportunities and challenges / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Breast cancer is globally the most common invasive cancer in women and remains one of the leading causes of cancer-related deaths. Surgery, radiotherapy, chemotherapy, immunotherapy, and endocrine therapy are currently the main treatments for this cancer type. However, some breast cancer patients are prone to drug resistance related to chemotherapy or immunotherapy, resulting in limited treatment efficacy. Consequently, traditional Chinese medicinal materials (TCMMs) as natural products have become an attractive source of novel drugs. In this review, we summarized the current knowledge on the active components of animal-derived TCMMs, including Ophiocordycepssinensis-derived cordycepin, the aqueous and ethanolic extracts of O.sinensis, norcantharidin (NCTD), Chansu, bee venom, deer antlers, Ostreagigas, and scorpion venom, with reference to marked anti-breast cancer effects due to regulating cell cycle arrest, proliferation, apoptosis, metastasis, and drug resistance. In future studies, the underlying mechanisms for the antitumor effects of these components need to be further investigated by utilizing multi-omics technologies. Furthermore, large-scale clinical trials are necessary to validate the efficacy of bioactive constituents alone or in combination with chemotherapeutic drugs for breast cancer treatment.

Current progress of iron metabolism and tumor development / 医学研究生学报

Iron is an essential nutrient that not only participates in cell oxidative phosphorylation, DNA synthesis and replication, but also regulates cancer associated genes through hypoxia-inducible factor (HIF).In the process of cancerization, cells change the way of iron metabolism resulting in a high consumption of iron.In this case, pathways of iron acquisition, efflux, storage and regulation are perturbed.Therefore, iron can significantly contribute to tumor growth, cell survival and metastasis.In this paper, we summarize the iron changes in cancer cells and the relationship between the changes and tumorigenesis.We also briefly state the potential problems of current clinical using iron chelating agents in oncotherapy.Targeting iron metabolic pathways may provide new tools for cancer prognosis and therapy.

Properties of realgar bioleaching using an extremely acidophilic bacterium and its antitumor mechanism as an anticancer agent

Realgar is a naturally occurring arsenic sulfide (or Xionghuang, in Chinese). It contains over 90% tetra-arsenic tetrasulfide (As4S4). Currently, realgar has been confirmed the antitumor activities, both in vitro and in vivo, of realgar extracted using Acidithiobacillus ferrooxidans (A. ferrooxidans). Bioleaching, a new technology to greatly improve the use rate of arsenic extraction from realgar using bacteria, is a novel methodology that addressed a limitation of the traditional method for realgar preparation. The present systematic review reports on the research progress in realgar bioleaching and its antitumor mechanism as an anticancer agent. A total of 93 research articles that report on the biological activity of extracts from realgar using bacteria and its preparation were presented in this review. The realgar bioleaching solution (RBS) works by inducing apoptosis when it is used to treat tumor cells in vitro and in vivo. When it is used to treat animal model organisms in vivo, such as mice and Caenorhabditis elegans, tumor tissues grew more slowly, with mass necrosis. Meanwhile, the agent also showed obvious inhibition of tumor cell growth. Bioleaching technology greatly improves the utilization of realgar and is a novel methodology to improve the traditional method.

Apoptosis of SMMC-7721 cells induced by the low-intensity pulsed ultrasound in vitro / 中华物理医学与康复杂志

Objective To explore whether the low-intensity pulsed ultrasound (LIPU) could induce apoptosis on SMMC-7721 cells and to explore the underlying mechanism.Methods The SMMC-7721 cells were randomly divided into 4 groups:a blank control group,which was subject to sham exposure to ultrasound,and 3 ultrasound intervention groups exposed to ultrasound at intensities of 0.5,1.3 and 2.0 W/cm2,respectively.Then they were incubated for 6 h.The cell apoptosis,necrosis and changes of cell cycles were measured using the flow cytometry.The transmission electron microscope (TEM) was used to observe microstructural changes in the cells.The agarose gel electrophoresis (AGE) was used to examine the DNA fragmentation,and Western-blotting was employed to assess the protein expression of caspase-3.Results The average cell apoptosis rate of the 3 intervention groups were 4.66％,8.99％ and 32.41％,respectively.The percentage of cells in G2 phase increased significantly and those in G1 phase decreased significantly in the 3 intervention groups compared to the blank control group at the same time points.In the intervention groups,significant cell apoptosis was observed under TEM,and DNA ladders was seen in AGE,with DNA fragments appearing obviously when cells were incubated for 6 h and 9 h after ultrasound exposure.In intervention groups subject to 1.3 and 2.0 W/cm2 ultrasound exposure,the protein expression of caspase-3 was significantly higher than that of the control group.Conclusion LIPU can inhibit the proliferation and induce apoptosis of SMMC-7721 cells with a dose-dependent feature.The possible mechanism underlying the LIPU-induced cell apoptosis might be related to the activation of the mitochondria pathway,and especially the caspase-3 protein.

