To investigate the effect of silencing the high-mobility group box-1 protein (HMGB1) combined with docetaxel (DTX) on the proliferation and apoptosis of PCa cells and its possible action mechanism.

To investigate the molecular mechanism of hsa_circ_0005221 regulating the progression of PCa through the miR-339-5p/STAT5a pathway.

The biomarkers targeting colorectal cancer (CRC) prognosis are short of high accuracy and sensitivity in clinic. Through bioinformatics analysis, we aim to identify and confirm a series of key genes referred to the diagnosis and prognosis of CRC.

To explore the molecular mechanism for thyroid cancer metastasis via analyzing the role of microRNA (miR)-21-5p and its target gene recombinant sclerostin domain containing protein 1 (SOSTDC1) in thyroid cancer.

Objective To investigate the role and mechanism of fatty acid binding protein 5 (FABP5) in hypoxia induced angiogenesis in hepatocellular carcinoma. Methods Huh7 cells were cultured under normal and anaerobic conditions; FABP5 siRNA was transfected to knock down the expression of FABP5 in Huh7 cells; the expression of FABP5 mRNA was detected by reverse transcription PCR; the expressions of FABP5 and vascular endothelial growth factor A (VEGFA) were detected by Western blot; the concentration of VEGFA in the supernatant of Huh7 cells was detected by ELISA; and the angiogenesis of human umbilical vein endothelial cells (HUVECs) induced by the supernatant of Huh7 cells was detected by tube formation assay. Results After anaerobic culture, the expressions of FABP5 mRNA and FABP5 and VEGFA proteins were increased; after FABP5 siRNA transfection, the expression and secretion of VEGFA in anaerobic cultured Huh7 cells were decreased and the angiogenesis of HUVECs induced by supernatant of anaerobic cultured Huh7 cells were decreased. Conclusion Hypoxia induces an increase in the expression of FABP5 in Huh7 cells, and knocking down FABP5 inhibits the expression of VEGFA in Huh7 cells and the angiogenesis of HUVEC.

Objective: To investigate the relationship between tumor angiogenesis and renal cancer stem cells. Methods: The primary cell culture method was used to extract and isolate RCSCs, and then qRT-PCR and Western blot methods were used to detect the expression levels of the kidney cancer stem cell markers CD105 and Sox2 genes and proteins from different MVD kidney cancer tissues. Using TCGA database, analyze the correlation between tumor angiogenesis markers and tumor stem cell regulatory genes. Results: The stem cell markers CD105 and Sox2 genes in RCSCs derived from high MVD kidney cancer tissues were respectively increased by (2.34±1.77) times and (3.92±1.41) times (PCD105<0.01, PSox2<0.05)and protein levels were increased by (5.12±3.31) times and (4.90±3.30) times(PCD105<0.05, PSox2<0.01).Meanwhile,up to 30% of stem cell promoting stemness regulatory genes are positively correlated with angiogenesis genes CD31/PECAM1 and KDR, and 64 genes are also strongly positively correlated with CD31/PECAM1 and KDR genes. Conclusion: The high microvessel density of kidney cancer is strongly correlated with the existence of renal carcinoma stem cells.

T-cell prolymphocytic leukemia (T-PLL) is a rare but highly aggressive and malignant mature T-lymphoid tumor. The diagnosis of T-PLL mainly depend on genetic characteristics, clinical manifestations, cell morphology and immunophenotype. At present, clinical treatment is mainly aimed at improving the response rate and prolonging the remission period. With the development of new molecular biology technologies, researchers have gained a deeper understanding of the pathogenesis and related genetics of T-PLL, targeted drugs, including HDAC inhibitors, JAK/STAT inhibitors, AKT inhibitors and BCL-2 inhibitors, are also under evolution and providing the new opportunities to improve the efficacy of therapy. In this review, the advances in genetics and treatment of T-PLL were summarized briefly.

To investigate the effect of silencing DNA methyltransferase 1(DNMT1) to the methylation of the promoter of the tumor suppressor gene wnt-1 (WIF-1) in human chronic myeloid leukemia (CML) cells.

To explore the clinical and cytogenetic characteristics of acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) based on morphology define.

To investigate the clinical characteristics and prognosis of acute myeloid leukemia(AML) patients with ASXL1 mutation.

To analyze the clinicobiological heterogeneity of NPM1 mutated (NPM1mut) acute myeloid leukemia (AML) detected by next generation sequencing (NGS) and their coexistence and mutual exclusivity relationship in the AML subtype.

To investigate the difference expression of circular RNA (circRNA) in acute myeloid leukemia (AML) by using bioinformatics method.

To investigate the regulation of chronic myelogenous leukemia （CML） imatinib resistant genes, in order to improve the therapeutic effect of CML imatinib resistant patients.

To investigate the expression of microRNA-143 (miR-143) in patients with acute myeloid leukemia (AML), and the effect of miR-143 over-expression on the proliferation and apoptosis of AML cells. And to verify the targeting relationship between miR-143 and long non-coding RNA MALAT-1. So as to explore the possible regulatory mechanism of miR-143 in the pathogenesis of AML.

To investigate the effect of paired related homeobox1 (PRRX1) on autophagy of salivary adenoidcystic carcinoma (SACC) cells.

This study focused on the role and mechanism of IGF2BP1 in cell cisplatin resistance of oral squamous cell carcinoma.