Transrectal versus transperineal prostate biopsy for cancer detection in patients with gray-zone prostate-specific antigen: a multicenter, real-world study.

Knowledge about the effect of different prostate biopsy approaches on the prostate cancer detection rate (CDR) in patients with gray-zone prostate-specific antigen (PSA) is limited. We performed this study to compare the CDR among patients who underwent different biopsy approaches and had rising PSA levels in the gray zone. Two hundred and twenty-two patients who underwent transrectal prostate biopsy (TRB) and 216 patients who underwent transperineal prostate biopsy (TPB) between June 2016 and September 2022 were reviewed in this study. In addition, 110 patients who received additional targeted biopsies following the systematic TPB were identified. Clinical parameters, including age, PSA derivative, prostate volume (PV), and needle core count, were recorded. The data were fitted via propensity score matching (PSM), adjusting for potential confounders. TPB outperformed TRB in terms of the CDR (49.6% vs 28.3%, P = 0.001). The clinically significant prostate cancer (csPCa) detection rate was not significantly different between TPB and TRB (78.6% vs 68.8%, P = 0.306). In stratified analysis, TPB outperformed TRB in CDR when the age of patients was 65-75 years (59.0% vs 22.0%, P < 0.001), when PV was 25.00-50.00 ml (63.2% vs 28.3%, P < 0.001), and when needle core count was no more than 12 (58.5% vs 31.5%, P = 0.005). The CDR ( P = 0.712) and detection rate of csPCa ( P = 0.993) did not significantly differ among the systematic, targeted, and combined biopsies. TPB outperformed TRB in CDR for patients with gray-zone PSA. Moreover, performing target biopsy after systematic TPB provided no additional benefits in CDR.

LncRNA B4GALT1-AS1 promotes non-small cell lung cancer cell growth via increasing ZEB1 level by sponging miR-144-3p.

Background: Long noncoding RNAs (lncRNAs) are emerging as key players in the development and progression of cancer. Several malignancies involve dysregulated long noncoding ribonucleic acids (lncRNAs) in non-small cell lung cancer cell growth and their aggressive phenotypes. LncRNA B4GALT1-AS1 is important in the advancement of various malignancies, although its contribution to non-small cell lung cancer (NSCLC) remains unexplored. Methods: LncRNA B4GALT1-AS1 in NSCLC tissues was detected and further validated in a cohort of non-small cell lung cancer tissues. The effects of lncRNA B4GALT1-AS1 on proliferation were determined by in vitro experiments. The B4GALT1-AS1-miR-144-3p-ZEB1 axis was assessed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Furthermore, the mechanism of B4GALT1-AS1 was investigated using loss-of-function assays in vitro. Results: We showed significant upregulation of B4GALT1-AS1 in cell lines and tissues of NSCLC. B4GALT1-AS1 knockdown impeded the in vitro proliferation-related characteristics of the NSCLC cells. The demonstration of the binding capacity of B4GALT1-AS1 and miR-144-3p was predicted by bioinformatics and luciferase reporter activity assay. The B4GALT1-AS1 and miR-144-3p interaction was shown by using rescue experiments. NSCLC has a positive association with its target, zinc finger e-box binding homeobox 1 (ZEB1). Conclusions: In summary, the progression of NSCLC was facilitated by lncRNA B4GALT1-AS1 via interaction with miR-144-3p and positive regulation of ZEB1 expression.

MALAT1 rs619586 polymorphism functions as a prognostic biomarker in the management of differentiated thyroid carcinoma.

This study aimed to explore the roles of miR-214 and MALAT1 rs619586 polymorphism in the control and survival of differentiated thyroid carcinoma (DTC) via Cox regression analyses. The levels of MALAT1, miR-214, and CTNNB1 in different experimental groups were compared to study the interaction among MALAT1, miR-214, and CTNNB1. MTT and colony assays were used to investigate the role of rs619586 polymorphism in cell growth. The G allele of rs619586 polymorphism obviously decreased the 5-year survival of patients with DTC. Additionally, compared with AA-genotyped patients, patients carrying the AG/GG genotypes of MALAT1 rs619586 polymorphism showed much higher levels of DTC grade and CTNNB1 expression, along with lower levels of MALAT1 and miR-214 expression. Furthermore, the transcription activity of MALAT1 was significantly lowered by the rs619586G allele or miR-214 mimic, while the miR-214 inhibitor upregulated the luciferase activity of MALAT1. Additionally, miR-214 inhibited CTNNB1 expression by targeting CTNNB1 3'-untranslated region. Finally, the G allele of MALAT1 rs619586 polymorphism apparently promoted cell proliferation. Our study indicated that miR-214 inhibited MALAT1 expression by directly binding to the G allele of MALAT1 rs619586 polymorphism, thus inhibiting CTNNB1 expression and promoting cell proliferation in the pathogenesis of DTC. Therefore, MALAT1 rs619586 polymorphism could be used to predict the prognosis of DTC.