Objective: To investigate the mechanism of microRNA-1290 （miR-1290） mediating the activation of NF-κB/interleukin-6 （IL-6） signaling by NMyc downstream-regulated gene 1 （NDRG1）, and further explore its impact on the migration and invasion of colorectal carcinoma cells. Methods: Immunohistochemistry were used to detect the expression of IL6 in the tumors and adjacent tissues in 48 cases of colorectal carcinoma. The expression of IL6 and miR-1290 in 20 samples selected at random from the 48 cases, colorectal carcinoma cells and normal colonic epithelial cells, HCoEpiC were detected by qRT-PCR. Western blotting was performed to detect the expression of p-NF-κB, NF-κB, NDRG1, E-cadherin, and vimentin; ELISA was used to test the levels of IL-6 after treatment with miR-1290 inhibitor or mimic, respectively. With the treatment of small interference RNA-IL-6 （siRNA-IL-6） or neutralizing antibody, the effect of miR-1290 in colorectal carcinoma cell migration was assessed by wound healing test, and cell invasion was tested by Matrigel invasion assay. Results: The expression levels of IL-6 were significantly higher in colon cancer tissues than adjacent normal tissues by immunohistochemical staining （P<0.01）, and there was a remarkably positive correlation between miR-1290 and IL-6 mRNA in colorectal carcinoma tissues （r=0.845 4, P<0.01）. Moreover, the expression of miR-1290 in colon cancer cells were significantly higher than in HCoEpiC cell （all P<0.01）. Upregulation of miR1290 by mimic inhibited the expression of NDRG1 and further induced the activation of NF-κB pathway and epithelial mesenchymal transformation（P<0.01）, while the treatment of miR-1290 inhibitor restored the expression of NDRG1 but increased the expression of p-NF-κB（P<0.01）. The scratch results showed miR-1290 upregulation increased the healing rate of colorectal carcinoma cells, which could be blocked by IL-6 silencing（P<0.01）. Coincidently, the number of invasive cells were elevated after miR-1290 mimic treatment, which could be effectively reversed by neutralizing antibody of IL-6（P<0.01）. Conclusion: miR-1290 promotes migration and invasion of colorectal carcinoma cell through the NF-κB/IL-6 axis, which is caused by targeting inhibition of NDRG1.

Objective: To explore the expression of C14ORF169 in patients with colorectal cancer, and analyze its impact on efficacy of chemotherapy and prognosis. Methods:C14ORF169 differences in expression level of colorectal adenoma, colorectal cancer and corresponding normal tissues were compared using Oncomine database. The correlation of C14ORF169 expression with patients′clinicopathological characteristics and prognosis was analyzed by using the GSE12945 and GSE17536 colorectal cancer datasets downloaded from the gene expression omnibus （GEO） database. The C14ORF169 over expression and knockdown colorectal cancer cell lines were constructed respectively, and the 5-fluorouracil （5-FU） halfmaximal inhibitory concentration （IC50） was detected by using CCK-8 method. Results: The level of C14ORF169 in colorectal adenomas and colorectal cancer tissues were significantly higher than that in normal tissues （P<0.05）. Overall survival and colorectal cancer specific survival of patients with high expression of C14ORF169 were significantly shorter than those with low C14ORF169 expression （P<0.05）. High expression of C14ORF169 was closely related to AJCC advanced stage of colorectal cancer. The sensitivity of colorectal cancer cells to 5FU increased after C14ORF169 knockdown, while C14ORF169 overexpression cell lines showed enhanced chemoresistance. Conclusion: C14ORF169 is highly expressed in colorectal cancer, which is associated with chemotherapy resistance and poor prognosis.

Objective: To investigate the effect of Polyphyllin A （PPA） on autophage of colorectal cancer （CRC） cells and its potential mechanism. Methods:Colorectal cancer RKO and HRT18 cells were selected as cell model. RKO and HRT18 cells were treated with different concentrations of PPA, MTT assay was used to detect the cell viability, and to screen the optimal experimental concentration. Colony formation assay was used to detect cell cloning ability. Western blotting was used to detect the expression of microtubule-associated protein Ⅱ light chain-3 （LC3Ⅱ）, expression of AMPactivated protein kinase （AMPK） and mammalian target of rapamycin （mTOR） and its phosphorylation. In addition, immunofluorescence was used to detect autophagosome formation. Molecular docking was used to analyze the interaction of PPA and AMPK. Results: Compared with the 0 μmol/L group, the cell viability in each concentration group of PPA was significantly reduced（P<0.05）. Compared with the 0 μmol/L group, the cloning ability of the two cell lines was significantly reduced （P<0.05）. With the gradual increase of PPA concentration, the expression of LC3Ⅱ in the two cell lines gradually increased, and autophagosomes aggregated. The expression of total AMPK and mTOR protein did not change significantly（P＞0.05）, while the phosphorylation of AMPK was increased and the phosphorylation of mTOR was decreased （P<0.05）. The molecular docking showed that PPA directly combined with AMPK. Conclusion: PPA induced autophagy in CRC cells by directly targeting and activating AMPK.

Objective: To screen the hub genes of colon cancer by bioinformatics methods and verify them through in vitro experiments to explore potential colon cancer molecular markers. Methods： GSE23878， GSE37182 and GSE74602 data sets were downloaded from the GEO database; R language was used to screen differentially expressed genes （DEGs） in colon cancer and adjacent tissues. DEGs was used to perform GO enrichment analysis and KEGG signaling pathway analysis; proteinprotein interaction（PPI） network of DEGs was constructed by using the STRING database， then the hub genes were screened by Cytoscape software. TCGA database was used to validate expression and prognostic value of hub genes. Finally， the functions of hub genes were further verified by cell transfection and MTT assays. Results： A total of 270 overlapping DEGs were obtained from 3 data sets. GO enrichment analysis showed that DEGs were mainly involved in negative regulation of growth， extracellular matrix organization and extracellular structure organization. KEGG signaling pathways analysis showed that DEGs were mainly enriched in Wnt， NFκB and cell cycle signaling pathways. A total of 11 hub genes were screened through the PPI. It was verified by GEPIA database that MYC， TIMP1， UBE2C， SOX9， AURKA， COL1A1， CDC20， TOP2A and CENPF were highly expressed in colon cancer tissues， while CAV1 and CXCL12 were lowly expressed. Survival analysis showed that high expression of AURKA was positively correlated with overall survival （OS） of colon cancer patients （P<0.05）， high expression of TIMP1 was negatively correlated with OS （P<0.05）， and high expression of COL1A1 was negatively correlated with diseasefree survival of colon cancer patients （P<0.05）. Cell transfection and MTT experiments further verified that overexpression of TIMP1 or AURKA could significantly promote the proliferation of colon cancer cells. Conclusion： A total of 11 hub genes of colon cancer were found being involved in the occurrence of colon cancer. The expression of AURKA and TIMP1 may be related to the prognosis of colon cancer.

结直肠癌是常见的消化道肿瘤之一，早期临床症状不明显，发现时往往是中晚期。自噬是一种进化保守的正常细胞中监视机制，它通过溶酶体清除分解受损的细胞器和聚集的蛋白质，并将产生的基础营养物质重新循环利用。在结直肠癌中，自噬对肿瘤的促进与抑制双重作用广泛得到认可，因此，明确自噬对结直肠癌肿瘤细胞的作用，将为结直肠癌的治疗提供更多的理论依据。本文对自噬在结直肠癌发展过程中的作用进展进行综述。