Objective To investigate the effect of circ0000601 on the proliferation of colorectal cancer cell and its possible mechanism.Methods High-throughput circRNA chip was used to screen circRNA gene between colorectal cancer tissues and paired normal tissues.PCR was used to detect the relative expression of circ0000601 in colorectal cancer tissues,paired normal tissues and colorectal cancer cell lines.circ0000601 expression was upregulated through transfecting with circ0000601 mimic and cell proliferation was analyzed by CCK -8 assay.Bioinformatics prediction software was used to analyze circ0000601 target miRNA and luciferasw reporter system was used to verificate circ0000601 target miRNA.The expression of miR-31-Sp was down-regulated through transfection of miR-31-5p inhibitor and cell proliferation was analyzed by CCK-8 assay.miRBase was used to predict the target gene of miR-31-5p and Luciferase reporter assay was used to confirm that NUMB was a direct target of miR-31-5p.The expression of miR-31-5p and NUMB protein expression in colorectal cancer cells was detected by Western blotting.circ0000601 expression was upregulated in colorectal cancer cells and NUMB mRNA expression in colorectal cancer cells were detected.Results T-test and Kruskal-Wallis test were used in data analysis.The expression of circ0000601 was lower in colorectal cancer tissues than paired normal tissues and overexpression of circ0000601 reduced colorectal cancer cell proliferation.miR-31-Sp was identified and validated to be a target miRNA of circ0000601.The knockdown of miR-31-5p suppressed the proliferation of colorectal cancer cells.Luciferase reporter assay confirmed that NUMB was a direct target of miR-31-5p.The protein level of NUMB was decreased by miR-31-5p Mimic.Also up-regulation of circ0000601 could increase the expression of NUMB mRNA.Conclusion circ0000601 can inhibit colorectal cancer cell proliferation by circ0000601/miR-31-5p/NUMB pathway,therefore,circ0000601 acts as a promising therapeutic target for colorectal cancer patients.

This study probed into North Sichuan Medical College to explore the problems existing in the cultivation of medical undergraduate, such as the low innovative and practical abilities, lack of pro-fessional knowledge and low level of literacy. Then the study analyzed the causes of the problem from the aspects of students, teachers, external factors and school environment. Basing on the analysis, the study put forward some talent quality promotion measures, such as improving the quality of enrollment, promoting the faculty building, exploration of scientific management of teaching expenditures, strengthening the construc-tion of discipline and curriculum, constructing teaching quality guarantee system and enhancing students' innovative and operative abilities.

Objective:To uncover the effect of circ0025847 on the proliferation of colorectal cancer cells and its molecular mechanisms.Methods:qRT-PCR was utilized to analyze the expression of circ0025847 and QK1 in human colorectal cancer cells (HCT116, SW480) and normal mucosa cells (NCM460) .CCK-8 was used to analyze the effect of circ0025847 and QK1 on proliferation in colorectal cancer cells. Bioinformatics method was used to screen RBP which could bind to circ0025847. RNA pulldown and RIP was utilized to confirm whether QK1 binds to circ0025847.Effects of circ0025847 over-expression on QK1 expression was analyzed by Western blot.NC group, circ0025847 overexpression group and circ0025847 overexpression+ QK1 inhibitor group were established and the proliferation effect was determined by CCK8.Results:circ0025847 (the expression levels in NCM460, HCT116 and SW480 cells were 1.01±0.05, 0.49±0.08, 0.45±0.10) and QK1 (the expression levels in NCM460, HCT116 and SW480 cells were 0.98±0.07, 0.50±0.07, 0.47±0.09) expression was significantly downregulated in colorectal cancer cells. Overpression of circ0025847 and QK1 suppressed colorectal cancer cells growth.RNA pull-down and RIP clarified that circ0025847 bind to QK1 and circ0025847 positively regulate QK1 expression (7 199.20±12.44 VS 3 889.80±11.03) . circ0025847 inhibiting the proliferation of colorectal cancer cells by promoting the expression of QK1 was confirmed by rescue experiment.Conclusion:circ0025847 inhibits colorectal cancer cells proliferation via positively regulating QK1 expression, indicating that circ0025847 may be potential therapeutic target of colorectal cancer.

Objective:To explore the effect of endoplasmic reticulum stressed (ER) on colorectal cancer (CRC) cell proliferation and invasion via ATG5-mediated autophagy pathway and the underlying mechanism.Methods:We performed bioinformatics analysis to identify the expression level of PERK, ATF6 and ATG5 in CRC tissues and adjacent tissues and the correlation between PERK and ATG5 expression in CRC tissues.The expression level of PERK in CRC cell lines was examined by qRT-PCR assay. Cell proliferation was quantified by CCK-8.The invasion of the cells was detected by Transwell.Western blot assay was performed to verify the levels of protein. The levels of autophagy were examined by electron microscopy.Results:PERK and ATF6 expression in CRC tissues was higher than that in the adjacent tissues and PERK expression was higher in CRC cells than intestinal mucosal cells. Expression level of PERK in CRC cell lines HCT116,SW480,HT29,LoVo and colonic mucosa cell lines FHC was 1.51±0.04,3.12±0.05,2.19±0.04,2.38±0.06 and 0.98±0.04 ( P<0.001) .The increased expression of PERK promoted CRC cell proliferation and invasion. PERK expression levels was positively associated with ATG5 expression levels ( r=0.52, P<0.001) and overexpression of PERK accelerated the protein expression of ATG5 (1.00±0.04,3.53±0.07, t=74.61, P<0.001) . ATG5 was highly expressed in CRC tissues. Overexpression of ATG5 could promote proliferation,invasion and accelerate autophagy of CRC cells (the number of autophagosomes in the blank control group,the negative control group and ATG5-Overexpression group was 4.33±1.53, 4.00±1.00, 9.67±2.52, and t=3.14,3.62, P=0.035,0.022, respectively) .ATG5 promoted colorectal cancer cell proliferation and invasion through autophagy pathway. Conclusion:ER stressed-CRC cells could promote CRC cell proliferation and invasion through ATG5-mediated autophagy pathway.