Sodium butyrate is a sodium salt of four-carbon short chain fatty acids produced by dietary fiber under the action of intestinal microorganisms,it can provide energy for intestinal epithelial cells,and plays an important role in maintaining the integrity of intestinal epithelial cells,inhibiting intestinal inflamma-tion and tumor.In recent years,many studies have indicated that sodium butyrate can mediate apoptosis of colorectal cancer cells by inhibiting histone deacetylase activity,cysteine protease mediation and endoplastic re-ticulum (ER) stress,suggesting that sodium butyrate may be a potential anti-colorectal cancer drug.This arti-cle aims to review the advance progress in the role and mechanism of sodium butyrate in colorectal cancer cell apoptosis,and briefly describe the relationship between sodium butyrate in maintaining intestinal microenvi-ronment and enhancing the immune barrier function of intestinal mucosa with inhibiting intestinal inflamma-tion in order to provide reference for the development of sodium butyrate as first-line anti-colorectal cancer drugs.

Objective:To understand the status quo of emotional intelligence, emotional labor, and humanistic caring ability of medical staff, and to clarify their internal relationship.Methods:Convenience sampling was used to select 713 medical staff from a grade A tertiary hospital in Chengdu, Sichuan Province, China. Emotional Intelligence Scale, Humanistic Caring Scale, and Emotional Labor Scale were used to measure the emotional intelligence, humanistic caring ability, and emotional labor of medical staff. SPSS 22.0 software was used to establish a database for statistical description and analysis. Process 3.2 software was used to analyze the mediating effect.Results:In humanistic caring ability, the average score of comprehension dimension was the highest (75.62±8.20) and the average score of patience dimension was the lowest (58.53±5.01). In emotional labor, the average score of the deep action dimension was the highest (23.39±3.85) and the average score of the surface action dimension was the lowest (17.73±3.18). In emotional intelligence, the average score of self-emotion evaluation dimension was the highest (21.76±3.30) and the average score of other-emotion evaluation dimension was the lowest (20.07±3.71). Positive correlations were found between humanistic caring ability and emotional intelligence, between humanistic caring ability and emotional labor, and between emotional intelligence and emotional labor ( P<0.01). Humanistic caring ability had a partial mediating effect between emotional intelligence and emotional labor. Humanistic caring ability had direct and indirect effects on emotional labor, and the effect sizes were 0.279 and 0.029, respectively. Conclusion:Emotional intelligence has a direct positive predictive effect on emotional labor, humanistic caring ability as an intermediary variable indirectly and positively predicts emotional labor. Humanistic caring ability plays a partial mediating role between emotional intelligence and emotional labor. Attention should be paid to the emotional labor of medical staff, and the emotional labor of medical staff should be improved through targeted training on emotional intelligence and humanistic caring ability. These efforts will improve the current situation and establish a harmonious doctor-patient relationship.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by the highest mortality among carcinomas. The pathogenesis of PDAC requires elevated autophagy, inhibition of which using hydroxychloroquine has shown promise. However, current realization is impeded by its suboptimal use and unpredictable toxicity. Attempts to identify novel autophagy-modulating agents from already approved drugs offer a rapid and accessible approach. Here, using a patient-derived organoid model, we performed a comparative analysis of therapeutic responses among various antimalarial/fungal/parasitic/viral agents, through which econazole (ECON), an antifungal compound, emerged as the top candidate. Further testing in cell-line and xenograft models of PDAC validated this activity, which occurred as a direct consequence of dysfunctional autophagy. More specifically, ECON boosted autophagy initiation but blocked lysosome biogenesis. RNA sequencing analysis revealed that this autophagic induction was largely attributed to the altered expression of activation transcription factor 3 (ATF3). Increased nuclear import of ATF3 and its transcriptional repression of inhibitor of differentiation-1 (ID-1) led to inactivation of the AKT/mammalian target of rapamycin (mTOR) pathway, thus giving rise to autophagosome accumulation in PDAC cells. The magnitude of the increase in autophagosomes was sufficient to elicit ER stress-mediated apoptosis. Furthermore, ECON, as an autophagy inhibitor, exhibited synergistic effects with trametinib on PDAC. This study provides direct preclinical and experimental evidence for the therapeutic efficacy of ECON in PDAC treatment and reveals a mechanism whereby ECON inhibits PDAC growth.

