Oral squamous cell carcinoma (OSCC) is a prevalent malignant tumor affecting the head and neck region (Leemans et al., 2018). It is often diagnosed at a later stage, leading to a poor prognosis (Muzaffar et al., 2021; Li et al., 2023). Despite advances in OSCC treatment, the overall 5-year survival rate of OSCC patients remains alarmingly low, falling below 50% (Jehn et al., 2019; Johnson et al., 2020). According to statistics, only 50% of patients with oral cancer can be treated with surgery. Once discovered, it is more frequently at an advanced stage. In addition, owing to the aggressively invasive and metastatic characteristics of OSCC, most patients die within one year of diagnosis. Hence, the pursuit of novel therapeutic drugs and treatments to improve the response of oral cancer to medication, along with a deeper understanding of their effects, remains crucial objectives in oral cancer research (Johnson et al., 2020; Bhat et al., 2021; Chen et al., 2023; Ruffin et al., 2023).
Humans ; Mouth Neoplasms/pathology* ; Carcinoma, Squamous Cell/metabolism* ; Luteolin/therapeutic use* ; Squamous Cell Carcinoma of Head and Neck/drug therapy* ; Head and Neck Neoplasms/drug therapy* ; Cell Line, Tumor

Objective:To identify the risk factors associated with postoperative adjuvant chemotherapy in patients with stage I gastric cancer and establish nomograms model based on risk factors.Methods:In this retrospective case-control study, 161 cases with stage Ⅰ primary gastric adenocarcinoma were included who underwent gastrectomy at the Department of General Surgery of the First Medical Center of Chinese PLA General Hospital from January to December in 2020, including 129 male cases and 32 females cases, with the average age of (59.90±0.80) years. Among them, 41 cases were treated with postoperative adjuvant chemotherapy (chemotherapy group), while 120 cases who did not receive postoperative adjuvant chemotherapy (no chemotherapy group). Univariate and multivariate Logistic regression analyses were used to identify the risk factors of adjuvant chemotherapy in stage Ⅰ gastric cancer patients and establish the nomograms predictive model. ROC curve and calibration curve were used to evaluate the performance of the model.Results:Multivariate analysis revealed that primary tumor site, tumor size, T stage, N stage lymph-vascular tumor embolus or perineural invasion were the independent risk factors of postoperative adjuvant chemotherapy for stage Ⅰ gastric cancer( P<0.05). The ROC curve indicated that area under the curve (AUC) of the multivariate model was 0.91(95% CI: 0.86-0.97). The calibration curve showed that probability predicted by nomograms was consistent with the actual situation(C-index: 0.91). Conclusions:The tumor located in the proximal stomach, tumor size>2 cm, T 2, N 1, lymph-vascular tumor embolus or perineural invasion maybe be the risk factors for chemotherapy decision in stage Ⅰ gastric cancer patients. The established model has good predictive ability for postoperative chemotherapy of stage Ⅰ gastric cancer patients, which might provide reference for the selection of clinical decisions in this part of patients.

【Objective】 To investigate the effects and molecular mechanism of Elafibranor (ELA) on the proliferation, migration and apoptosis of human prostate cancer (PCa) cells. 【Methods】 After PCa DU145 cells were treated with culture media containing different dosages of ELA, the proliferation, migration and apoptosis were determined with MTT assay, wound healing assay and Transwell assay, respectively. The expressions of genes related to lipid metabolism were detected with real-time quantitative polymerase chain reaction (real-time qPCR). 【Results】 The relative cell proliferation rate at 48 h was 100% in the blank control group, (86.9±7.8)% in the low-dose (5 μmol/L) group and (58.5±9.4)% in the high-dose (15 μmol/L) group;the wound healing rate at 24 h was (74.7±3.2)%, (61.8±2.9)% and (53.2±3.3)%;the relative percentage of migrated cells at 24 h was 100%, (32.4±11.2)% and (15.4±3.2)%;the cell apoptosis rate at 48 h was (9.3±1.4)%, (11.3±0.3)%, and (15.2±4.5)%, respectively, all P<0.05. After ELA treatment for 48 h, the genes related to fatty acid intake (SCPX, PLTP) and fatty acid oxidation (PDK1, ACOX2) were significantly down-regulated in the high-dose group, while the gene related to fatty acid deposition (PLIN2) was significantly up-regulated, indicating that the lipid metabolism pathway of DU145 cells was seriously interfered by the ELA treatment. 【Conclusion】 ELA can inhibit the proliferation and migration, and promote the apoptosis of prostate cancer cells by interfering in the lipid metabolism pathway, which exhibits remarkable potential of clinical translation in the field of anti-tumor chemotherapy.