Antitumor Effects of Fucoidan on Human Colon Cancer Cells via Activation of Akt Signaling

We identified a novel Akt signaling mechanism that mediates fucoidan-induced suppression of human colon cancer cell (HT29) proliferation and anticancer effects. Fucoidan treatment significantly inhibited growth, induced G1-phase-associated upregulation of p21WAF1 expression, and suppressed cyclin and cyclin-dependent kinase expression in HT29 colon cancer cells. Additionally, fucoidan treatment activated the Akt signaling pathway, which was inhibited by treatment with an Akt inhibitor. The inhibition of Akt activation reversed the fucoidan-induced decrease in cell proliferation, the induction of G1-phase-associated p21WAF1 expression, and the reduction in cell cycle regulatory protein expression. Intraperitoneal injection of fucoidan reduced tumor volume; this enhanced antitumor efficacy was associated with induction of apoptosis and decreased angiogenesis. These data suggest that the activation of Akt signaling is involved in the growth inhibition of colon cancer cells treated with fucoidan. Thus, fucoidan may serve as a potential therapeutic agent for colon cancer.

Anti-cancer Activity of Osmanthus matsumuranus Extract by Inducing G2/M Arrest and Apoptosis in Human Hepatocellular Carcinoma Hep G2 Cells

BACKGROUND: Osmanthus matsumuranus, a species of Oleaceae, is found in East Asia and Southeast Asia. The bioactivities of O. matsumuranus have not yet been fully understood. Here, we studied on the molecular mechanisms underlying anti-cancer effect of ethanol extract of O. matsumuranus (EEOM). METHODS: Inhibitory effect of EEOM on cell growth and proliferation was determined by WST assay in various cancer cells. To investigate the mechanisms of EEOM-mediated cytotoxicity, HepG2 cells were treated with various concentration of EEOM and analyzed the cell cycle arrest and apoptosis induction by flow cytometry, Western blot analysis, 4,6-diamidino-2-phenylindole (DAPI) staining and DNA fragmentation. RESULTS: EEOM showed the cytotoxic activities in a dose-dependent manner in various cancer cell lines but not in normal cells, and HepG2 cells were most susceptible to EEOM-induced cytotoxicity. EEOM induced G2/M arrest in HepG2 cells associated with decreased expression of cyclin-dependent kinase 1 (CDK1), cyclin A and cylcin B, and increased expression of phospho-checkpoint kinase 2, p53 and CDK inhibitor p21. Immunofluorescence staining showed that EEOM-treated HepG2 increased doublet nuclei and condensed actin, resulting in cell rounding. Furthermore, EEOM-mediated apoptosis was determined by Annexin V staining, chromatin condensation and DNA fragmentation. EEOM caused upregulation of FAS and Bax, activation of caspase-3, -8, -9, and fragmentation of poly ADP ribose polymerase. CONCLUSIONS: These results suggest that EEOM efficiently inhibits proliferation of HepG2 cells by inducing both G2/M arrest and apoptosis via intrinsic and extrinsic pathways, and EEOM may be used as a cancer chemopreventive agent in the food or nutraceutical industry.

Anticancer Effect of Lycopene in Gastric Carcinogenesis

Gastric cancer ranks as the most common cancer and the second leading cause of cancer-related death in the world. Risk factors of gastric carcinogenesis include oxidative stress, DNA damage, Helicobacter pylori infection, bad eating habits, and smoking. Since oxidative stress is related to DNA damage, smoking, and H. pylori infection, scavenging of reactive oxygen species may be beneficial for prevention of gastric carcinogenesis. Lycopene, one of the naturally occurring carotenoids, has unique structural and chemical features that contributes to a potent antioxidant activity. It shows a potential anticancer activity and reduces gastric cancer incidence. This review will summarize anticancer effect and mechanism of lycopene on gastric carcinogenesis based on the recent experimental and clinical studies.

