Journal of Buon最新文献

Purpose: The aim was to demonstrate the progression of glioma influenced by Vitamin C (VC) and the potential molecular mechanism.

Methods: Proliferative and migratory rates of U87 and U251 cells induced with 0, 50 and 100 µM VC were examined by CCK-8 and Transwell assay, respectively. Clinical significance of SYNPO2 in glioma patients was analyzed. Relative level of SYNPO2 in VC-induced glioma cells was detected. By intervening SYNPO2, the involvement of SYNPO2 in the anti-cancer role of VC in inhibiting glioma cell phenotypes was finally confirmed.

Results: VC induction dose-dependently attenuated proliferative and migratory potentials of glioma cells. A low level of SYNPO2 indicated poor prognosis of glioma. Protein and mRNA levels of SYNPO2 were upregulated in glioma cells induced with VC. The inhibitory effects of VC on proliferative and migratory potentials of glioma cells were partially reversed by knockdown of SYNPO2.

Conclusions: VC blocks glioma cells to proliferate and migrate by upregulating SYNPO2.

Purpose: Postoperative chyle leak, termed 'chylous ascites', is a rare complication with a reported frequency of only one in 20464 abdominal operations. The purpose of this study was to summarize the available scientific data reviewing the most relevant studies for this type of postoperative complication after pancreatic surgery, highlighting at the same time the necessity for pancreatic surgeons to retain a high level of clinical suspicion for the early diagnosis and its therapeutic management.

Methods: A thorough literature search in Pubmed and Google Scholar, under the terms' chylous ascites OR chyle leak AND pancreas OR pancreatic', since the year of inception until 19th of February 2021 was conducted by the authors and the associated results are presented in this narrative review.

Results: Chyle leak is a rare complication following pancreatic surgery. Patients may suffer from exudative enteropathy and malnutrition leading to repeated infections and impaired wound healing or even death secondary to sepsis. Several studies have highlighted the issue of increased hospital stay, while others failed to reach statistical significance as far as hospital stay or survival are concerned. Researchers found that patients with diffuse chyle leak tended to have a worse 3-year survival rate (18.8%), which can be attributed to postoperative complications and early demise due to immunosuppression associated with the leak, or delayed adjuvant chemotherapy Conclusion: Further clinical research is needed to enhance prevention, diagnosis, treatment and long-term prognosis of this relevant surgical problem that shows trends of increase due to the great number of major operations which are performed nowadays.

Purpose: To investigate the potential function of FAT10 in the development of osteosarcoma (OS) and its mechanism.

Methods: Relative level of FAT10 in OS specimens and cell lines was detected by qRT-PCR. The correlation between FAT10 level and clinical features of OS patients was assessed by χ2 test. After intervention of FAT10 in MG-63 and U2OS cells, changes of FAT10 level, cell viability, clonality and proliferative capacity were respectively detected by qRT-PCR, CCK-8, colony formation and EdU assay. Moreover, dynamic change of FAT10 in OS cells induced with pro-inflammatory factors was examined by qRT-PCR. Protein levels of FAT10, p-STAT1, p-STAT3 and p-STAT5 in OS cells induced with TNF-α were determined by Western blot. The JAK2 inhibitor AZ960 was used to further confirm the role of the JAK signaling in FAT10-regulated development of OS.

Results: FAT10 was upregulated in OS specimens and cell lines, which was correlated to tumor size, WHO grade and distant metastasis of OS patients. Knockdown of FAT10 inhibited viability, clonality and proliferative capacity of MG-63 and U2OS cells. FAT10 was time-dependently upregulated in OS cells stimulated with IFN-γ and TNF-α, which was dose-dependently downregulated by the treatment of AZ960. Protein levels of FAT10, p-STAT1, p-STAT3 and p-STAT5 in OS cells induced with AZ960 were remarkably downregulated.

Conclusion: FAT10 is upregulated in OS samples, which stimulates the development of OS by activating the JAK/STAT signaling pathway.

Purpose: In this study, we aimed to determine the factors which affect post-progression survival (PPS) and overall survival (OS) in patients with metastatic colorectal cancer.

Methods: 87 patients with metastatic colorectal cancer had been followed up with palliative care due to disease progression or ECOG performance status after receiving at least two cycles of chemotherapy. PPS was estimated as the time between the last progression date and last control or death date in patients who were followed up with palliative care.

Results: 87 patients with metastatic colorectal cancer were included in the study. Evaluation with multivariate analysis of factors affecting PPS revealed a significantly longer PPS (10.8 weeks) in patients with ECOG score 0 or 1 than the PPS of patients with ECOG score 2-5 (3 weeks) (p=0.01). It was also found that PPS was 14.4 weeks in patients with CEA levels <5ng/ml,while it was 6.7 weeks in patients with CEA levels ≥5 ng/ml (p=0.001) and PPS was 13.7 weeks in patients with controlled disease after first-line chemotherapy while it was 8 weeks in patients with progression (p=0.03); both were statistically significant. No significant association was found between PPS and age, gender, tumor location, sites of metastasis, and RAS status.

Conclusion: ECOG performance status score of 0-1, CEA levels below 5 ng/ml, and disease control with first-line chemotherapy are related to longer PPS in patients with metastatic colorectal cancer.

Purpose: To clarify how ZCCHC14 affects the development of hepatocellular carcinoma (HCC).

