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Aim To investigate the effect of licochalcone A (LCA) on proliferation and apoptosis of osteosarcoma HOS and U2OS cells and to explore its possible molecular mechanism. Methods The HOS and U2OS cells were cultured in vitro. MTT assay was used to detect the proliferation of the cells after being treated with different concentrations of LCA at different intervention time. Then HOS and U2OS cells were treated with 0. 1% DMSO, or different concentrations of LCA (5, 10, 20 μmol/L), and flow cytometry was used to assess the cell apoptosis. The expression of apoptosis-related protein cleaved PARP1, Bcl-2, Bax, and Akt, ERK were detected by Western blot. The antitumor effect of LCA was detected on U2OS xenograft mice in vivo. Results LCA could inhibit the proliferation of HOS and U2OS cells in a time-and dose-dependent manner. Flow cytometry showed that LCA treatment could induce cell apoptosis. Western blot results showed that LCA could inhibit the phosphorylation of Akt and ERK, increase the expression of cleaved PARP1 and Bax, and decrease the expression of Bcl-2. In the tumor-bearing mouse models, LCA significantly decreased the tumor volume (P < 0. 05) and weight (P < 0. 01). Conclusions LCA could inhibit the proliferation of HOS and U2OS and induce apoptosis possibly by inhibiting the Akt/ERK signaling pathway.
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Objective:To establish the patient derived xenograft (PDX) model of liver malignant tumor, analyze the related factors affecting the carcinogenesis of PDX model, and analyze the differences of biological characteristics between the primary tumor and PDX model.Methods:Fresh liver malignant tumor tissue samples were collected from the patients who received the surgery from the Tianjin First Central Hospital and the samples were inoculated subcutaneously into BALB/c-nu mice. The correlations between clinicopathological information and tumor formation rate were analyzed, and the pathological morphology and specific protein expression of PDX model and primary tumor were compared.Results:Thirty-three PDX models were successfully established from 63 cases of liver malignant tumors. The overall tumor formation rate was 52.4% (33/63), including 46.3% (25/54) of primary liver cancer and 88.9% (8/9) of liver metastasis. The main factors affecting the tumor formation rate were tumor pathological type, distant metastasis and TNM stage (all P<0.05). The pathological morphology and specific protein expression of PDX model and primary tumor were similar. Conclusion:The PDX model of liver malignant tumor was successfully constructed, and the tumor formation rate was high, and can maintain the biological characteristics of the primary tumor.
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Recent studies have shown that miR-338-3p plays an important role in the proliferation and invasion of lung cancer, but whether miR-338-3p regulates lung cancer proliferation and invasion through targeting ring finger protein 121 (RNF121) is still unclear. In order to explore its mechanism, the normal lung cell line MRC-5 and the non-small cell lung cancer line A549 were cultured in vitro. Using qRTPCR and Western blotting detection, we found that the expression of miR-338-3p in A549 lung cancer cells was lower than that in MRC-5 cells, while RNF121 expression increased (P0. 05). In summary, miR-338-3p can target the expression of RNF121 to inhibit the proliferation and invasion of A549 cells and inhibit the growth of subcutaneous transplanted tumors in nude mice. RNF121 is expected to become a new target for the treatment of non-small cell lung cancer.
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Purpose To study the malignant transformation after treating rat oval cell line ( WB-F344 ) with chemical carcinogen N-methyl-N′-nitro-N-nitrosoguanidine ( MNNG) . Methods WB-F344 cells were cultured with MNNG for severe times. The biological characteristics of induced cells were detected through the following methods:to check proliferation activity by flow cytometry analysis, to examine malignant transformation degree of induced cells by soft agar assay and tumor formation in NOD/SCID mice, and to investi-gate the transcriptional and protein levels of hepatocellular carcinoma marker GGT, GST-P by real time-PCR. Results Oval cells in-duced by MNNG showed changes in biological characteristics and malignant molecular markers. Conclusion Hepatic oval cells model is successfully established, which can be confirmed by tumor formation in NOD/SCID mice.
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tumours was found to be slightly faster than those of the controls.Conclusion:Hes1 is overexpressed in colon cancer than that in normal tissue, and Hes1 is upregulated in poorly differentiated cancer samples compared with well-differentiated tumour samples. Hes1 has a positive inlfuence on the ability of tumour-formation in SW620 cellsin vivo.