Two-way effects on nasopharyngeal carcinoma CNE2 cells growth and mechanisms of different dose naringenin / 中国药学杂志

OBJECTIVE: To explore the influence and the mechanisms of different dose naringenin on nasopharyngeal carcinoma CNE2 cells growth. METHODS: Different concentrations of naringenin (0, 5, 10, 20, 40, 60, 80, 100, 200, 400, 800 μg · mL-1) were used to detect their effects on CNE2 cells growth for 24 to 72 h by MTT Method. High concentrations of naringenin (0, 200, 400 μg · mL-1) for 48 h were used to detect apoptosis by Hochest 33 258 staining. High concentrations of naringenin (0, 200, 400 μg · mL-1) for 48 h were used to detect the cell cycle by flow cytometry. Different concentrations of naringenin (0, 40, 200 μg · mL-1) for 24 and 48 h were used to detect the level of reactive oxygen species (ROS) by flow cytometry, and mRNA expression levels of P53 and C-fos were determined by qPCR. RESULTS: After different concentrations of naringenin administration, CNE2 cells were changed growth rate. Relatively low dose can induce the low level rise of ROS, the low level rise of ROS can induce the up-regulation of the expression levels of c-fos (P < 0.01) and the down-regulation of the expression levels of P53(P < 0.01), so relatively low dose can promote CNE2 cells growth rate. However, relatively high dose can induce the high level rise of ROS, the high level rise of ROS can induce the up-regulation of the expression levels of P53(P < 0.01) and the down-regulation of the expression levels of C-fos (P < 0.01), so relatively high dose can induce apoptosis, also possess the effect of S and G2/M phase blockage(P < 0.01), significantly suppress CNE2 cells growth rate. CONCLUSION: Different dose naringenin has two-way effects on CNE2 cells growth, relatively low dose has carcinogenic effect, relatively high dose has good anticancer effect.

Application of hypericin in cancer therapy and diagnosis / 国际药学研究杂志

Hypericin, used as a medicinal heifo since ancient times, is a natural photosensitizer derived from the plant Hypericum perforantum. Hypericin would produce peroxides to induce apoptosis and inhibit the growth of oncocytes. Meanwhile, hypericin has a specific affinity with tumor pathology organization (underlying accumulation in pathology organization) which has been widely used in optical diagnosis. The present review gives a comprehensive summary of the anticancer effect based on photodynamic therapy, and photodynamic diagnosis of hypericin optical properties, with the purpose of making full use of the hypericin natural resources, and providing a basis for research and development of hypericin derivatives. © 2006 Editorial office of Foreign Medical Sciences.

Chestnut extract induces apoptosis in AGS human gastric cancer cells

In Korea, chestnut production is increasing each year, but consumption is far below production. We investigated the effect of chestnut extracts on antioxidant activity and anticancer effects. Ethanol extracts of raw chestnut (RCE) or chestnut powder (CPE) had dose-dependent superoxide scavenging activity. Viable numbers of MDA-MD-231 human breast cancer cells, DU145 human prostate cancer cells, and AGS human gastric cancer cells decreased by 18, 31, and 69%, respectively, following treatment with 200 microg/mL CPE for 24 hr. CPE at various concentrations (0-200 microg/mL) markedly decreased AGS cell viability and increased apoptotic cell death dose and time dependently. CPE increased the levels of cleaved caspase-8, -7, -3, and poly (ADP-ribose) polymerase in a dose-dependent manner but not cleaved caspase-9. CPE exerted no effects on Bcl-2 and Bax levels. The level of X-linked inhibitor of apoptosis protein decreased within a narrow range following CPE treatment. The levels of Trail, DR4, and Fas-L increased dose-dependently in CPE-treated AGS cells. These results show that CPE decreases growth and induces apoptosis in AGS gastric cancer cells and that activation of the death receptor pathway contributes to CPE-induced apoptosis in AGS cells. In conclusion, CPE had more of an effect on gastric cancer cells than breast or prostate cancer cells, suggesting that chestnuts would have a positive effect against gastric cancer.

