Bernsteinware1724
ors of halitosis.
The incidence of cholangiocarcinoma (CCA) is on the rise in recent years, and its pathogenesis may be associated with the deregulation of circular RNAs (circRNAs). Hence, we aimed to investigate the role of circRNA homeodomain interacting protein kinase 3 (circ_HIPK3) in CCA.
The expression of circ_HIPK3, miR-148a-3p and unc-51 like kinase 3 (ULK1) mRNA was detected using quantitative real-time polymerase chain reaction (qPCR). The role of circ_HIPK3 in cell proliferation was detected by 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromide (MTT) assay and colony formation assay. Cell apoptosis and cell cycle progression were investigated using flow cytometry assay. Cell migration and invasion were detected by transwell assay. The protein levels of ULK1 and migration/invasion-associated markers were measured using Western blot. The putative relationship between miR-148a-3p and circ_HIPK3 or ULK1 was validated by dual-luciferase reporter assay. The role of circ_HIPK3 was also investigated in vivo.
Circ_HIPK3 was overexpressed in CCA tissues and cells. In function, circ_HIPK3 knockdown inhibited CCA cell proliferation, migration and invasion and induced apoptosis and cycle arrest. It was confirmed that miR-148a-3p was a target of circ_HIPK3, and ULK1 was a target of miR-148a-3p. Circ_HIPK3 regulated ULK1 expression by targeting miR-148a-3p. Rescue experiments showed that miR-148a-3p inhibition reversed the effects of circ_HIPK3 knockdown. Besides, miR-148a-3p enrichment-blocked cell proliferation, migration and invasion were recovered by ULK1 overexpression. In vivo, circ_HIPK3 knockdown inhibited solid tumor growth.
Circ_HIPK3 knockdown blocked CCA malignant development partly via regulating the miR-148a-3p/ULK1 pathway.
Circ_HIPK3 knockdown blocked CCA malignant development partly via regulating the miR-148a-3p/ULK1 pathway.
Ovarian cancer has one of the highest mortality rates among all gynaecological malignancies, and increasing evidence suggests that lncRNAs are widely involved in the development of ovarian tumours. This study aimed to investigate the mechanism of the LNC00115/miR-7/ERK axis in the cisplatin resistance of ovarian cancer cells.
The expression of miR-7 and LNC00115 in ovarian cancer cell lines and tissues was detected by qRT-PCR. The ovarian cancer cell lines were constructed by overexpressing or knocking down the expression of LNC00115 or miR-7. CCK-8, transwell invasion, Western blot, immunohistochemistry, and luciferase reporter assays were carried out to identify the targets of LNC00115 and explore its roles and mechanisms in ovarian cancer. A nude mouse model was established, and the expression of LNC00115, miR-7 and ERK was detected. The changes in the tumours and body weights of the nude mice were measured.
LNC00115 was upregulated in ovarian cancer tissues and cisplatin-resistant ovarian cancer celn resistance and provide a new clinical strategy for combating cisplatin resistance in ovarian cancer.
A diagnosis of testicular cancer (TC) at a relatively young age can have a dramatic impact on the psychological well-being of those affected. The aim of this review was to synthesize recent evidence to provide an updated account of the prevalence, severity and correlates of anxiety, depression, fear of cancer recurrence (FCR) and distress in TC survivors.
A systematic literature review was conducted from September 2017 until June 2020 using electronic databases including Embase, MEDLINE, PsycINFO, Scopus and Web of Science. Study eligibility and quality were independently assessed by two reviewers. Narrative synthesis was used to depict the severity (mean/median scores), prevalence (proportions above standard clinical thresholds) and correlates of study outcomes.
A total of 988 articles were identified for screening after duplicate removal. Fifty-six full-text articles were screened, and eight articles met the inclusion criteria. The reported prevalence of the outcomes varied across studies (clinical le TC survivors most likely to need one of the increasing number of psychological interventions being developed for TC survivors.
Gastric cancer (GC) is a common and deadly malignancy in the world. CircRNAs have emerged as important regulators in human diseases, including GC. In this work, we intended to explore the role of circ_CORO1C in GC progression and potential mechanism.
