Journal of Buon最新文献

Purpose: To explore the role of lncRNA MANCR in regulating in vitro proliferation and apoptosis in esophageal carcinoma cells and in vivo growth of esophageal carcinoma in nude mice.

Methods: MANCR levels in 15 pairs of esophageal carcinomas and non-tumoral tissues were detected by qRT-PCR. In vitro regulations of MANCR on proliferative and apoptotic potentials in TE-1 and EC-109 cells were explored by CCK-8, colony formation assay and flow cytometry. In addition, dual-luciferase reporter assay and rescue experiments were conducted to clarify the potential mechanisms of MANCR on regulating PDE4D. Finally, in vivo role of MANCR in mediating esophageal carcinoma growth was determined in nude mice implanted with EC-109 cells.

Results: MANCR was highly expressed in esophageal carcinomas tissues than non-tumoral ones. MANCR promoted proliferative ability and inhibited apoptosis in TE-1 and EC-109 cells. In nude mice with xenografted esophageal carcinoma, knockdown of MANCR markedly slowed down tumor growth. PDE4D was the target gene binding MANCR, which was downregulated in esophageal carcinoma tissues. Its level was negatively regulated by MANCR. Importantly, PDE4D could abolish the role of MANCR in stimulating the malignant progression of esophageal carcinoma.

Conclusions: LncRNA MANCR is upregulated in esophageal carcinoma cases. Through negatively regulating PDE4D level, MANCR stimulates proliferative ability and inhibits apoptosis in esophageal carcinoma, thus driving the malignant progression.

Retraction of "Acetylshikonin inhibits in vitro and in vivo tumorigenesis in cisplatin-resistant oral cancer cells by inducing autophagy, programmed cell death and targeting m-TOR/PI3K/Akt signalling pathway", by Peng Wang, Weiyue Gao, Yibin Wang, Jun Wang. JBUON 2019;24(5):2062-2067; PMID: 31786876 Following the publication of the above article, readers drew to our attention that part of the data was unreliable. We requested the authors to provide the raw data to prove the originality. Then the corresponding author contacted with our journal and stated below: Our group tried to repeat the results presented in this paper, but found that some data was not able to be reproducible. The authors then asked to retract this article. At the same time, our journal's investigation into this article also showed that part of the results in this article can not be supported by the data. Given above, we decided to retract this article. All the authors were informed of the retraction. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.

Retraction of "HHIP gene overexpression inhibits the growth, migration and invasion of human liver cancer cells", by Xiaobin Wang, Wenjie Ma, Jun Yin, Meizhu Chen, Hong Jin. JBUON 2020;25(5):2424-2429; PMID: 33277865 Following the publication of the above article, readers drew to our attention that part of the data was unreliable: Figures of this article appeared in other articles (by totally different authors). The authors were requested to provide the raw data and were also asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. Given above, we decided to retract this article. Authors were informed of the retraction. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.

Gross chromosomal and specific gene alterations are genetic aspects that are involved in rise, progression, and metastatic expansion of malignances. Concerning Uveal melanoma (UM), a variety of chromosome and gene functional and numerical imbalances in crucial molecular pathways such as cell cycle regulation, signaling transduction, apoptosis or angiogenesis have been identified and explained. UM is the most common primary ocular malignancy demonstrating increased rates, especially in middle-aged white (Caucasian) populations. Chronic exposure to ultraviolet rays/sunlight, race, gender (males), or some familial hereditary syndrome in sub-groups of patients are major factors correlated to increased risk for UM rise and progression. Specific genetic signatures at the level of chromosomal instability (CI) or at the gene mutations status characterize sub-groups of patients affecting the biological behaviour of the tumour leading to aggressive phenotypes (advanced stage-distant metastases, poor response, and survival rates). Sporadic or hereditary mediated mutations in genes including BAP1, EIF1AX, GNA11, GNAQ CHEK2, PALB2, SMARCE1, MBD4, MSH6 and MLH1. In the current molecular review, we present specific mutations -as a landscape- that are implicated in UM genetic substrate and create a variety of genetic signatures in the corresponding patients.