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Wireless technologies are ubiquitous today and the mobile phones are one of the prodigious output of this technology. Although the familiarization and dependency of mobile phones is growing at an alarming pace, the biological effects due to the exposure of radiations have become a subject of intense debate. The present evidence on mobile phone radiation exposure is based on scientific research and public policy initiative to give an overview of what is known of biological effects that occur at radiofrequency (RF)/ electromagnetic fields (EMFs) exposure. The conflict in conclusions is mainly because of difficulty in controlling the affecting parameters. Biological effects are dependent not only on the distance and size of the object (with respect to the object) but also on the environmental parameters. Health endpoints reported to be associated with RF include childhood leukemia, brain tumors, genotoxic effects, neurological effects and neurodegenerative diseases, immune system deregulation, allergic and inflammatory responses, infertility and some cardiovascular effects. Most of the reports conclude a reasonable suspicion of mobile phone risk that exists based on clear evidence of bio-effects which with prolonged exposures may reasonably be presumed to result in health impacts. The present study summarizes the public issue based on mobile phone radiation exposure and their biological effects. This review concludes that the regular and long term use of microwave devices (mobile phone, microwave oven) at domestic level can have negative impact upon biological system especially on brain. It also suggests that increased reactive oxygen species (ROS) play an important role by enhancing the effect of microwave radiations which may cause neurodegenerative diseases.
Subject(s)
Animals , Apoptosis , Biophysics/methods , Brain/radiation effects , Brain Neoplasms/etiology , Cell Cycle , Cell Line, Tumor , Cell Phone , Central Nervous System/radiation effects , DNA Damage/radiation effects , Electromagnetic Fields , Environmental Exposure , Free Radicals , Humans , Mice , Models, Biological , Mutagens , Neoplasms, Radiation-Induced/diagnosis , Radiometry , Rats , Reactive Oxygen SpeciesABSTRACT
The CCN family involves a group of six secreted proteins that specifically associate with the extracellular matrix.Cyr61 is the first cloned gene of the CCN family.CYR61 can promote cell growth,adhesion,migration,differentiation,apoptosis and extracellular matrix production.The synthesis of CYR61 is highly inducible by serum growth factors,cytokines,and environmental stresses.CYR61 can also modulate the activities of several growth factors and cytokines,including transforming growth factor-β(TGF-β),tumor necrosis factor-α(TNF-α),vascular endothelial growth factor(VEGF),bone morphogenetic proteins(BMPs)and Wnt proteins.Cyr61 is an important regulator in angiogenesis,osteogenesis,and chondrogenesis,and plays an important role in embryonic development,wound healing,tumor formation and development.It is reported that CYR61 plays a role in the course of ocular neovascular diseases.It can promote the proliferation,migration and tube formation of retinal endothelial cells in vitro.Expression of Cyr61 is upregulated in the retinas of diabetic rats and the vitreous of proliferative diabetic retinopathy (PDR)patients.CYR61 is likely to be involved in the pathogenesis of diabetic retinopathy(DR).Research progress on CYR61 in recent years is reviewed in this article.
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This study examined the differences in tumor formation of three bladder tumor cell lines (BIU-87,T24 and E J) after subcutaneously transplanted into nude mice,in order to find the best technique for establishing in vivo bladder tumor model.BIU-87,T24 and EJ cells at logarithmic phase were re-suspended in serum-free medium.The cells suspensions of the identical concentration were subcutaneously transplanted into nude mice and then the success rate and tumor growth were compared among the three cell groups.The results of tumor formation were pathologically evaluated.Lung,liver and kidney tissues were also pathologically examined for distant metastasis.The proliferation of the three cells were determined by immunohistochemically detecting the PCNA expression in the tumors.The results showed that the success rates of EJ and T24 cells were significantly higher than that of BIU-87 cells and no distant metastasis was noted among the three groups.The proliferation levels of EJ and T24 cells was significantly higher than that of BIU-87.But at the later stage of tumor formation,as compared with T24 cells,EJ grew more vigorously,soon resulting in the central necrosis of tumor,which affected the measurement of the actual size of the tumors.Moreover,PCNA staining exhibited that the proliferation of EJ and T24 was significantly higher than that of BIU-87 cells.It is concluded that as compared with BIU-87 cells,EJ and T24 cells had higher success rates,with not significant differences in death rate and distant metastasis found among them.There existed no significant difference in tumor formation between EJ and T24 cells and T24 cells do not rupture easily,which makes it a better cell line for the establishment of in vivo bladder tumor model.