Quantitative real-time PCR (qRT-PCR) or Western blot assay was performed to examine the expression of circRNA coronin-like actin-binding protein 1C (circ_CORO1C), microRNA (miR)-138-5p and Krueppel-like factor 12 (KLF12) in clinical samples and cells. Cell colony formation ability and viability were measured by colony formation assay and methyl thiazolyl tetrazolium (MTT) assay, respectively. Expression of cell proliferation and epithelia-mesenchymal transition (EMT) biomarker was detected by Western blot analysis. And cell metastasis, including migration and invasion, and apoptosis were analyzed via Transwell assay and flow cytometry, respectively. Target relationship among circ_CORO1C, miR-138-5p and KLF12 was validated by dual-luciferase reporter assay. The in vivo role of circ_CORO1C was investigated by tumor xenograft assay.
Circ_CORO1C and KLF12 were upregulated, while miR-138-5p was downregulated in GC tissues and cells. Circ_CORO1C knockdown suppressed colony formation ability, viability, migration, invasion and EMT in GC cells, while promoted cell apoptosis in vitro. Circ_CORO1C targeted miR-138-5p, the inhibition of which could attenuate silenced circ_CORO1C-induced inhibitory effects on GC progression. MiR-138-5p repressed the aggressive malignant behaviors of GC cells by directly targeting KLF12. Circ_CORO1C deficiency inhibited GC tumor growth in vivo.
Depletion of circ_CORO1C suppressed GC progression by regulating miR-138-5p/KLF12 axis, offering a potential molecular target for GC therapy.
Depletion of circ_CORO1C suppressed GC progression by regulating miR-138-5p/KLF12 axis, offering a potential molecular target for GC therapy.
NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development.
The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319.
PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo.
In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC.
In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC.
The aim of our study was to identify the diagnostic ability of free fatty acids (FFAs) in younger colorectal cancer (CRC) patients by comparing carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9).
Patients screened for CRC at Fujian Medical University Union Hospital from January 2011 to December 2014 were recruited. Patients pathologically diagnosed with CRC or colorectal adenoma (CA) and healthy control participants were included. The enzyme endpoint method was applied to measure FFA levels. Receiver operating characteristic (ROC) curve analysis was performed to further evaluate the diagnostic ability of FFAs.
FFA levels in late-stage patients (tumour-node-metastasis (TNM) stages III-IV) were higher than those in early-stage patients (TNM stages I-II) (P=0.02). The FFA levels in CRC patients were higher than those in controls of all ages, those younger than 50 years, males and females (P<0.001), and this difference was larger for patients younger than 50 years and females than for ability in female and younger patients with CRC. FFA levels may have a potential role in triage screening of early CRC.
Medication error is one of the most common medical errors in the practice of modern medicine. Among cancer patients receiving chemotherapy, medication errors can be potentially harmful given the narrow therapeutic index, complex dosing, and toxic nature of anti-cancer drugs.
This study aimed to determine the incidence and factors associated with medication errors among cancer patients.
The study was a prospective observational study carried out at the cancer unit of Mbarara Regional Referral Hospital, Southwestern Uganda. The study included 110 participants, both adults and children receiving chemotherapy. The study was carried out for a period of five months from January to May 2020. A checklist was used to collect patient, medication, and disease information to identify the prescription, transcription, dispensing, and administration errors.
Of the 110 participants, 52 (47.3%) experienced a total of 78 medication errors (MEs). Of these, 33 (42.31%) were prescription errors, 29 (37.18%) administrationferral Hospital. Prescription errors were the most common type of error followed by administration errors, and dispensing errors were the least common. Residence, education level, and alkylating agent chemotherapy were significantly associated with occurrence of medication errors.
This study aimed to assess the effectiveness of a psycho-education intervention programme in improving the coping strategies of Jordanian breast cancer patients.
A double-blinded randomised control trial involving 200 participants between the ages of 20 to 65 years old breast cancer patients was performed. Apart from those who refused participation, patients with chronic diseases and extreme baseline depression scores were also excluded. Lusutrombopag The control group received standard care twice a week from the social welfare services team facilitator compared to the intervention group that received additional psycho-education intervention programme (PEIP). The coping strategies were measured using the Brief-COPE inventory consisting of 28 items. It was administered on the second and 12th week of trial. The primary end point was compared between pre- and post-intervention. The effect of the intervention between groups, time, and covariates was measured using the generalised linear mixed model (GLMM) analysis.
The mean (SD) of adaptive coping score among the intervention group increased from 5.