In recent years, with the continuous studies on tumor metabonomics, more and more results have shown that changes of metabolism play important roles in the occurrence and development of malignant tumor. Carcinogenic factors can destroy the metabolic balance of human body, induce metabolic reprogramming, and then mediate a variety of biological behaviors to partici-pate in the proliferation and invasion of cancer cells. Lipids provide the body with the necessary energy and essential fatty acids, and a variety of lipid molecules and metabolites are involved in cell signal transduction. Lipid metabolism is an important link in the metabolic system of the body, and the relationship between the occurrence and development of pancreatic cancer and lipid metabo-lism is not clear. The purpose of this paper is to reveal the changes of lipid metabolism in pancreatic cancer, summarize some preclinical studies and clinical trials, and deeply explain the research status of abnormal lipid metabolism associated with pancreatic cancer, so as to provide new ideas for the study of pancreatic cancer pathogenesis and accurate treatment.

Pancreatic cancer is a rapidly progressive and highly malignancy of the digestive system. In recent years, the diagnosis and treatment of pancreatic cancer has been in a slow stage of development, and the 5-year survival rate of patients remains very low. The main objective of translational medicine is to remove the barriers between basic medical research and clinical medical applications, to achieve practical integration between laboratory and clinic, and to accelerate the translation of the results obtained from basic research into clinical diagnosis, evaluation and treatment of diseases, thus promoting the development of life sciences. With the rapid development of the concept and technology of translational medicine, its application in the early diagnosis of pancreatic cancer can bring new hope for effectively improving the overall prognosis of patients. The authors comprehensively analyzed the latest research progress of translational medicine in the early diagnosis of pancreatic cancer in order to improve the early diagnosis and long-term survival of pancreatic cancer patient.

Objective:To observe the protective effects of Clostridium butyricum and butyrate on pancreas, liver and intestinal mucosa in rats with acute necrotizing pancreatitis (ANP), and to explore the possible mechanism.Methods:Forty Sprage-dawley rats were randomly divided into control group, ANP group，Clostridium butyricum treated group(CB group) and butyrate treated group(SB group), with 10 rats in each group by random number method. The ANP rat models were prepared by retrograde injection of sodium taurocholate into the biliopancreatic duct. Rats in CB and SB group were given intragastic administration of Clostridium butyricum 1×10 9 CFU or sodium butyrate (100 mg/kg) in 10 days once a day before modeling. Serum amylase (SAMY), lypase, ALT, AST, TBil, tumor necrosis factor alpha(TNF-α), IL-6 and HMGB1were measured after 24 h. Protein from intestinal mucosa was extracted and Western Blotting was used to measure expression of tight-junction proteins ZO-1, claudin-1 and occludin. Pancreas and liver tissues were stained with hematoxylin-eosin and scored by pathology. Results:The levels of amylase [(9365.1±716.5), (5947.3±512.0), (6517.7±269.6)U/L], lipase[(8343.7±1041.4), (6600.4±899.7), (6754.4±1046.4)U/L], AST[(560.5±72.7), (432.0±76.2), (429.8±40.5)U/L], ALT[(499.9±65.2), (385.7±46.0), (395.8±45.8)U/L], TBil[(134.2±56.2), (74.3±65.2), (81.3±35.3)U/L], TNF-α[(162.0±14.4), (100.4±6.3), (119.2±12.5)ng/L], IL-6[(161.4±26.0), (104.8±15.2), (105.5±12.7)ng/L], HMGB1[(100.1±6.7), (58.0±7.7), (63.4±7.2)ng/L] in ANP group, CB group and SB group were detected; and the pathological scores of pancreas[(11.2±1.08)，(9.45±1.06), (9.04±0.89)] and liver[(2.89±0.73), (2.09±0.49), (2.12±0.52)] in ANP group，CB group and SB group were higher than those in control group[(100.6±5.20)U/L, (966.5±301.9)U/L，(30.2±6.3)U/L, (27.6±5.9)U/L, (2.4±0.6)U/L, (29.5±4.8)ng/L，(36.9±7.6)ng/L，(35.5±5.7)ng/L，(1.18±0.05)，(0.56±0.09)]. However, those indexes in CB group and SB group were lower than those in ANP group, and the difference was statistically significant (all P<0.05). The expression of ZO-1 in control group, ANP group, CB group and SB group was 1.83, 0.79, 1.25 and 1.16. The expression of claudin-1 in control group, ANP group, CB group and SB group was 0.58, 0.13, 0.43 and 0.37. The expression of occludin in control group, ANP group, CB group and SB group was 1.06, 0.38, 0.82 and 0.79. The expression of TJ proteins in ANP group was significantly lower than that in other groups and the difference was statistically significant (all P<0.05). Conclusions:Clostridium butyricum and metabolites butyrate can alleviate the inflammatory response in ANP rats with liver injury, maintain the function of intestinal mucosal barrier and prevent the liver injury.