ERK pathway regulated the programmed death ligand-1 (PD-L1) expression which was linked to the response of programmed death-1 (PD-1)/PD-L1 blockade therapy. So it is deducible that ERK inhibitor could enhance the efficacy of PD-1 inhibitor in cancer immunotherapy. In this study, PD0325901, an oral potent ERK inhibitor, strongly enhanced the efficacy of PD-1 antibody

Objective:To investigate the effects and the mechanism of FoxO6 on the proliferation and invasion of colorectal cancer cells.Methods:FoxO6 siRNA was transfected into colorectal cancer cell HCT116 and SW480. The overexpression vector pcDNA.3.1-c-Myc was constructed and co-transfected into HCT116 and SW480 cells with FoxO6 siRNA. Real-time fluorescent quantitative PCR (RT-qPCR) and western blot were used to detect the mRNA and protein expressions of FoxO6, c-Myc, and p21 in HCT116 and SW480 cells. Bromodeoxyuridine (BrdU) was used to detect cell proliferation and Transwell assay was performed to detect the invasion ability of these cells. SW480 cells transfected with FoxO6 shRNA lentivirus (LV-FoxO6) and were injected into the right armpit of BAL b/c nude mice to construct a tumor-bearing mode and the tumor volumes were measured on the days of 10, 13, 16, 19, 22, and 25 after injection.Results:The FoxO6 mRNA were 0.91±0.04, 1.72±0.07, and 2.03±0.06, and protein expression were 0.70±0.04, 1.35±0.08, and 1.56±0.07 in normal colon cell FHC, colorectal cancer cells HT116 and SW480, respectively. The protein and mRNA levels of FoxO6 in HCT116 and SW480 were significantly higher than those in FHC (both P<0.05). Knockdown of FoxO6 in HCT116 and SW480 cells decreased the mRNA and protein expressions of FoxO6 (both P<0.05), the cell proliferation ability (absorbances were 0.26±0.07 and 0.27±0.06, both P<0.05), cell invasion ability (the invaded cell numbers were 42.3±3.3 and 45.7±4.1, both P<0.05), and the mRNA and protein expressions of c-Myc, while increased the mRNA and protein expressions of p21 (both P<0.01). Overexpression of Myc in FoxO6 silenced HCT116 and SW480 cells decreased the expression of p21, while increased the cell proliferation ability (absorbances were 0.54±0.09 and 0.58±0.07, both P<0.01) and invasion ability (the invaded cell numbers were 79.2±5.9 and 80.5±6.4, both P<0.01). On the 25th day after cell inoculation in nude mice, the tumor volume of LV-FoxO6 group was (190.6±36.2) mm 3, significantly lower than (437.8.6±69.2) mm 3 of LV-NC group ( P<0.05). Conclusion:FoxO6 promotes the proliferation and invasion of colorectal cancer cells through facilitating c-Myc mediated p21 expression inhibition.

