ALKBH3 partner ASCC3 mediates P-body creation as well as frugal discounted associated with MMS-induced 1-methyladenosine and 3-methylcytosine from mRNA.
 027) were significantly associated with poor PFS; and LMR≤3.8 (HR = 0.459, 95% CI 0.306-0.688, P = 34 U/ml (HR = 1.946, 95% CI 1.256-3.015, P = 0.003) were significantly associated with OS. Furthermore, the area under the curve of COLC was higher (0.713) than that of LMR (0.709) or CA125 (0.583), the specificity of COLC was higher (75.9%) than that of LMR (62%) or CA125 (40.5%) in predicting mortality in OC patients. Conclusions LMR alone and combined with CA125 might be used as predictive markers in OC. Furthermore, as a prognostic factor, COLC might have a higher specificity to predict the outcome. © The author(s).Objective DUSP6 is a negative regulator of the ERK signaling pathway and plays an important role in chemotherapy-resistance. Previously we showed that DUSP6 is overexpressed in ovarian cancer side population (SP) cells that possess cancer stem cell-like properties and are quiescent and chemotherapy-resistant. Here, we explore the effects of DUSP6 on chemotherapy-resistance by examining its regulation of the ERK signaling pathway and G0/G1 cell cycle arrest. Methods mRNA and protein expression of DUSP6 and G0/G1 cell cycle checkpoint regulating proteins (CyclinD1, CyclinD3 and CyclinE2) was evaluated among ovarian cancer cell lines and tissue samples. Ovarian cancer cells were transiently transfected to overexpress DUSP6. After treatment with cisplatin, cell viability was measured by the MTS assay at 48 hours and the half maximal inhibitory concentration (IC50) for each cell line was calculated. Subcellular localization and cell cycle analysis were determined by using immunofluorescence and FACS, respectively.rest in DUSP6-overexpressing ovarian cancer cells.  https://www.selleckchem.com/products/turi.html  This suggests that overexpression of DUSP6 promotes chemotherapy-resistance through the negative regulation of the ERK signaling pathway, increasing the G0/G1 phase ratio among ovarian cancer cells, and leading to cellular quiescence. © The author(s).Background Platinum-based therapy (PBT) can be limited by gastrointestinal adverse events, particularly PBT-related colitis and diarrhea (PCD). We studied clinical features, treatments, and outcomes of PCD. Methods This was a retrospective study of cancer patients who received PBT and colonoscopic evaluation for PCD symptoms from 2009 to 2018. Results Of 36,595 patients who received PBT, 86 (0.2%) met inclusion criteria. Median time from PBT initiation to PCD was 66 days.  https://www.selleckchem.com/products/turi.html  Regarding PBT type, 47% of the patients received carboplatin, 31% cisplatin, and 22% oxaliplatin. Median duration of PCD symptoms was 20 days. Colonoscopy revealed mucosal ulceration in 34% of the patients and nonulcerative inflammation in 33%. Half of the cohort needed hospitalization for PCD (49%). The majority received treatment for PCD (59%) immunosuppressive therapy in 21%, antibiotics in 27%, antimotility agents in 22%, and intravenous fluids in 51%. Eight patients (9%) were admitted to the intensive care unit for PCD management. Six patients (7%) experienced colonic perforation that required surgical intervention; two of them had gastrointestinal tumors. Physicians restarted PBT in 37 (43%) patients; 8 (22%) of them had PCD recurrence that was managed expectantly. Colonic perforation occurred more frequently with use of oxaliplatin and cisplatin than carboplatin (P=0.05). The median duration of PCD symptoms was longer in patients receiving carboplatin or cisplatin than in those receiving oxaliplatin (P=0.182). Conclusions PCD is rare, but in a small subset of patients, it can lead to serious complications. Treatment of PCD is mainly supportive, but immunosuppressive therapy may be required. © The author(s).Background Peroxiredoxins (PRDXs) were reported to be associated with inflammation response in previous studies. In colon adenocarcinoma (COAD), however, their correlations and clinical significance were unclear. Methods The RNA-seq data of 452 COAD patients with clinical information was downloaded from The Cancer Genome Atlas (TCGA) and transcripts per million (TPM) normalized. Comparisons of relative expressions of PRDXs between COAD tumor and normal controls were applied. PRDXs dy-regulations in COAD were validated via Oncomine, Human Protein Atlas (HPA) and Gene Expression Omnibus (GEO) repository. Through Tumor Immune Estimation Resource (TIMER), the immune estimation of TCGA-COAD patients was downloaded and the dy-regulated PRDXs were analyzed for their correlations with immune infiltrations in COAD. The TCGA-COAD patients were divided into younger group (age≤65 years) and older group (age>65 years) to investigate the prognostic roles of age, TNM stage, dy-regulated PRDXs and the immune infiltrations inr its early diagnosis. Age was prognostic and should be considered in the treatments of the older patients. Dy-regulated PRDXs were negatively correlated with immune infiltration levels. CD4+ T cell and CD8+ T cell infiltrations were prognostic in COAD and their potential as immune targets needed further investigation. © The author(s).Gallbladder cancer is one of the most common malignant tumors in the biliary tract. In recent years, the chemotherapy treatment for gallbladder carcinoma has exhibited obvious characteristics of drug resistance and insensitivity, and one of the main factors is the existence of cancer stem cells. Here in this study, the effect of Bufalin on gallbladder cancer (GBC-SD) cells and the related mechanism were studied. The results indicated that Bufalin could inhibit the growth of gallbladder carcinoma both in vivo and in vitro. According to the biological behavior analysis, Bufalin induced apoptosis, inhibited the propagation, migration and invasion of GBC-SD cells, and blocked cell cycle at the G2/M stage. Besides, Bufalin inhibited the tumor sphere formation capability of gallbladder carcinoma in matrigel, reduced the expression of multiple stemness-associated proteins, including Oct4, Sox2 and the stem cell-surface marker proteins CD133 and CD44. Western blot assay showed that Bufalin inhibited MEK/ERK and PI3-K/AKT signaling pathways by inhibiting the expression of p-c-Met, which in turn affected the expression of apoptosis-related protein Mcl-1, and the invasion-associated proteins E-cadherin, MMP9 and Snail. Bufalin was found to have an inhibitory effect on the GBC-SD cell growth and reduce the self-renewal and characteristic of gallbladder cancer stem cells. It enhanced the chemotherapeutic sensitivity and reduced the metastasis of gallbladder carcinoma. In conclusion, Bufalin can be used as a new promising anticancer drug for gallbladder cancer patients who are resistant to traditional chemotherapy. © The author(s).