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@#Objective: To study the regulatory effects and possible mechanism of long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) on chemotherapy sensitivity to cisplatin (DDP) of colorectal cancer (CRC)．Methods: A total of 112 pairs of matched cancer and adjacent non-cancerous tissues were obtained from the CRC patients who underwent surgical resection in the First Affiliated Hospital of Xinxiang Medical University betweenApril 2006 and March 2011.All specimens were confirmed by pathological examinations. Tumor tissues and corresponding adjacent non-cancerous tissues from 30 cisplatin-sensitive CRC patients and 30 cisplatin-resistant patients were selected. Human CRC cell lines (HT29, SW480, HCT116, RKO and LoVo) and normal colonic epithelial cell line NCM460 were also collected for this study; and DDP-resistant RKO/DDP and LoVo/DDP cell lines were constructed. siPVT1, siNC, LV-PVT1 and LV-NC were transfected into LoVo and RKO cells or LoVo/DDP and RKO/DDP cells using lipofectamineTM2000. The expression of lncRNA PVT1 in CRC tissues and cells was tested by Real-time qPCR. CCK-8 assay, flow cytometry and WB were performed to test the effect of PTV1 knockout or enforcement on cell proliferation, apoptosis and expressions of apoptosis-related proteins, respectively. The CRC subcutaneous transplanted xenograft model was established on athymic nude mice to study the effect of PVT1 over-expression on tumor growth and DDP resistance. Results: PVT1 was highly expressed in the cancer tissues and CRC cells, and its expression was positively associated with cisplatin resistance of CRC. After knockdown of PVT1, the proliferation of cisplatinresistant CRC cells was significantly suppressed, while the apoptosis was significantly enhanced (P<0.05 or P<0.01); Mechanically, the levels of drug resistance-associated molecules, including MDR1 and MRP1, as well as the expression of anti-apoptotic Bcl-2 were significantly downregulated whereas the levels of pro-apoptotic Bax and cleaved caspase-3 were increased in PVT1-silenced DDP-resistant CRC cells. Over-expression of PVT1 reversely increased proliferation and decreased apoptosis of CRC cells (P<0.05 or P<0.01). In addition, PVT1 over-expression in CRC cells significantly promoted DDP-resistance in vivo (P<0.05). Conclusion: Collectively, knockdown of PVT1 expression can significantly suppress cell proliferation and promote apoptosis of DDP-resistant CRC cells. Overexpression of PVT1 can significantly promote the growth of CRC cells in vitro and transplanted xenograft in vivo. PVT1 regulates endogenous apoptosis pathways and further promotes the sensitivity of CRC cells to cisplatin chemotherapy via inhibiting the expressions of MDR1 and MRP1.
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Objective To Study the effects of high mechanical index ultrasound radiation microbubble on colon cancer cell skeletal.Methods Lovo cell were cultured in vitro,and this study was divided into control group,simple contrast agent group,microbubble plus ultrasound radiation group and simple ultrasound radiation group.Ultrasound contrast agent SonoVue and ultransound (frequency 1.5 MHz and MI 1.7) were used.Results In the control group,the microtubes were densest in dyeing silk,and extended to the edge of a cell.In the ultrasound and microbubble group,the microtubes were weaker and thin,the.network was mainly in the structure of the long axis.The cells arranged in a slight pigmentation to the density cell,to reach out many fine short hair,there were obviously a sense of silk and directional.In the microbubble and ultrasound group,Lovo cells streamed of the central significantly reduced,fluorescent lighting,with short hair.There was no difference in the ultrasound group and the microbubble group with microfilament and microtubule.Conclusions High mechanical index ultrasound radiation can changed into vacant,a trace of the assembly and distributed to the tumor cells are attacking,the transfer of restraining.
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Objective To clone cDNA of trichosanthin (TCS) and purify TCS, and to study its influence on apoptosis and growth inhibition of colorectal carcinoma LoVo cells in vitro. Methods MTT assay was adopted to measure the growth inhibition ratio of LoVo cells treated with TCS, and apoptosis was assayed by agarose gel eletrophoresis. Results The results showed that the higher concentration of TCS and the longer testing time, the stronger growth inhibition of LoVo cells. DNA agarose gel eletrophoresis showed a gradient, which confirmed that TCS could induce the apoptosis of LoVo cells. Conclusions TCS can inhibit the growth of LoVo cells in vitro and induce its apoptosis. Our study provides evidence for the application of TCS in clinical treatment of human colorectal carcinoma.
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Objective To study the anti-tumor effects of SFPS against human colon cancer cells.Methods Inhibition of the cell proliferation was measured by MTT assay.SFPS induced apoptosis of lovo and RKO cells was observed by electron microscopy and flow cytometry.The potential of SFPS in inhibiting lovo and RKO cells viability was assessed by MTT assay.Results SFPS significantly exhibited antiproliferative activity which depended on dosage.Morphological examination showed chromosomal condensation, karyotheca margination,cell shrinkage and the presence of apoptosis bodies.The overall effect of SFPS on the cell cycle distribution was examined by flow cytometry.However,it was also found that SFPS arrested the human colon cancer cell line RKO at G0/G1 phase,and the RKO cells at S phase decreased significantly,while no change in cell cycle distribution from SFPS treated lovo cells was observed.Conclusion SFPS may induce the apoptosis of lovo and RKO cells in vitro through anti-tumor proliferation.