Objective:To investigate the effects and the mechanism of FoxO6 on the proliferation and invasion of colorectal cancer cells.Methods:FoxO6 siRNA was transfected into colorectal cancer cell HCT116 and SW480. The overexpression vector pcDNA.3.1-c-Myc was constructed and co-transfected into HCT116 and SW480 cells with FoxO6 siRNA. Real-time fluorescent quantitative PCR (RT-qPCR) and western blot were used to detect the mRNA and protein expressions of FoxO6, c-Myc, and p21 in HCT116 and SW480 cells. Bromodeoxyuridine (BrdU) was used to detect cell proliferation and Transwell assay was performed to detect the invasion ability of these cells. SW480 cells transfected with FoxO6 shRNA lentivirus (LV-FoxO6) and were injected into the right armpit of BAL b/c nude mice to construct a tumor-bearing mode and the tumor volumes were measured on the days of 10, 13, 16, 19, 22, and 25 after injection.Results:The FoxO6 mRNA were 0.91±0.04, 1.72±0.07, and 2.03±0.06, and protein expression were 0.70±0.04, 1.35±0.08, and 1.56±0.07 in normal colon cell FHC, colorectal cancer cells HT116 and SW480, respectively. The protein and mRNA levels of FoxO6 in HCT116 and SW480 were significantly higher than those in FHC (both P<0.05). Knockdown of FoxO6 in HCT116 and SW480 cells decreased the mRNA and protein expressions of FoxO6 (both P<0.05), the cell proliferation ability (absorbances were 0.26±0.07 and 0.27±0.06, both P<0.05), cell invasion ability (the invaded cell numbers were 42.3±3.3 and 45.7±4.1, both P<0.05), and the mRNA and protein expressions of c-Myc, while increased the mRNA and protein expressions of p21 (both P<0.01). Overexpression of Myc in FoxO6 silenced HCT116 and SW480 cells decreased the expression of p21, while increased the cell proliferation ability (absorbances were 0.54±0.09 and 0.58±0.07, both P<0.01) and invasion ability (the invaded cell numbers were 79.2±5.9 and 80.5±6.4, both P<0.01). On the 25th day after cell inoculation in nude mice, the tumor volume of LV-FoxO6 group was (190.6±36.2) mm 3, significantly lower than (437.8.6±69.2) mm 3 of LV-NC group ( P<0.05). Conclusion:FoxO6 promotes the proliferation and invasion of colorectal cancer cells through facilitating c-Myc mediated p21 expression inhibition.

Objective: To observe the expressions of periostin (Postn) in colon cancer tissues and cells, and to investigate its biological effect and mechanism in colon cancer cells. Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to detect the expressions of Postn, let-7a and miR-98 in 20 pairs of colon cancer tissues and adjacent normal tissues, colon cancer cell lines including SW480, HT-29, HCT-116 and human normal colon epithelial cell NCM460. Small interfering RNAs (siRNAs) of Postn, pcDNA3.1-Postn plasmids, let-7a mimic and its negative control let-7a mimic-NC, miR-98 mimic and its negative control miR-98 mimic-NC were transfected into HCT-116 cells. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) was used to detect cell viability. Flow cytometry was used to detect cell apoptosis. Luciferase reporter gene assay was used to determine the targeting relationship between miRNAs and Postn. Results: Compared with adjacent normal tissues, Postn expression was up-regulated (P<0.05) while let-7a/miR-98 expression was down-regulated (P<0.05) in colon cancer tissues. Compared with NCM460 cells, Postn expression was up-regulated (P<0.05) while let-7a/miR-98 expression was down-regulated (P<0.05) in SW480, HT-29 and HCT-116 cells. In colon cancer tissues, the expression of Postn was negatively correlated with the expressions of let-7a and miR-98 (r=-0.69, P<0.001; r=-0.80, P<0.001). Inhibition of Postn in vitro reduced the viability of HCT-116 cells [(53.73±7.63)%, P<0.05], increased the apoptotic rate [(22.88±3.40)%, P<0.05], enhanced the expression of epithelial-mesenchymal transition (EMT) marker E-cadherin (2.44±0.39, P<0.05), while down-regulated the expressions of N-cadherin and Vimentin (0.44±0.07 and 0.38±0.06, P<0.05). Overexpression of Postn in vitro enhanced the cell viability of HCT-116 cells [(134.41±8.82) %, P<0.05], decreased the expression of E-cadherin (0.55±0.09, P<0.05), increased the expressions of N-cadherin and Vimentin (2.93±0.42 and 2.24±0.34, P<0.05), but had no effect on the apoptotic rate (P>0.05). Overexpression of let-7a or miR-98 partially reversed the biological effects of Postn overexpression in colon cancer cells, which implicated that Postn was a target gene of let-7a/miR-98. Conclusions Postn is a cancer-promoting molecule of colon cancer, and inhibition of Postn expression can increase the apoptotic rate of colon cancer cells and repress EMT. Postn expression and function is regulated by let-7a/miR-98.

