Combining prognostic value of serum carbohydrate antigen 19-9 and tumor size reduction ratio in pancreatic ductal adenocarcinoma.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a common cancer with increasing morbidity and mortality due to changes of social environment. AIM: To evaluate the significance of serum carbohydrate antigen 19-9 (CA19-9) and tumor size changes pre- and post-neoadjuvant therapy (NAT). METHODS: This retrospective study was conducted at the Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital. This study specifically assessed CA19-9 levels and tumor size before and after NAT. RESULTS: A total of 156 patients who completed NAT and subsequently underwent tumor resection were included in this study. The average age was 65.4 ± 10.6 years and 72 (46.2%) patients were female. Before survival analysis, we defined the post-NAT serum CA19-9 level/pre-NAT serum CA19-9 level as the CA19-9 ratio (CR). The patients were divided into three groups: CR < 0.5, CR > 0.5 and < 1 and CR > 1. With regard to tumor size measured by both computed tomography and magnetic resonance imaging, we defined the post-NAT tumor size/pre-NAT tumor size as the tumor size ratio (TR). The patients were then divided into three groups: TR < 0.5, TR > 0.5 and < 1 and TR > 1. Based on these groups divided according to CR and TR, we performed both overall survival (OS) and disease-free survival (DFS) analyses. Log-rank tests showed that both OS and DFS were significantly different among the groups according to CR and TR (P < 0.05). CR and TR after NAT were associated with increased odds of achieving a complete or near-complete pathologic response. Moreover, CR (hazard ratio: 1.721, 95%CI: 1.373-3.762; P = 0.006), and TR (hazard ratio: 1.435, 95%CI: 1.275-4.363; P = 0.014) were identified as independent factors associated with OS. CONCLUSION: This study demonstrated that post-NAT serum CA19-9 level/pre-NAT serum CA19-9 level and post-NAT tumor size/pre-NAT tumor size were independent factors associated with OS in patients with PDAC who received NAT and subsequent surgical resection.

ACY1 regulating PTEN/PI3K/AKT signaling in the promotion of non-small cell lung cancer progression.

BACKGROUND: Non-small cell lung cancer (NSCLC) has a poor prognosis and is the most common cause of cancer-related deaths worldwide. Aminoacylase 1 (ACY1) plays a promoting role in some cancers, but its role in NSCLC is still unclear. METHODS: Immunohistochemistry, Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting assays were used to determine ACY1 expression patterns in NSCLC tissues and cell lines. The clinical significance of ACY1 in NSCLC was evaluated by χ2 test and Kaplan-Meier analysis. MTT, flow cytometry, wound healing, and Transwell assays were performed to assess cell growth, apoptosis, migration, invasion, and tumorigenesis under different treatments. Male athymic BALB/C nude mice were used for xenotransplantation experiments. RESULTS: The results showed that ACY1 expression was elevated in NSCLC tissue samples and cells, and high ACY1 expression predicted an advanced clinical process and shorter overall survival in patients with NSCLC. Overexpression of ACY1 significantly increased cell growth, migration, invasion, and tumorigenesis, and reduced cell apoptosis, indicating that ACY1 functions as an oncogene in NSCLC. Moreover, ACY1 decreased phosphatase and tensin homolog (PTEN) expression, increased its ubiquitination, and activated PI3K/AKT signaling. Overexpression of PTEN diminished the effects of ACY1 upregulation on cell tumorigenesis promotion. CONCLUSIONS: This study reveals that ACY1 may promote the progression of NSCLC via activating PI3K/AKT signaling in a PTEN-dependent manner. Our study may provide a better understanding of the pathogenesis and development of NSCLC.

Radiation induces submandibular gland damage by affecting Cdkn1a expression and regulating expression of miR-486a-3p in a xerostomia mouse model.

BACKGROUND: Radiotherapy has been proven to be an effective treatment strategy for inhibiting head-and-neck cancer. However, side effects are common when using high-dosage irradiation, and the mechanism of action of this therapy has not been fully clarified. OBJECTIVES: To discover targeting molecules involved in an electron radiation-induced xerostomia murine model. MATERIAL AND METHODS: The xerostomia model mice were divided into Gy-3 (n = 5), Gy-7 (n = 5), and Gy-21 (n = 5) groups, and were compared to a negative control (NC) group. Drinking water amount, saliva volume, submandibular gland weight, and body weight were recorded. Real-time polymerase chain reaction (RT-PCR) was performed to amplify gene transcription. Hematoxylin and eosin (H&E) staining was used to identify submandibular gland damage. The dual-luciferase assay was used to observe the interaction between the Cdkn1a gene and miR-486a-3p. RESULTS: Electron radiation significantly increased the drinking water amount, and decreased saliva volume and body weight compared to mice without radiation treatment (p < 0.05). The H&E staining showed that electron radiation damaged the submandibular gland. Electron radiation also triggered significantly higher transcription of the Cdkn1a gene in the submandibular gland of xerostomia mice compared to those without radiation treatment (p < 0.05). The dual-luciferase assay demonstrated that miR-486a-3p interacted with the Cdkn1a gene (miRNA-mRNA). CONCLUSIONS: Radiation was found to induce damage of the submandibular gland and affect Cdkn1a expression by regulating the expression of miR-486a-3p in a xerostomia murine model. Therefore, modulation of miR-486a-3p and the Cdkn1a gene in a xerostomia murine model might improve damage of the submandibular gland.

Discovered differentially expressed lncRNA AC010973.2 can act as a diagnostic and prognostic biomarker for colon adenocarcinoma.

BACKGROUND: The identification of prognostic genes that can distinguish the prognostic risks of cancer patients remains a significant challenge. Recent studies show that long noncoding RNAs (lncRNAs) might act as prognostic biomarkers in a variety of cancers. This study aimed to identify and assess a prognostic lncRNA signature in patients with colon adenocarcinoma (COAD). METHODS: We downloaded expression profiles and corresponding clinicopathological data from The Cancer Genome Atlas (TCGA) database. We selected samples with lncRNA expression data and relevant clinical prognostic data for subsequent analysis. The association between lncRNA and prognostic function was analyzed by Cox regression analysis. The potential biofunctions of target lncRNA were investigated through bioinformatic analysis. RESULTS: LncRNAs expression profiles and corresponding clinicopathological data of 480 COAD patients and 41 normal samples were obtained from TCGA database. A multivariate Cox analysis model was used to identify the lncRNA signature. AC010973.2 lncRNA was found to be significantly related to the survival of COAD patients. The area under the curve (0.758) and the C-index (0.753) further confirmed the prediction accuracy of our model. Through nucleic acid sequence comparison and literature search, we found that the homologous host gene SLC4A2 of AC010973.2 is significantly related to COAD. CONCLUSIONS: We provide here a new biomarker for COAD diagnosis and a new direction for further research on the pathogenesis of COAD.