Objective: To explore the relationship between plasma coagulation factor XIII (FXIII) and bleeding events. Methods: A total of 55 cases of acute leukemia (AL) at the myelosuppression phase after chemotherapy hospitalized in our hospital from August 2017 to March 2018 were enrolled, with 35 normal controls. The concentration of plasma coagulation factor XIII (FXIII) was detected by ELISA to determine the relationship between the plasma FXIII levels in AL patients at the myelosuppression phase after chemotherapy with bleeding events. Results: The level of FXIII in AL patients at the myelosuppression phase after chemotherapy was significantly lower than that in controls (P<0.001) . The level of FXIII was inversely related with the bleeding severity (the Spearman correlation coefficient -0.761) . Given the diagnosis cut-off point of FXIII concentration as 103.9 μg/L, the sensitivity of diagnosing bleeding in AL patients at the myelosuppression phase after chemotherapy was 0.939, and the specificity 0.909. Conclusion AL patients at the myelosuppression phase after chemotherapy had low level of plasma FXIII, and patients with lower plasma FXIII associated with higher incidence and severity of bleeding. FXIII level was an independent influencing factor of bleeding in AL patients at the myelosuppression phase after chemotherapy.

Objective: To evaluate the protective effect of granulocyte-colony stimulating factor(G-CSF) on neonatal rats after hypoxic-ischemic brain damage(HIBD)and its effect on endoplasmic reticulum (ER) stress. Methods: According to the random number table, a total of 54 Sprague-Dawley (SD) rats aged 7 days were divided into 3 groups(18 rats in each group): Sham group, HIBD group and G-CSF group, and the improved Rice method was used to establish a neonatal rat model of HIBD.A dose of 50 μg/kg of G-CSF was administered intraperitoneally 1 hour after HIBD (G-CSF group), while the rats in HIBD group and Sham group received saline only.At 24 hours of HIBD, pups were euthanized to quantify brain infarct volume by using 2, 3, 5-Triphenyltetrazolium chloride.Hematoxylin-Eosin (HE) staining was used to observe the changes of brain structure.Neuronal cell death was determined by using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). Then the expressions of glucose-regulated protein 78 (GRP78), cysteinyl aspartate specific proteinase 12 (Caspase-12), CCAAT/enhancer binding-protein homologous protein (CHOP) were assessed by Western blot and immunofluorescence staining. Results: Twenty-four hours after operation, HE staining showed that no significant neuronal damage was observed in Sham group.The brain tissue structure of rats in the HIBD group was significantly damaged, while some improvement was observed in the G-CSF group.The infarction volume in HIBD group[(25.40±5.15)%] increased compared with that in the Sham group[(0.31±0.15)%] and the G-CSF group[(16.36±4.97)%], and the differences were statistically significant(all P<0.05). There was increased positive expression of GRP78 protein in HIBD group, compared with that in the Sham group and the G-CSF group[(49.38±10.06)% vs.(9.12±4.50)%, (30.61±6.35)%], and the differences were statistically significant (all P<0.05). The percentage of apoptosis in the hippocampal CA1 region and conex in HIBD group [(44.84±11.54)%, (48.23±14.07)%] were higher than those in the G-CSF group [(17.87±7.20)%, (26.18±9.96)%], and the differences were statistically significant (all P<0.05). The expression of GRP78, CHOP and Caspase-12 in the HIBD group (0.63±0.24, 0.72±0.21, 0.68±0.25) were higher than those in the Sham group (0.20±0.08, 0.28±0.08, 0.23±0.07), and the G-CSF group (0.39±0.13, 0.51±0.18, 0.48±0.16), and the differences were statistically significant (all P<0.05). Conclusions G-CSF exerts neuroprotective effect on the neonatal rats after HIBD.G-CSF may be an effective treatment of HIBD by reducing ER stress-induced neuronal apoptosis.

