OBJECTIVETo investigate the expression of metastasis-associated colon cancer 1 (MACC1) protein in colorectal cancer and its clinical significance.

METHODSImmunohistochemistry method was used to determine the expression of MACC1 protein in colorectal cancer and normal colorectal mucosal tissues (>5 cm distance to cancer tissue). Statistic analysis was performed to investigate the association between clinicopathologic features and MACC1 expression.

RESULTSThe positive rate of MACC1 protein in colorectal cancer tissues was significantly higher than that in normal tissues [75%(72/96) vs. 14.6%(14/96), P<0.01, χ(2)=68.43]. Expression of MACC1 protein was associated with TNM staging (P<0.01, χ(2)=16.82) and distant metastasis (P<0.01, χ(2)=10.53), but not with age, gender, tumor size, differentiation degree, invasion depth, and lymph node metastasis(all P>0.05). Positive rate of MACC1 expression increased with the advanced TNM staging. When distant metastasis occurred, high expression of MACC1 protein in cancer tissues was found. During median 13(4 to 21) months of follow-up, 7 patients died, including 6(8.3%, 6/72) with high expression and 1(4.2%, 1/24) with low expression. Distant metastasis occurred in 9 patients, including 7 with high expression and 2 with low expression. Two patients had local relapse, whose MACC1 expressions were both high.

CONCLUSIONMACC1 protein is highly expressed in colorectal cancer tissues, which may be associated with the invasion and metastasis of colorectal cancer.

Objective:To investigate the changes of reactive oxygen species (ROS) in pancreatic cancer cells under the effect of pulsed electric fields (PEF).Methods:Murine-derived pancreatic cancer cells Panc02 were treated with PEF at electric field strengths of 0, 250, 500, 750, and 1 000 V/cm, respectively. The intracellular ROS generation patterns under the different field strengths and at different times after the PEF were investigated in vitro by flow cytometry and immunofluorescence, meanwhile exploring the apoptosis of murine and human pancreatic cancer cells under different field strengths. Twenty 6- to 8-week-old male C57BL/6 SPF mice were prepared as orthotopic pancreatic cancer models and divided into five groups of four mice each: 250 V/cm PEF group, 500 V/cm PEF group, 750 V/cm PEF group, 1 000 V/cm PEF group, and sham operation group. ROS expression in the residual tumor tissues of mice in each group was detected by immunofluorescence.Results:Under the 500 V/cm, 750 V/cm and 1 000 V/cm electric field strength, the proportion of cells with intracellular ROS expression was decreased after 6 h, 12 h, 24 h and 48 h of the PEF compared with 2 h after the PEF, and the differences were statistically significant (all P<0.05). Compared with 0 V/cm PEF group, ROS expression increased in Panc02 cells treated with 500 V/cm and 750 V/cm PEF groups, and the differences were statistically significant (all P<0.05). Compared with 250 V/cm PEF group under the same time, ROS in Panc02 cells treated with 500 V/cm and 750 V/cm electric field strengths increased, and the differences were statistically significant (all P<0.05). The proportions of apoptosis of both Panc02 cells and MIA-PaCa-2 cells increased with rising field strength and peaked at the field strength of 750 V/cm. Compared with the sham-operated group, the expression of ROS was increased in pancreatic cancer tissues of mice in the 500 V/cm PEF-treated group (16.65±6.01 vs. 2.38±1.21, t=-6.53) and 750 V/cm PEF-treated group (16.54±4.41 vs. 2.38±1.21, t=-6.48), and the differences were statistically significant in both cases (both P<0.001). Conclusion:PEF treatment was able to increase the level of ROS in both pancreatic cancer cells and tissues, and more ROS were produced when the electric field strength was 500 and 750 V/cm.