Purpose: This study aimed to illustrate the biological role of hsa_circ_0005721 in the development of osteosarcoma and the molecular mechanism.

Methods: hsa_circ_0005721 levels in 30 pairs of osteosarcoma and non-tumor tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Functional experiments were conducted to assess the influence of hsa_circ_0005721 on proliferative, metastatic and apoptotic rates of osteosarcoma cells. The downstream target of hsa_circ_0005721 and their co-regulatory mechanism in malignant development of osteosarcoma were analyzed by dual-luciferase reporter assay and rescue experiments, respectively.

Results: hsa_circ_0005721 was upregulated in osteosarcoma tissues and cell lines. Knockdown of hsa_circ_0005721 suppressed proliferative and metastatic rates of U-2OS and Saos-2 cells, and stimulated apoptosis. Serving as a ceRNA, hsa_circ_0005721 upregulated the linear transcript TEP1 by competitively binding miR-16-5p, thus exerting its biological functions in regulating osteosarcoma development.

Conclusions: This study for the first time identified the upregulated hsa_circ_0005721 in osteosarcoma, which triggers the malignant development of osteosarcoma by upregulating the linear transcript TEP1.

Purpose: The objective of this study was to investigate the therapeutic effect and safety of three-dimensional digital subtraction angiography (3D-DSA) in interventional therapy for hepatocellular carcinoma (HCC) patients.

Methods: A total of 62 HCC patients who underwent interventional therapy were selected and divided into control group (n=31, receiving ordinary two-dimensional DSA) and observation group (n=31, undergoing 3D-DSA). The dosage of contrast agent, operation time and exposure dose were compared between the two groups. Besides, the effective rate, success rate of superselective arterial catheterization, lipiodol deposition rate and the incidence rate of complications of the two groups were observed and recorded.

Results: Compared with those in control group, the dose of contrast agent and exposure dose were lower in observation group, and the operation time in the former was significantly shorter than that in the latter. The effective rate was 74.19% in observation group and 48.39% in control group. Moreover, in comparison with control group, operation group exhibited a higher effective rate, a higher success rate of superselective arterial catheterization and a higher lipiodol deposition rate, showing statistically significant differences (p<0.05). Besides, the incidence rate of complications (including myelosuppression, gastrointestinal discomfort and infection, 4.88%) in observation group was markedly lower than that in control group (25.81%) (p<0.05).

Conclusion: 3D-DSA under contrast guidance during interventional treatment of patients with HCC can significantly improve the therapeutic effect, and it is of great importance to reduce the incidence rate of complications and enhance the safety of interventional treatment.

Purpose: Patients over the age of 65 constitute approximately 54% of newly diagnosed cancers and approximately 70% of cancer-related deaths. These patients aged ≥65 years, who form the majority of clinical practice, are represented less in clinical studies than in real life. We designed this retrospective study to examine the treatment and response of patients to pancreatic cancer in patients over 70 years of age.

Methods: Our study is a retrospective study that included patients from 5 centers in Turkey. Inclusion criteria were being over the age of 18 years, diagnosed with pancreatic cancer, and with ECOG performance score between 0-2. These patients were divided into two groups according to their age. The classification was made as patients over 70 years of age in the first group (geriatric group) and patients under 70 years of age (<70 age group) in the second group.

Results: Overall survival of the <70 age group was statistically significantly longer (median 10 months vs 9.1 months p=0.027). When the patients who underwent only curative surgery were examined, the survival was statistically significant in favor of the <70 age group (median 20.96 months vs 14.5 months p=0.011). No statistically significant difference was found between the two groups in terms of the overall survival of patients with metastatic diagnosis (median 8.1 months vs 8.4 months p=0.182).

Conclusion: The survival of patients with pancreatic cancer aged 70 and over was shorter than other age groups. While this difference was significant in patients who could undergo surgery at an early stage, it was not found in the metastatic patient group. Prospective larger-scale studies are needed to evaluate the treatment of geriatric patients better.