Synthetic Bile Acid Derivative HS-1200-induced Apoptosis of Human Osteosarcoma Cells / 대한해부학회지

Bile acids and synthetic its derivatives induced apoptosis in various kinds of cancer cells and had anticancer effects. However, it wasn`t discovered those materials have apoptosis induced effects on osteosarcoma cells. The present study was done to examine the synthetic bile acid derivatives induced apoptosis on osteosarcoma cells and such these apoptosis events. The synthetic bile acid derivatives, chenodeoxycholic acid (CDCA) induced the cell death on human osteosarcoma (HOS) cells contrary to ursodeoxycholic acid (UDCA). HS-1200, a synthetic derivative of CDCAs, was chosen to experiment apoptosis events in HOS cells. HOS cells treated with HS-1200 showed nucleus condensation, cytochrom c release, Bax/Bcl-xL alteration, activation of caspase-3 and caspase-activated deoxyribonuclease (CAD), and degradation of poly (ADP-ribose) polymerase (PARP). Though this study needs more investigations, these in vitro data suggest that treatment of the synthetic bile acid derivatives can give medical therapy on HOS cells.

Anticancer Effect of Persimmon Leaf Extracts on Korean Gastric Cancer Cell

This study was performed to investigate the in vitro and in vivo anticancer effects of persimmon leaf extracts on human gastric cancer cells. In vitro anticancer effects of persimmon leaf extracts (water extract at 80 degrees C for 3 hours, water extract at room temperature for 48 hours, 50% ethanol extract at 80 degrees C for 3 hours, 50% ethanol extract at room temperature for 48 hours, 75% ethanol extract at 80 degrees C for 3 hours and 75% ethanol extract at room temperature for 48 hours) on SNU16 (Korean gastric cancer cell) were investigated by MTT assay. Persimmon leaf extracts exhibited strong in vitro anticancer effects. We found that the higher the ethanol content of the solvent, the stronger the in vitro anticancer effects. Extraction yields, contents of flavonoids, vitamin A, vitamin C and vitamin E were measured. We found that the higher the ethanol content of the solvent, the higher the extraction yields and the contents of flavonoids, vitamin A and vitamin E. Among persimmon leaf extracts, 75% ethanol 80 degrees C extract showed the highest extraction yield, the highest contents of flavonoids, vitamin A and vitamin E and exhibitied the strongest in vitro anticancer effect on SNU16. Therefore, 75% ethanol 80 degrees C extract was chosen as the material to investigate in vivo anticancer effects. In vivo anticancer effect of persimmon leaf 75% ethanol 80 degrees C extract was investigated in SNU16 transplanted nude mice. Twenty five female nude mice (BALB/c) were blocked into five groups according to body weight and raised for 4 weeks with diets containing 4% (w/w), 8% (w/w) persimmon leaf 75% ethanol 80 degrees C extract, with IT (intratumoral) injection treatment with 1.65 mg/100 microliter, 3.3 mg/100 microliter concentration every other day 3 weeks after SNU16 was transplanted. Persimmon 75% ethanol 80 degrees C extract significantly lowered tumor weight and tumor volume in SNU16 transplanted nude mice. Tumor weight and tumor volume in all experimental groups were significantly lower than those in the control group. Helper T cell (CD4) levels of mice injected with 3.3 mg/100 microliter extract significantly increased. Cytotoxic T cell (CD8) levels in all experimental groups significantly increased and helper/cytotoxic T cell ratios in all experimental groups significantly decreased. Natural killer cell and MHC class II molecule in all experimental groups significantly increased. In conclusion, persimmon leaf 75% ethanol 80 degrees C extract exhibited strong in vitro and in vivo anticancer effects against SNU16 cells and it increased cytotoxic T cell, natural killer cell and MHC classII molecule in experimental groups in SNU16 transplanted nude mice.

