Effect of hypoxia-inducible factor-1α on proliferation and invasion of prostate cancer PC-3 cell in hypoxic situation

Objective We transfected recombinant expression plasmid of pcDNA3. 1-HIF-1α into prostate cancer cells, to research effect of HIF-1α on proliferation of prostate cancer cell PC-3. Methods We selected a stable expression cell line with G418 we selected by transfection

Neamine Inhibits Growth of Pancreatic Cancer Cells In Vitro and In Vivo

Neamine, a non-toxic derivative of neomycin, has recently been shown to have antitumor activities in various types of cancers. However, its effect on pancreatic cancer is still unknown. The study aimed to investigate its antitumor activity on pancreatic cancer and the underlying mechanisms. MTT assay was used to observe the effect of neamine on angiogenin（ANG）-induced As PC-1 cell proliferation. Tissue microassay and immunofluorescence staining were used to detect the expression of ANG and its nuclear translocation, respectively. Tumor xenografts were established by subcutaneous inoculation of As PC-1 pancreatic cancer cells into the right flanks of nude mice, and neamine was injected subcutaneously. Immunohistochemistry was done to observe the expression of ANG, CD31 and Ki-67 in tumor xenografts. It was found that neamine blocked the nuclear translocation of ANG effectively and inhibited ANG-induced As PC-1 cell proliferation in a dose-dependent manner. Neamine had anti-tumor effects on As PC-1 xenograft models. Consistently, neamine reduced the expression levels of ANG, Ki-67 and CD31 in tumor xenografts. It was concluded that neamine may be a promising agent for treatment of pancreatic cancer.

Knockdown of GRHL3 Inhibits Activities and Induces Cell Cycle Arrest and Apoptosis of Human Colorectal Cancer Cells

The Grainyhead-like 3（GRHL3） is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer（CRC） has not been clarified yet. Our microarray analysis has indicated predominant GRHL3 expression in CRC. The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues, as well as using distinct CRC cell lines（HT29 and DLD1）. We observed increased GRHL3 expression at both m RNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction（q RT-PCR） and Western blotting. Moreover, silencing GRHL3 with si RNA could suppress CRC cell proliferation, viability and migration in vitro. We also found that knockdown of GRHL3 could promote cell cycle arrest at G0/G1 phase in HT29 cells and DLD1 cells, and induce cell apoptosis in HT29 cells. Together, our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G0/G1 phase and apoptosis.

Cellular metabolic energy modulation by tangeretin in 7,12-dimethylbenz(a) anthracene-induced breast cancer

Breast cancer is the leading cause of death among women worldwide.Chemoprevention and chemotherapy play beneficial roles in reducing the incidence and mortality of cancer.Epidemiological and experimental studies showed that naturally-occurring antioxidants present in the diet may act as anticancer agents.Identifying the abnormalities of cellular energy metabolism facilitates early detection and management of breast cancer.The present study evaluated the effect of tangeretin on cellular metabolic energy fluxes in 7,12-dimethylbenz（a）anthracene（DMBA）-induced proliferative breast cancer.The results showed that the activities of glycolytic enzymes significantly increased in mammary tissues of DMBA-induced breast cancer bearing rats.The gluconeogenic tricarboxylic acid（TCA） cycle and respiratory chain enzyme activities significantly decreased in breast cancer-bearing rats.In addition,proliferating cell nuclear antigen（PCNA） was highly expressed in breast cancer tissues.However,the activities of glycolytic enzymes were significantly normalized in the tangeretin pre- and post-treated rats and the TCA cycle and respiratory chain enzyme activities were significantly increased in tangeretin treated rats.Furthermore,tangeretin down-regulated PCNA expression on breast cancerbearing rats.Our study demonstrates that tangeretin specifically regulates cellular metabolic energy fluxes in DMBA-induced breast cancer-bearing rats.

