AIM： TO study the effect of some genes especially those involved in cell cycle regulation on hepatocellular carcinoma. METHODS： Paraffin-embedded tissue samples of 25 patients （18 males and 7 females） with hepatoc...AIM： TO study the effect of some genes especially those involved in cell cycle regulation on hepatocellular carcinoma. METHODS： Paraffin-embedded tissue samples of 25 patients （18 males and 7 females） with hepatocellular carcinoma were collected from 22 pathology centers in Tehran during 2000-2001, and stained using immunohistochemistry method （avidin-biotin-peroxidase） for detection of p53, cyclinD1, RB1, c-los and N-ras proteins. RESULTS： Six （24%）, 5 （20%）, 12 （48%） and 2 samples （8%） were positive for p53, cyclinDl, C-los and N-ras expression, respectively. Twenty-two （88%） samples had alterations in the （31 cell-cycle checkpoint protein expression （RBI or cyclinD1）. P53 positive samples showed a higher （9 times） risk of being positive for RBI protein than p53 negative samples. Loss of expression of RBI in association with p53 over-expression was observed in 4 （66.7%） of 6 samples. Loss of expression of RBI was seen in all cyclinD1 positive, 20 （90.9%） N-ras negative, and ii （50%） C-fos positive samples, respectively. CyclinD1 positive samples showed a higher （2.85 and 4.75 times） risk of being positive for c-los and N-ras expression than cyclinD1 negative samples. CONCLUSION： The expression of p53, RB1 and c-los genes appears to have a key role in the pathogenesis of hepatocellular carcinoma in Iran. Simultaneous overexpression of these genes is significantly associated with their loss of expression during development of hepatocellular carcinoma.展开更多
Ras gene mutation has been observed in more than 30%of cancers,and 90%of pancreatic,lung and colon cancers.Ras proteins(K-Ras,H-Ras,N-Ras)act as molecular switches which are activated by binding to GTP.They play a rol...Ras gene mutation has been observed in more than 30%of cancers,and 90%of pancreatic,lung and colon cancers.Ras proteins(K-Ras,H-Ras,N-Ras)act as molecular switches which are activated by binding to GTP.They play a role in the cascade of cell process control(proliferation and cell division).In the inactive state,transforming GTP to GDP leads to the activation of GTpase in Ras gene.However,the mutation in Ras leads to the loss of internal GTPase activity and permanent activation of the protein.The activated Ras can promote the cell death or stop cell growth,which are facilitated by Ras-association domain family.Various studies have been conducted to determine the importance of losing RASSF proteins in Rasinduced tumors.This paper examines the role of Ras and RASSF proteins.In general,RASSF proteins can be used as a suitable means for targeting a large group of Ras-induced tumors.展开更多
AIM: To investigate the targeted inhibition of proliferation and migration of SW620 human colon cancer cells by upregulating mi RNA-145(mi R-145).METHODS: Forty-five samples of colon cancer tissues and 45 normal contr...AIM: To investigate the targeted inhibition of proliferation and migration of SW620 human colon cancer cells by upregulating mi RNA-145(mi R-145).METHODS: Forty-five samples of colon cancer tissues and 45 normal control samples were obtained from the biological database of the First Affiliated Hospital of Liaoning Medical University. We performed quantitative analysis of mi R-145 and N-ras expression in tissues; reverse transcriptase polymerase chain reaction analysis of mi R-145 expression in SW620 colon cancer cells and normal colonic epithelial cells; construction of mi R-145 lentiviral vector and determination of mi R-145 expression in SW620 cells transduced with mi R-145 vector; analysis of the effect of mi R-145 overexpression on SW620 cell proliferation; analysis of the effect of mi R-145 overexpression on SW620 cell migration using a wound healing assay; and analysis of the effect ofmi R-145 on N-ras expression using Western blotting. RESULTS: mi R-145 expression was significantly downregulated in colon cancer tissues, with its expression in normal colonic tissues being 4-5-fold higher(two sample t test, P < 0.05), whereas N-ras expression showed the opposite trend. mi R-145 expression in SW620 cells was downregulated, which was significantly lower compared to that in colonic epithelial cells(two sample t test, P < 0.05). mi R-145 vector and control were successfully packaged; expression of mi R-145 in SW620 cells transduced with mi R-145 was 8.2-fold of that in control cells(two sample t test, P < 0.05). The proliferation of mi R-145-transduced SW620 cells was significantly decreased compared to control cells(two sample t test, P < 0.05). At 48 h in the wound healing experiment, the migration indexes and controls were(97.27% ± 9.25%) and(70.22% ± 6.53%), respectively(two sample t test, P < 0.05). N-ras expression in mi R-145-tranduced SW620 cells was significantly lower than others(one-way analysis of variance, P < 0.05). CONCLUSION: mi R-145 is important in inhibiting colon cancer cell proliferation a展开更多