Objective To explore the effect of Clostridium butyricum ( C. butyricum ) and its metabolite butyrate on the function of intestinal mucosal barrier and intestinal flora in acute necrotizing pancreatitis ( ANP) rats with intra-abdominal hypertension ( IAH) . Methods Eighty SD rats were randomly divided into normal control group (A group, n=20), ANP with IAH group(B group, n=20), ANP with IAH and C. butyricum treated group ( C group, n=20 ) , ANP with IAH and sodium butyrate treated group ( D group, n=20). Rats of C and D group were given intragastric administration of C. butyricum 1 × 109 CFU once a day or 100 mg/kg sodium butyrate once a day from 10 days before modeling. Sodium taurocholate injection method via pancreatobiliary ducts was used to establish ANP with IAH rat model, and the intra-abdominal pressure was measured by direct puncture of left lower belly 24 h after modeling. Blood samples were collected for detecting serum amylase(AMY), tumor necrosis factor alpha (TNF-α), diamine oxidase( DAO ) , lipopolysaccharide ( LPS ) and D-Lactate, and the pathological changes of terminal ileum was observed. Real-time quantitative PCR was used to detect the populations of 6 bacteria in ileum mucosa. Results The levels of AMY, TNF-α, LPS,DAO, D-Lactate and ileum mucosa score were obviously higher in B, C and D group than those in A group, but the number of piobiotic flora in ileum mucosa was lower than that in A group, while the number of pathogenic bacteria was higher than that in A group. The levels of LPS, DAO, D-Lactate and ileum mucosa pathological score were lower in C group and D group than those in B group, but the number of piobiotic flora in ileum mucosa was lower than that in B group, while the number of pathogenic bacteria was higher than that in B group. All the differences above were statistically different (P<0.05). Conclusions C. butyricum and butyrate can maintain the function of intestinal mucosal barrier in ANP rats with IAH, and also readjust the imbalance of intestinal flora.

Objective To investigate the effect of ERH gene knockdown on the proliferation and apoptosis of human bladder cancer T24 cells. Methods T24 cells infected by lentivirus with interference on ERH gene sequence were cloned to establish stable T24 cells clone in ERH gene suppression. The expression of ERH mRNA gene in bladder cancer was detected by using quantitative real time polymerase chain reaction (qPCR). The effects of ERH knockout on the cell proliferation and apoptosis were examined by using methylthiazolyl tetrazolium (MTT) assay, colony formation assay and flow cytometry. The effect of ERH knockout on the tumorigenic effect of T24 cells in vivo was verified by subcutaneous tumor formation in nude mice. Results After lentiviral transfection, qPCR results showed that the knockdown effect of ERH mRNA in ERH normal group (untreated T24 cells) was better than that in ERH gene knockdown group, and the difference was statistically significant [(1.006±0.126) vs. (0.079±0.007); t=12.72, P=0.0002]. After knocking out ERH gene, MTT assay showed that the proliferation ability of T24 cells in ERH gene knockdown group was weakened compared with ERH normal group, and the difference was statistically significant [A490 value: (0.13±0.00) vs. (0.66±0.01);t=104.61, P<0.0001]. Colony formation assay indicated that the ability of clone in ERH normal group was weakened compared with ERH gene knockdown group [(10.5 ±1.2) vs. (196.4 ±4.0); t= 73.63, P< 0.0001]. Flow cytometry showed that the cell apoptosis rate in ERH gene knockdown group was higher than that in ERH normal group [(11.0 ±0.5) ％ vs. (4.2 ±0.5) ％; t= 16.06, P<0.0001]. Imaging results of subcutaneous tumor formation in nude mice showed that the total fluorescence intensity of the tumor area in ERH gene knockdown group was (4.67 ±0.59) × 1010 μW/cm2, and the corresponding part in ERH normal group was (9.54±4.20) × 1010μW/cm2 (t=3.64, P=0.0051);tumor weight in ERH gene knockdown group was (0.80±0.62) g, and in ERH normal group was (1.79±0.71) g (t=3.33, P=0.0037). Conclusion ERH gene knockout can inhibit the proliferation of human bladder cancer T24 cells, and promote the cell apoptosis.