Methods: Differential levels of ZCCHC14 in HCC tissues and cells were examined. Proliferative and migratory changes in HCC cells with overexpression or knockdown of ZCCHC14 were detected using 5-Ethynyl-2'- deoxyuridine (EdU) and Transwell assay, respectively. Expression changes of p-Akt/Akt, p-GSK3β/GSK3β and β-catenin in HCC cells mediated by ZCCHC14 were determined. Intervened by the p-Akt activator SC79 or overexpression of β-catenin, further validated the involvement of the Akt/GSK3β/β-catenin signaling in HCC cell phenotypes mediated by ZCCHC14.

Results: Upregulated ZCCHC14 in HCC accelerated in vitro proliferative potential of HCC cells. Knockdown of ZCCHC14 inactivated the Akt/GSK3β/β-catenin signaling and inhibited malignant phenotypes of HCC, which were partially reversed by SC79 induction or overexpression of β-catenin.

Conclusions: By activating the Akt/GSK3β/β-catenin signaling, ZCCHC14 accelerates HCC cells proliferation.

Purpose: To uncover the biological role of LINC00355 in regulating the proliferative and apoptotic potentials in hepatocellular carcinoma (HCC), and the underlying mechanism.

Methods: LINC00355 levels in HCC tissues and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). After knockdown of LINC00355 or miR-217-5p in Hub7 and Hep3B cells, proliferative and apoptotic potentials were assessed by cell counting kit-8 (CCK-8), colony formation assay and flow cytometry. The interaction between LINC00355 and miR-217-5p was determined by dual-luciferase reporter assay and Pearson correlation test. Western blot analysis was conducted to illustrate the regulatory effects of LINC00355 and miR-217-5p on the Wnt/β-catenin signaling.

Results: LINC00355 was upregulated in HCC tissues and cell lines. Knockdown of LINC00355 reduced viability in Hub7 and Hep3B cells, which was much pronounced on days 3 and 4. Clonality was attenuated by transfection of shLINC00355 as well. In addition, apoptosis rate increased by knockdown of LINC00355 in HCC cells. Protein levels of β-catenin, GSK3β, c-myc and cyclin D1 were downregulated in Hub7 and Hep3B cells transfected with shLINC00355. MiR-217-5p was the target gene binding LINC00355. It displayed exactly opposite regulations on HCC cell phenotypes and protein levels of vital genes in the Wnt/β-catenin signaling to those of LINC00355.

Conclusions: LINC00355 is upregulated in HCC specimens, LINC00355 triggers proliferative rate and inhibits apoptosis in HCC cells by negatively regulating miR-217-5p and activating the Wnt/β-catenin signaling.

Purpose: To assess patient satisfaction from chemotherapy and investigate the effect of demographic factors, disease symptoms and treatment on satisfaction.

Methods: A non-randomized cross-sectional survey was conducted on a sample of 100 patients undergoing chemotherapy at "Metaxa" Cancer Hospital, Piraeus, Greece for 6 months. A demographic data questionnaire, a Cancer Treatment Satisfaction Questionnaire (CTSQ) and visual analog scales were used to evaluate pain, anxiety, fatigue, and nausea while presence or absence of vomit were also assessed.

Results: The majority of the patients in the sample were men (51%), with a mean age of 58.5 ± 10.82 years. The mean value of expectations from treatment was 60.55, from treatment's satisfaction was 75.86 and from feelings about treatment's side effects was 44.56. The most serious symptoms were fatigue and anxiety (7.2 ± 1.95 and 6.71 ± 2.5, respectively). Statistical tests have shown that sub-dimensions of CTSQ are associated with pain, anxiety, fatigue, and nausea.

Conclusions: Generally, chemotherapy meets patients' expectations with cancer. Symptoms such as fatigue, anxiety, pain, and nausea affect their satisfaction. Treatment's satisfaction can be improved by evaluating symptoms, which will lead to appropriate interventions.

Purpose: To compare the efficacy and safety between endoscopic submucosal dissection (ESD) and conventional surgical treatment in the treatment of colorectal cancer (CRC) and the precancerous lesions.

Methods: A retrospective analysis was performed on the clinical data of 65 patients with CRC or precancerous lesions (ESD group) and another 65 patients receiving surgical treatment at the same period (Surgery group). The surgical indicators, incidence of complications, and quality of life score were compared between the two groups, and the survival and tumor progression were followed up and recorded.

Results: The rate of en bloc tumor resection was 89.2% (58/65) and 100% (65/65) and the rate of tumor curative resection was 92.3% (60/65) and 100% (65/65) in ESD group and Surgery group. Moreover, ESD group had markedly shorter operation time and mean hospital stay. After treatment, ESD group had higher scores of emotional functioning, fatigue, constipation, and diarrhea symptoms and general quality of life on the European Organization for Research and Treatment of Cancer quality of life questionnaire Core 30 (EORTC QLQ-C30) than Surgery group. The follow-up results showed no statistically significant difference in the 5-year recurrence rate between ESD group and Surgery group (7.7% vs. 0%, p=0.208).

Conclusion: ESD and surgery have similar long-term clinical efficacy in treating early CRC and precancerous lesions, but ESD is more minimally invasive and safer, and is superior in accelerating postoperative recovery and improving the overall survival of patients.