Objective: To analyze the clinical efficacy of thalidomide combined with TP regimen (taxol+cisplatin) in treatment of advanced gastric cancer. Methods: A total of 60 patients with advanced gastric cancer in the Affiliated Cancer Hospital of Zhengzhou University from February 2016 to March 2018 were enrolled. The patients were divided into two groups by using random number table method: the observation group (32 cases) taking thalidomide, oral administration 100 mg based on TP regimen before going to bed; the control group (28 cases) taking TP regimen chemotherapy only. Both groups received 75 mg/m² doses of cisplatin, intravenous infusion, 25 mg/m² per day, for 3 d. Paclitaxel dose was 150 mg/m², intravenous infusion for 1 day, 3-week was one course, and the efficacy was evaluated after at least 2 course of treatment. Results: The incidence of gastrointestinal adverse reactions including nausea and vomiting was 21.8% (7/32) in the observation group, and was 64.3% (18/28) in the control group, and the difference was statistically significant (χ ² = 11.051, P = 0.001), but there were no statistically significant differences in the incidence of morning faint, constipation, bone marrow suppression, liver and kidney injury and other adverse reactions between the two groups (all P > 0.05). The effective rates in the observation group and the control group were 43.8% (14/32) and 39.3% (11/28), respectively, and the disease control rates in the observation group and the control group were 84.4% (27/32) and 78.6% (22/28), respectively. There were no significant differences in the effective rates and the disease control rates between the two groups (χ ² = 0.122, P = 0.726; χ² = 0.336, P = 0.562). The improvement and significant improvement rate of sleeping quality, pain, Eastern Cooperative Oncology Group (ECOG) score was 71.9% (23/32), 53.1% (17/32), 56.2% (18/32), respectively in the observation group, and 17.9% (5/28), 14.3% (4/28), 21.4% (6/28), respectively in the control group, and the difference between the two groups was statistically significant (all P < 0.05). Conclusions Thalidomide combined with TP regimen in treatment of advanced gastric cancer patients can improve the efficacy of chemotherapy and the quality of life. It also has a good tolerance to side effects.

Objective: To explore the clinical characteristics, treatment strategy and prognosis of adenoid cystic carcinoma of the head and neck (ACCHN). Methods: A retrospective analysis of the clinical and follow-up treatment of 79 patients with ACCHN from June 2008 to July 2017 was conducted in the Cancer Hospital of Zhengzhou University. Results: A total of 79 ACCHN cases, including 31 males and 48 females. The age ranged from 19 to 77 (median, 52). The clinical manifestations of ACC were related to the locations of primary tumor.The mean size of the tumor was 2.6 cm (range from 1.5 to 7.7 cm). 50 of 79 patients with a definitive pathological diagnosis received surgical resection. 59 cases received chemotherapy and 62 cases received radiotherapy. With a median follow-up of 55 months, the 5-year, 10-year survival rate of these patients were 69.6% and 54.4%, respectively. Conclusions ACCHN is an uncommon neoplasm with the characteristics of epithelial nerve growth, being inclined to distant metastasis, and high early misdiagnosis rate. The clinical manifestation, imaging and pathological result are need to be combined together to diagnose ACCHN.

Objective: To investigate the role of microRNA-96-5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods: From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA-96-5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para-cancerous tissues were quantified by quantitative real-time PCR (qRT-PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA-96-5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA-96-5p in gastric cancer tissue and adjacent normal tissue were detected by qRT-PCR. miRNA-96-5p mimics was transfected to BGC-823 gastric cancer cells. The effects of miRNA-96-5p on cell proliferation and invasion were detected by cell counting kit-8 (CCK-8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E-cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA-96-5p expressed in BGC-823 cells was detected by dual-luciferase reporter assay. Results: The median expression of miRNA-96-5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para-cancerous tissues (P<0.05). The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para-cancerous tissues (P<0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA-96-5p (r=-0.613, P=0.006). The expression of miRNA-96-5p in gastric cancer cell BGC-823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84±0.15, P<0.05). The results of CCK-8 assay and Transwell assay showed that overexpression of miRNA-96-5p significantly reduced the proliferation and invasion abilities of gastric cancer cells (P<0.05). Overexpression of miRNA-96-5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E-cadherin and downregulated the expression of vimentin. The result of dual-luciferase-3′-UTR reporter assay confirmed that miRNA-96-5p binds to the 3′UTR of FoxQ1. Conclusion miRNA-96-5p may suppress the proliferation, migration and epithelial-mesenchymal transition (EMT) of gastric cancer cell by down-regulation of FoxQ1.