The research of transcription factor CEBPB activates FJX1 to promote the proliferation,invasion,migration and angiogenesis of colon cancer cells / 中国现代医生

Objective To explore the regulatory relationship between CCAAT enhancer binding protein beta(CEBPB)and four-jointed box kinase 1(FJX1)in colon cancer and their effect on colon cancer(CC)malignant progression and angiogenesis.Methods Bioinformatics was used to analyze the expression of FJX1 and CEBPB in CC and the regulatory relationship between them.Real-time quantitative reverse transcription polymerase chain reaction(qRT-PCR)was used to verify the expression of FJX1 and CEBPB in CC cells,and chromatin immunoprecipitation(CHIP)and dual luciferase assay were used to verify the binding relationship between FJX1 and CEBPB.The effects of FJX1 and CEBPB on the viability,migration,invasion and angiogenesis of CC cells were detected by cell counting kit-8(CCK-8),scratch test,Transwell and angiogenesis test.Results This study revealed that FJX1 was highly expressed in CC.Inhibiting the expression of FJX1 could significantly inhibit the cell viability,migration,invasion and angiogenesis of CC cells.Subsequently,we found that CEBPB was an upstream regulatory gene of FJX1,and CEBPB was highly expressed in CC.CHIP and dual luciferase experiments showed that CEBPB could bind to FJX1.The results of cell experiments showed that the transcription factor CEBPB could promote the proliferation,migration,invasion and angiogenesis of CC cells by activating FJX1.Conclusion CEBPB/FJX1 axis played a cancer-promoting role in the progression of CC,suggesting that CEBPB and FJX1 may be potential therapeutic targets for CC.

Blocking of tripartite motif 8 protects against lipopolysaccharide (LPS)-induced acute lung injury by regulating AMPKα activity.

Acute lung injury (ALI) and its more serious form, respiratory distress syndrome (ARDS), are considered as an acute and severe inflammatory process existing in lungs, and still remain high mortality rates. Tripartite motif 8 (TRIM8) contains an N-terminal RING finger, which is followed by two B-boxes and a coiled-coil domain, belonging to the TRIM/RBCC family and playing significant role in meditating inflammation, oxidative stress and apoptosis. In the study, we investigated the role of TRIM8 in ALI induced by lipopolysaccharide (LPS) and the underlying molecular mechanisms. The in vitro results indicated that LPS time-dependently enhanced TRIM8 expression in lung epithelial cells. Suppressing TRIM8 markedly ameliorated LPS-elicited inflammatory response, as evidenced by the down-regulated mRNA levels of interleukin-1ß (IL-1ß), IL-6 and tumor necrosis factor-α (TNF-α) in cells mainly through inactivating nuclear factor-kappa B (NF-κB) signaling pathway; however, over-expressing TRIM8 markedly promoted inflammation in LPS-challenged cells. In addition, LPS-induced oxidative stress was accelerated by TRIM8 over-expression, while being alleviated by TRIM8 knockdown by regulating Nrf2 signaling. Importantly, TRIM8 could negatively meditate AMP-activated protein kinase-α (AMPKα) activation to modulate LPS-triggered inflammatory response and ROS generation in vitro. Additionally, our in vivo findings suggested that TRIM8 knockdown effectively attenuated LPS-induced lung injury nu decrease of lung wet/dry (W/T) ratio, protein concentrations, neutrophil infiltration, myeloperoxidase (MPO) activity, reactive oxygen species (ROS) production and superoxide dismutase (SOD) depletion. Meanwhile, the loss of TRIM8 markedly lessened IL-1ß, IL-6 and TNF-α expression in lung tissues of LPS-challenged mice, and reduced NF-κB phosphorylation. Furthermore, TRIM8 knockdown evidently improved nuclear factor-erythroid 2 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expressions in lung of LPS-treated mice. The anti-inflammation and anti-oxidant role of TRIM8-silence might be associated with AMPKα phosphorylation. Together, our study firstly provided a support that TRIM8 knockdown effectively protected LPS-induced ALI against inflammation and oxidative stress largely dependent on the promotion of AMPKα pathway.

Observation of the curative effect of colonoscopy combined with laparoscope in the treatment of colonic polyps / 中国基层医药

Objective To explore the curative effect of colonoscopy combined with laparoscope in the treatment of colonic polyps.Methods The clinical data of 48 cases with colonic polyps were retrospectively analyzed.According to the operation pattern,the patients were divided into observation group(23 cases)and control group(25 cases).The observation group received colonoscopy combined with laparoscopy for radical surgery of colon polyps,the control group used the traditional open surgery to remove polyps.The operation time,bleeding volume, exhaust and defecation time,hospital days and cost as well as postoperative complications were observed.Results The two groups were successfully completed surgery.The operative time,bleeding volume of the observation group were (78.3 ±8.2)min and (1 3.1 ±4.5)mL respectively,which of the control group were (1 1 5.5 ±1 0.1 )min, (63.6 ±1 8.1 )mL,the differences between the two groups were statistically significant(t =1 3.93,1 3.01 ,all P 0.05).Conclusion For simple colonoscopy treatment difficulties of colon polyps,colonoscopy,laparoscopy combined treatment is minimally invasive and can improve the safety,strictly control surgical indications,can give full play to the double mirror combined advantage.