BACKGROUND Increasing evidence reveals that aberrant microRNAs (miRNAs) expression play a crucial role in the tumorigenesis of cancers, including hepatocellular carcinoma (HCC), whereas the role of miR-654-3p in HCC remains unclear. This study aimed to investigate the role of miR-654-3p in HCC. Pargyline METHODS Real-time quantitative PCR was performed to detect miR-654-3p expression in HCC tissues and cell lines. The association of miR-654-3p expression with clinical characteristics of HCC patients were analyzed. And the prognostic value of miR-654-3p was examined using Kaplan-Meier curve and Cox regression analysis. CCK-8 and Transwell assays were used to observe the effects of miR-654-3p on proliferation, migration, and invasion of HCC cells. RESULTS The miR-654-3p expression was downregulated in both HCC tissues and cell lines, which was significantly associated with lymph node metastasis and TNM stage. Downregulation of miR-654-3p predicted poor prognosis of HCC patients. Overexpression of miR-654-3p inhibited HCC cell proliferation, migration, and invasion, while knockdown of miR-654-3p promoted these cellular behaviors in vitro. CONCLUSION Our study suggested that miR-654-3p expression was downregulated in HCC and might serve as a potential prognostic marker and therapeutic target for the survival of HCC patients. miR-654-3p might exert a suppressor role in HCC through inhibiting tumor cell proliferation, migration, and invasion.BACKGROUND LncRNA MEG3 rs7158663 has been shown to confer cancer susceptibility, maybe through altering its gene expression level. OBJECTIVE We aimed to weigh the effect of rs7158663 on MEG3 serum level and breast cancer susceptibility. METHODS We genotyped rs7158663 G > A and measured serum MEG3 in 150 breast cancer, 95 FA, and 154 controls by the TaqMan method. RESULTS The presence of rs7158663 G > A is a risk factor for breast cancer among fibroadenoma patients and controls, AA vs. GG genotypes (OR = 6.320, 95% CI = 2.587-15.439, P 5 cm. CONCLUSION The presence of both rs7158663 and low MEG3 are diagnostic and unfavorable prognostic factors for BC patients.BACKGROUND Minimal invasive blood-based molecular markers are evaluated as promising biomarkers in malignant diseases these days. OBJECTIVE In this pilot study, we investigated the potential of cell-free DNA (cfDNA) concentration and cell-free DNA Integrity (cfDI) as blood-based diagnostic markers for ovarian cancer patients in a retrospective study cohort. METHODS cfDNA concentration and cfDI were determined in the plasma of 37 ovarian cancer patients and 28 healthy controls, by measuring ALU and LINE1 repetitive DNA elements using quantitative real-time PCR. RESULTS A high correlation was observed between the results of ALU and LINE1. The correlated co-efficiency between the values of cfDNA concentration and cfDI was 0.86 and 0.71. As for the results between cases and controls, no or just borderline significant difference was observed in cfDI after age adjustment (P= 0.40 for ALU and P= 0.05 for LINE1) while cfDNA concentration showed a significant difference between ovarian cancer patients and healthy controls groups (P= 0.03 for ALU and P= 3.00 E-03 for LINE1). cfDNA concentration of ALU and LINE1 had an AUC of 0.81 (0.70-0.91). ALU and LINE1 cfDI reached an AUC of 0.60 (95% CI 0.46-0.73). The combination of these markers reached the best diagnostic power with an AUC of 0.84. CONCLUSIONS cfDNA variables might be potentially diagnostic biomarkers in ovarian cancer, in combination with additional molecular markers. However, further studies are needed to confirm the diagnostic ability of cfDNA variables (cfDNA concentration and cfDI).BACKGROUND Elevated Anoctamin 7 (ANO7) expression is associated with poor survival in prostate cancer patients. OBJECTIVE The aim was to discover proteins that interact with ANO7 to understand its functions and regulatory mechanisms. METHODS The proximity-dependent biotin identification (BioID) method was utilized. ANO7 fused to biotin ligase was transiently transfected into LNCaP cells, and the biotinylated proteins were collected and analysed by mass spectrometry. Four identified proteins were stained with dual fluorescent immunostaining and visualized using Stimulated emission depletion microscopy (STED). RESULTS After bioinformatic filtering steps, 64 potentially ANO7-interacting proteins were identified and analysed with the GO enrichment analysis tool. One of the most prominently enriched cellular components was cellular vesicle. Co-localization was showed for staphylococcal nuclease and tudor domain containing 1 (SND1), heat shock protein family A (Hsp70) member 1A (HSPA1A), adaptor related protein complex 2 subunit beta 1 (AP2B1) and coatomer protein complex subunit gamma 2 (COPG2). CONCLUSIONS This is the first study in which ANO7 interacting proteins have been identified. Although further studies are needed, the findings reported here expand our understanding of the role and regulation of ANO7 in prostate cancer cells. Furthermore, these results are likely to introduce new targets for the novel cancer therapies.BACKGROUND Glioma is considered to be one of the most common and lethal malignant brain tumors, accounting for 40% to 50% of brain tumors. Long non-coding RNAs (lncRNAs) have been widely proved to play an irreplaceable role in the tumorigenesis and progression. Nevertheless, the role of LINC00467 in glioblastoma remained unclear. AIM The current study was aimed to explore the functional mechanism of LINC00467 in glioblastoma. METHODS The expression of LINC00467/miR-339-3p/IP6K2 glioblastoma tissues and cells was evaluated by RT-qPCR. The protein expression of genes (cleaved PARP, PARP, cleaved caspase 3, caspase 3, Bax, Bcl-2 and IP6K2) was measured by western blot assay. Then role of LINC00467 was demonstrated by EdU, colony formation, flow cytometry and TUNEL assays. The relationship between miR-339-3p and LINC00467/IP6K2 was validated by RNA pull down and luciferase reporter assays. RESULTS The expression of LINC00467 was upregulated in glioblastoma tissues and cells. LINC00467 knockdown suppressed cell proliferation but activated cell apoptosis.