Purpose: To uncover the role of FBXL19-AS1 in aggravating the progression of hepatocellular cancer (HCC) by downregulating kruppel-likefactor2 (KLF2).

Methods: FBXL19-AS1 level in HCC tissues and adjacent normal tissues were firstly determined. Its level in HCC with different tumor sizes (≤ 5 cm or > 5 cm) and different tumor stages (stage I-II or III-IV) was examined as well. Subcellular distribution of FBXL19-AS1 was detected. The regulatory effect of FBXL19-AS1 on viability, apoptosis and cell cycle progression of HCC cells was assessed. RNA immunoprecipitation (RIP) assay was conducted to explore the interaction between FBXL19-AS1 with EZH2 and SUZ12. Moreover, chromatin immunoprecipitation (ChIP) assay was carried out to identify the recruitment ability of FBXL19-AS1 on EZH2 and H3K27me3. Finally, the potential role of KLF2 in FBXL19-AS1-mediated HCC proliferation was investigated.

Results: FBXL19-AS1 was highly expressed in HCC tissues, especially in those larger than 5 cm in tumor size and worse tumor stage. FBXL19-AS1 was mainly distributed in nucleus and interacted with EZH2 and SUZ12. Knockdown of FBXL19-AS1 suppressed proliferation, cell cycle progression and induced apoptosis of HCC cells. Moreover, silence of FBXL19-AS1 attenuated the recruitment ability of EZH2 on KLF2. Knockdown of KLF2 reversed the regulatory effect of FBXL19-AS1 on proliferative ability of HCC cells.

Conclusions: Long non-coding RNA (lncRNA) FBXL19-AS1 is upregulated in HCC. It accelerates proliferative ability, cell cycle progression and suppresses apoptosis of tumor cells through interacting with KLF2, thus aggravating the progression of HCC.

Purpose: Colorectal cancer (CRC) is a frequent fatal cancer worldwide. 5-Fluorouracil (5-FU) is extensively used in its chemotherapy. This drug resistance, however, should be well concerned. Ring finger proteins (RNF) are vital regulators involved in CRC development. In this article, HCT116R cells were first established. The roles of RNF38 and Wnt signaling in 5-FU-resistant CRC were further illustrated. Our study provides novel evidence for improving 5-FU chemotherapy outcome in CRC patients.

Methods: The phenotype of established HCT116R cells was first examined. Next, the regulatory effect of RNF38 on 5-FU resistance in CRC was mainly explored. Nude mice bearing CRC were treated with 5-FU and in vivo overexpression of RNF38.

Results: 5-FU-resistant HCT-116 cells (HCT116R) were first established. 5-FU treatment markedly killed survival and induced apoptosis in HCT-116 cells. P53 was downregulated in HCT116R cells. Through microarray analysis, RNF38 was found to be upregulated in HCT116R cells compared to parental cells.

Conclusions: Overexpression of RNF38 enhanced 5-FU resistance in CRC. Furthermore, Wnt signaling was activated by RNF38 and involved in 5-FU resistance in CRC.

Purpose: In this study, we developed a CAUTI risk factor evaluation index system for postoperative patients with gynecologic malignant tumors and provided scientific evidence for the prevention of catheter-related urinary tract infection (CAUTI).

Methods: A comprehensive method, including literature review, group discussion and Delphi method, was adopted to establish a CAUTI risk factor evaluation index system for postoperative patients with gynecologic malignant tumors.

Results: Two rounds of expert consultations resulted in effective response rates of 100%, with authority coefficients of 0.94, and coordination coefficients of 0.473 and 0.388 respectively (p<0.01). The risk factor indicator system consisted of 4 first-level indicators, 13 second-level indicators, and 56 third-level indicators.

Conclusion: The experts showed high enthusiasm, good authority, and coordination. The CAUTI risk factor evaluation index system for postoperative patients with gynecologic malignant tumors is comprehensive and scientific, and could serve as an important guide for assessment and prevention of CAUTI in patients with gynecologic malignant tumor postoperatively.