LINC-PINT suppresses tumour cell proliferation, migration and invasion through targeting miR-374a-5p in ovarian cancer.

LncRNA LINC-PINT acts as an important regulator in the development of many cancers. The current study aimed to explore the role of LINC-PINT in the progression of ovarian cancer (OC). LINC-PINT expression level in different FIGO stages of OC and its adjacent tissues, normal HOSE and OC cell lines (A2780, SKOV3, OVCAR3 and HO-8910) was determined by qRT-PCR. Survival analysis on LINC-PINT and OC patients was conducted by Kaplan-Meier. CCK-8, flow cytometry, wound-healing, Transwell assays and western blot were performed to detect the effects of LINC-PINT on proliferation, apoptosis, migration, invasion and EMT process in OC cells. Target gene of LINC-PINT was predicted by Starbase and verified by dual-luciferase reporter assay. The expression of miR-374a-5p in normal and OC tissues, LINC-PINT- or siLINC-PINT-modified OC cells was determined. Moreover, rescue assay was carried out to confirm whether LINC-PINT contributes to the development of OC cells through targeting miR-374a-5p. Low expression of LINC-PINT was observed in OC tissues and cells, noticeably, LINC-PINT expression was even lower in OC tissues with higher FIGO stage. Increased LINC-PINT expression significantly inhibited cell proliferation, promoted apoptosis and suppressed migration, invasion and EMT process, while silencing of LINC-PINT caused the opposite results. Moreover, LINC-PINT sponged miR-374a-5p and overexpressed miR-374a-5p attenuated the effect of up-regulated LINC-PINT on cell viability, migration, invasion and apoptosis. LINC-PINT acts as a tumour suppressor, as it could inhibit cell proliferation, migration, invasion and EMT process, and promote cell apoptosis through down-regulating miR-374a-5p. SIGNIFICANCE OF THE STUDY: Ovarian cancer (OC), which is a frequently diagnosed tumour in female reproductive organs, has a high incidence rate behind cervical cancer and endometrial cancer. LncRNA LINC-PINT acts as an important regulator in the development of many cancers. The current study aimed to explore the role of LINC-PINT in the progression of ovarian cancer (OC) and found that LINC-PINT inhibited cell proliferation, migration invasion and EMT process of OC cell via regulating miR-374a-5p; it might be a potential target for OC treatment.

The Role of Tumor Oxygenation Tested by Magnetic Resonance Imaging (MRI) in Prostate Cancer Grading.

BACKGROUND Prostate cancer is a common malignant tumor in males. Prostate cancer grading is an important basis for evaluation of invasion. The purpose of this article was to use dynamic enhanced scan magnetic resonance imaging (MRI) to quantitatively investigate the relationship between tumor oxygenation value and prostate cancer pathological Gleason score. MATERIAL AND METHODS A total of 312 prostate cancer patients diagnosed by needle biopsy who received MRI dynamic enhanced scan were enrolled in this study. Multiparameter oxygen concentration image based on MRI was applied to test pO2 in tumors. Multiple spin resonance image relaxation time edit sequence and weak field diffusion model were used to estimate oxygen saturation level and pO2. hematoxylin and eosin staining and Gleason score were used to determine biological behavior and prognosis. RESULTS According to the Gleason score system, there were 28 cases with a score of 10, 112 cases with a score of 9, 56 cases with a score of 8, and 116 cases with a score lower than 7. The enrolled patients were divided into groups: 116 cases into the middle-to-well differentiation group (Gleason score ≤7) and 196 cases into the poorly differentiation group (Gleason score at 8 to 10). Prostate cancer tumor oxygenation value was positively correlated with Gleason score (r=0.349, P<0.05) or PSA (r=0.432, P<0.05). Tumor oxygenation value in Gleason ≤7 group was obviously different from that in the group with Gleason score between 9 and 10 (P<0.05). CONCLUSIONS Tumor oxygenation value in prostate cancer was positively correlated with Gleason score. Tumor oxygenation value might be useful in clinics to evaluate prostate cancer grading and prognosis.

Hepatitis B virus pre-existing drug resistant mutation is related to the genotype and disease progression.

INTRODUCTION: Previous studies have indicated that the drug-resistant mutations of hepatitis B virus (HBV) are a major obstacle to antiviral therapy. However, it is still unclear whether there are pre-existent resistance mutations in patients with HBV infection and the relationship between drug-resistant mutation, genotypes, and progression of hepatitis B disease. METHODOLOGY: A total of 357 treatment-naïve patients with HBV infection were involved in this retrospective study. The drug-resistant mutations of HBV reverse transcriptase domain were screened by direct gene sequencing. RESULTS: Lamivudine (LAM) resistance was detected in 8 patients (3.7%) with chronic hepatitis B (CHB), 13 (11.7%) patients with liver cirrhosis (LC), and 6 (21.4%) patients with hepatocellular carcinoma (HCC). Adefovir(ADV)-resistant mutations were detected in 10 (4.6%) patients with CHB, 15 (13.5%) patients with  LC and 4 (14.5%) patients with HCC. Both LAM and ADV resistant mutations were detected in 2 patients (0.9%) with CHB, 1 patient (0.9%) with LC and 1 patient (3.6%) with HCC. Significant differences (p <0.01) were observed in the drug-resistance rates among patients with CHB, LC and HCC. Meanwhile, all the drug-resistant mutations were found in patients with HBV genotype C. CONCLUSIONS: This study demonstrated higher risk of pre-existing drug-resistant mutations in patients with HBV genotype C comparing to patients with HBV genotype B. Likewise, increasing prevalence of pre-existing drug-resistant mutations was shown, alongside with the progression of the disease.

[Dynamic variations of hepatitis B virus polymerase gene in lamivudine-treated hepatitis B patients].

OBJECTIVE: To study variation features of the hepatitis B virus polymerase gene in chronic hepatitis B patients before and after lamivudine treatment. METHODS: From the serum samples of five CHB patients both before and after 12 months' lamivudine treatment, HBV polymerase gene was amplified and positive DNA fragments were cloned into JM105. Twenty positive clones of every sample were checked with mismatched polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and YMDD variants were sequenced. RESULTS: Among five patients after 12 months lamivudine treatment, M552I mutations in two patients with HBV DNA rebounding and D553G mutation in one non-responder were detected except in two patients with negative HBV DNA. CONCLUSIONS: D553G mutation is probably one of the reasons which caused non-responsiveness to the lamivudine treatment. The mutations of YMDD motif that occurred after lamivudine treatment are caused by the induction of the drug.