Studies on anticancer effects of extracts caesalpinia sappan on oral carcinoma and osteosarcoma cells

Anticancer effect of methanol extract of Caesalpinia sappan L. on oral carcinoma (KB) and osteosarcoma (HOS) cells were investigated in this study. In order to elucidate the anticancer mechanism of Caesalpinia sappan L, we analyzed telomerase inhibitory effect of the methanol extract of Caesalpinia sappan L. In addition we prepared 5 fraction samples according to its polarity differences and analyzed anticancer effects on oral carcinoma and osteosarcoma cells. Following results are obtained in this study. 1. 50% cell proliferation inhibitory value (IC50) of the methanol extract of Caesalpinia sappan L. against oral carcinoma (KB) cells and osteosarcoma (HOS) cells were 9.0 microgram/ml and 10.9 microgram/ml, respectively. 2. The methanol extract of Caesalpinia sappan L. showed inhibitory effect of telomerase which is required for cancer cell immortality. Therefore, it seems that the anticancer effect of methanol extract of Caesalpinia sappan is at least partially due to telomerase inhibitory effect. 3. Five fraction samples were prepared according to its polarity and 88.7% of ingredient of total methanol extract was transferred to ethylacetate fraction. Thin layer chromatography analysis showed that dichloromethane fraction contained ingredient with relatively high polarity and ethylacetate fraction contained similar ingredient found in total methanol extract. 4. Anticancer effect was observed in n-hexane, dichloromethane, and ethylacetate fractions. The highest anticancer effect was found in dichloromethane fraction which had IC50 value of 4.4 and>4.0 microgram/ml against oral carcinoma (KB) cells and osteosarcoma (HOS) cells, respectively.

Anticancer Effect and Apoptosis of All-trans-retinoic Acid on the Human Ovarian Epithelial Carcinoma Cell Lines

Ovarian carcinoma is a serious disease in women. Some reports revealed all-trans-retinoic acid (tRA) inhibited the proliferation of ovarian carcinoma cell lines and induced apoptosis. The aim of this study was to evaluate the anticancer and apoptotic effects of tRA and the expression of the retinoic acid receptor (RAR) alpha, beta, gamma, p53, bcl-2, and c-myc genes on the ovarian carcinoma cell lines, NIH OVCAR3 and SKOV3. In both cell lines, the proliferation of tumor cells was inhibited and characteristic morphologic patterns of apoptosis were shown after treatment of tRA. The number of apoptotic cells and the percentage of apoptosis were increased after treatment of tRA. The gel electrophoresis revealed the DNA ladder pattern in the NIH OVCAR3. Gene expressions were observed using northern blotting. There was no RARalpha expression in both cell lines. In NIH OVCAR3, there was no changes in the expression of RARbeta and bcl-2 gene. The RARgamma gene expression of tRA treated group was slightly increased, but p53 gene expression was decreased, and c-myc gene was not expressed. In SKOV3, the expressions of RARbeta, gamma, and p53 genes were increased and that of bcl-2 was decreased in the tRA treated group. There was no change in c-myc gene expression. These results suggest tRA has anticancer and apoptotic effect on both ovarian carcinoma cell lines. RARbeta, RARgamma, bcl-2, and p53 gene expressions were correlated with these effects of tRA on SKOV3 but not on NIH OVCAR3.

Prophylactic efficacy of BCG and polyinosinic : Polycytidylic acid on implanted murine bladder tumor / 대한비뇨기과학회지

A study was done to evaluate whether intraperitoneal Polyinosinic: Polycytidylic acid (Poly I:C) administration in addition to BCG could enhance the anticancer effect of BCG on subcutaneously implanted syngeneic murine bladder tumor. The appropriate administration schedules of Poly I:C and BCG were defined by evaluating the change of natural killer cell activity and cell mediated cytotoxic effect against syngeneic bladder tumor cells or splenic and peritoneal lymphocyte at regular time interval. The prophylactic anticancer effect of Poly I:C alone and Poly I:C plus BCG were evaluated by observing the tumor take rate and growth change of the taken tumor compared to the control group. Bladder tumor take rate and growth of the taken tumor were suppressed after administration of Poly I:C alone. Natural killer cell activity of the splenic and peritoneal lymphocytes were enhanced and in vitro cytotoxicity against MBT-2 was increased after Poly I:C administration. When Poly I:C was administrated in addition to BCG, tumor take rate and tumor growth were more suppressed and the time for appearance of the visible tumor was prolonged compared to BCG therapy alone. In conclusion, Poly I:C showed prophylactic anticancer effect against subcutaneously implanted murine bladder tumor when used alone or in combination with BCG, and the cell mediated cytotoxicity including enhanced NK cell activity seemed to play an important role in their anticancer effect. These results suggest a possibility of Poly I:C, alone or in combination with BCG, would become a new prophylactic treatment modality against bladder tumors.