文摘AIM： TO study the effect of some genes especially those involved in cell cycle regulation on hepatocellular carcinoma. METHODS： Paraffin-embedded tissue samples of 25 patients （18 males and 7 females） with hepatocellular carcinoma were collected from 22 pathology centers in Tehran during 2000-2001, and stained using immunohistochemistry method （avidin-biotin-peroxidase） for detection of p53, cyclinD1, RB1, c-los and N-ras proteins. RESULTS： Six （24%）, 5 （20%）, 12 （48%） and 2 samples （8%） were positive for p53, cyclinDl, C-los and N-ras expression, respectively. Twenty-two （88%） samples had alterations in the （31 cell-cycle checkpoint protein expression （RBI or cyclinD1）. P53 positive samples showed a higher （9 times） risk of being positive for RBI protein than p53 negative samples. Loss of expression of RBI in association with p53 over-expression was observed in 4 （66.7%） of 6 samples. Loss of expression of RBI was seen in all cyclinD1 positive, 20 （90.9%） N-ras negative, and ii （50%） C-fos positive samples, respectively. CyclinD1 positive samples showed a higher （2.85 and 4.75 times） risk of being positive for c-los and N-ras expression than cyclinD1 negative samples. CONCLUSION： The expression of p53, RB1 and c-los genes appears to have a key role in the pathogenesis of hepatocellular carcinoma in Iran. Simultaneous overexpression of these genes is significantly associated with their loss of expression during development of hepatocellular carcinoma.
文摘Ras gene mutation has been observed in more than 30%of cancers,and 90%of pancreatic,lung and colon cancers.Ras proteins(K-Ras,H-Ras,N-Ras)act as molecular switches which are activated by binding to GTP.They play a role in the cascade of cell process control(proliferation and cell division).In the inactive state,transforming GTP to GDP leads to the activation of GTpase in Ras gene.However,the mutation in Ras leads to the loss of internal GTPase activity and permanent activation of the protein.The activated Ras can promote the cell death or stop cell growth,which are facilitated by Ras-association domain family.Various studies have been conducted to determine the importance of losing RASSF proteins in Rasinduced tumors.This paper examines the role of Ras and RASSF proteins.In general,RASSF proteins can be used as a suitable means for targeting a large group of Ras-induced tumors.
基金Supported by Liaoning Medical "Principal Fund" special fund clinical construction,No.XZJJ20130214Liaoning Provincial Science and Technology Department of Science and Technology Program,No.2013225305
文摘AIM: To investigate the targeted inhibition of proliferation and migration of SW620 human colon cancer cells by upregulating mi RNA-145(mi R-145).METHODS: Forty-five samples of colon cancer tissues and 45 normal control samples were obtained from the biological database of the First Affiliated Hospital of Liaoning Medical University. We performed quantitative analysis of mi R-145 and N-ras expression in tissues; reverse transcriptase polymerase chain reaction analysis of mi R-145 expression in SW620 colon cancer cells and normal colonic epithelial cells; construction of mi R-145 lentiviral vector and determination of mi R-145 expression in SW620 cells transduced with mi R-145 vector; analysis of the effect of mi R-145 overexpression on SW620 cell proliferation; analysis of the effect of mi R-145 overexpression on SW620 cell migration using a wound healing assay; and analysis of the effect ofmi R-145 on N-ras expression using Western blotting. RESULTS: mi R-145 expression was significantly downregulated in colon cancer tissues, with its expression in normal colonic tissues being 4-5-fold higher(two sample t test, P < 0.05), whereas N-ras expression showed the opposite trend. mi R-145 expression in SW620 cells was downregulated, which was significantly lower compared to that in colonic epithelial cells(two sample t test, P < 0.05). mi R-145 vector and control were successfully packaged; expression of mi R-145 in SW620 cells transduced with mi R-145 was 8.2-fold of that in control cells(two sample t test, P < 0.05). The proliferation of mi R-145-transduced SW620 cells was significantly decreased compared to control cells(two sample t test, P < 0.05). At 48 h in the wound healing experiment, the migration indexes and controls were(97.27% ± 9.25%) and(70.22% ± 6.53%), respectively(two sample t test, P < 0.05). N-ras expression in mi R-145-tranduced SW620 cells was significantly lower than others(one-way analysis of variance, P < 0.05). CONCLUSION: mi R-145 is important in inhibiting colon cancer cell proliferation a