Study on the Mechanism of Xiaotan Sanjie Recipe for Inhibiting Proliferation of Gastric Cancer Cells

Objective:To explore the mechanism of Xiaotan Sanjie Recipe (XtSjR, Recipe for dissolving phlegm to eliminate stagnation) in inhibiting proliferation of gastric cancer cells. Methods: The nude mouse human gastric cancer MKN-45 in situ transplantation tumor model was established by use of OB glue, and 40 model mice were randomized into 5 groups, model group, low-dose XtSjR group, middle-dose XtSjR group, high-dose XtSjR group, and 5-Fu group, 8 rats in each group. Human gastric cancer MKN-45 telomerase reverse transcriptase (hTERT) protein and mRNA expressions were assayed by immunohistochemical method and real-time fluorescence quantitative RT-PCR, and influences of XtSjR on the expressions of hTERT protein and mRNA were investigated in the nude mouse human gastric cancer MKN-45 in situ tumor transplantation model. Results: 1) There were significant differences in the mean tumor weight between the low-, middle-, high-dose XtSjR groups and the model group (all P<0.01); 2) There were significant differences in the hTERT positive expression rate between the middle-and high-dose XtSjR groups and the model group (P<0.05 or P<0.01); 3) There were significant differences in the hTERT mRNA content between the middle-and high-dose XtSjR groups and the model group (P<0.05 or P<0.01). Conclusion: 1) XtSjR has a marked inhibitory effect on the growth of gastric cancer cells; 2) XtSjR inhibits telomerase activity by down-regulating the expressions of hTERT protein and mRNA, shortening the length of cancer cell telomeres gradually, losing the ability to infinitely proliferate, and finally inhibiting the growth and proliferation of tumor cells.

Effects of human microRNA-181a-5p on proliferation and migration of gastric cancer cells

Objective To preliminarily explore the effects of human microRNA-181a on migration of gastric cancer cells and its mechanism.Methods The expression of miRNA-181a-5p in gastric cancer cell line GC9811 and peritoneal high metastasis gastric cancer cell line GC9811-P were tested by quantitative real-time polymerase chain reaction(qRT-PCR).GC9811 cell line was

Effects of insulin-like growth factor binding protein 7 on cell cycle and proliferation of gastric cancer in vitro and in vivo

Objective To investigate the effects of insulin-like growth factor binding protein 7(IGFBP7)on the proliferation,cell cycle of gastric cancer cell and the expression of cynlin D1,cyclin-dependent kinase(CDK)4,and to observe the effects of IGFBP7 on the growth of gastric tumor xenografts in nude mice.Methods The MKN-28cell line was interfered by small interfere ribonucleic acid(siRNA)(interfered group),and blank control group,

Inorganic arsenic： A non-genotoxic carcinogen

Inorganic arsenic induces a variety of toxicities including cancer. The mode of action for cancer and non-cancer effects involves the metabolic generation of trivalent arsenicals and their reaction with sulfhydryl groups within critical proteins in various cell types which leads to the biological response. In epithelial cells, the response is cell death with consequent regenerative proliferation. If this continues for a long period of time, it can result in an increased risk of cancer. Arsenicals do not react with DNA. There is evidence for indirect genotoxicity in various in vitro and in vivo systems, but these involve exposures at cytotoxic concentrations and are not the basis for cancer development. The resulting markers of genotoxicity could readily be due to the cytotoxicity rather than an effect on the DNA itself. Evidence for genotoxicity in humans has involved detection of chromosomal aberrations, sister chromatid exchanges in lymphocytes and micronucleus formation in lymphocytes, buccal mucosal cells, and exfoliated urothelial cells in the urine. Numerous difficulties have been identified in the interpretation of such results, including inadequate assessment of exposure to arsenic, measurement of micronuclei, and potential confounding factors such as tobacco exposure, folate deficiency, and others. Overall, the data strongly supports a non-linear dose response for the effects of inorganic arsenic. In various in vitro and in vivo models and in human epidemiology studies there appears to be a threshold for biological responses, including cancer.