Search

The article presents the discussion on tongue squamous cell carcinoma being a common type of cancer of the oral cavity. Topics include lncRNAs in cancer initiation and progression, dysregulation serving as a promising indicators of tumor characteristic; and considering the vital role of HPV infection contributed to the initiation and progression of TSCC.

Background: Myeloid ecotropic viral integration site 1 (MEIS1) protein plays a synergistic causative role in acute myeloid leukemia (AML). However, MEIS1 has also shown to be a potential tumor suppressor in some other cancers, such as non-small-cell lung cancer (NSCLC) and prostate cancer. Although multiple roles of MEIS1 in cancer development and progression have been identified, there is an urgent demand to discover more functions of this molecule for further therapeutic design.Methods: MEIS1 was overexpressed via adenovirus vector in clear cell renal cell carcinoma (ccRCC) cells. Western blot and real-time qPCR (quantitative Polymerase Chain Reaction) was performed to examine the protein and mRNA levels of MEIS1. Cell proliferation, survival, in vitro migration and invasion were tested by MTT, colony formation, soft-agar, transwell (in vitro invasion/migration) assays, and tumor in vivo growthwas measured on nude mice model. In addition, flow-cytometry analysis was used to detect cell cycle arrest or non-apoptotic cell death of ccRCC cells induced by MEIS1.Results: MEIS1 exhibits a decreased expression in ccRCC cell lines than that in non-tumor cell lines. MEIS1 overexpression inhibits ccRCC cells proliferation and induces G1/S arrest concomitant with marked reduction of G1/S transition regulators, Cyclin D1 and Cyclin A. Moreover, MEIS1-1 overexpression also induces non-apoptotic cell death of ccRCC cells via decreasing the levels of pro-survival regulators Survivin and BCL-2. Transwell migration assay (TMA) shows that MEIS1 attenuates in vitro invasion and migration of ccRCC cells with down-regulated epithelial-mesenchymal transition (EMT) process. Further, in nude mice model, MEIS1 inhibits the in vivo growth of Caki-1 cells.Conclusions: By investigating the role of MEIS1 in ccRCC cells' survival, proliferation, anchorage-independent growth, cell cycle progress, apoptosis and metastasis, in the present work, we propose that MEIS1 may play an important role in clear cell renal cell carcinoma (ccRCC) development. [ABSTRACT FROM AUTHOR]

Resonance Raman spectra (RRs) and quantum chemical calculations were used to investigate the photodissociation dynamics of diuron in S2 state. The RRs indicate that the photorelaxation dynamics for the S0 → S2 excited state is predominantly along nine motions: the ring C = C stretch vibration ν12 (1593 cm−1), Ph-N-H wag ν14 (1517 cm−1), CO-N(CH3)2 stretch ν23 (1365 cm−1), CCH wag in plane/ring C = C stretch ν24 (1297 cm−1), ring CH rock in plane/ring deformation ν27 (1233 cm−1), CCH wag in plane ν29 (1151 cm−1), Ph-Cl (para) stretch ν35 (1028 cm−1), Ph-N-H wag ν37 (913 cm−1) and ring breath ν44 (685 cm−1). Dissociation by Ph-Cl (para) cleavage at S2 state directly or relaxation to T2 state by internal conversion (S2 → S1) and intersystem crossing (S1/T2) is expected by ~250 nm irradiation based on the RRS, complete active space self-consistent field, configuration interaction singles and time-dependent density functional theory calculations. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Objective To establish a human bladder cancer cell line stably co-expressing human sprouty2 (hSPRY2) and luciferase (Luc) genes simultaneously, and develop its subcutaneous tumor xenograft model in nude mice. Methods The hSPRY2 and Luc gene segments were amplified by PCR, and were cloned into lentiviral vector pCDH and pLVX respectively to produce corresponding lentivirus particles. The J82 human bladder cancer cells were infected with these two kinds of lentivirus particles, and then further screened by puromycin and G418. The expressions of hSPRY2 and Luc genes were detected by bioluminescence, immunofluorescence and Western blot analysis. The screened J82-hSPRY2/Luc cells were injected subcutaneously into BALB/c nude mice, and the growth of tumor was monitored dynamically using in vivo fluorescence imaging system. Results J82-hSPRY2/Luc cell line stably expressing hSPRY2 and Luc genes was established successfully. Bioluminescence, immunofluorescence and Western blot analysis validated the expressions of hSPRY2 and Luc genes. The in vivo fluorescence imaging system showed obvious fluorescence in subcutaneous tumor xenograft in nude mice. Conclusion The J82-hSPRY2/Luc bladder cancer cell line and its subcutaneous tumor xenograft model in nude mice have been established successfully.

Objective: To determine the effect of obesity on prostate specific antigen (PSA) in men with benign prostatic hyperplasia (BPH) and develop a PSA-related parameter that can eliminate the effect of obesity., Methods: We reviewed the clinical data of 706 patients with BPH. Two PSA-related parameters, namely PSA mass (total circulating PSA protein) and PSA mass ratio (total circulation PSA protein per prostate volume), were calculated for all the patients and the association of BMI with PSA, PSA mass, and PSA mass ratio was assessed., Results: A higher BMI was significantly associated with a greater plasma volume and prostate volume (P<0.05). Linear regression analysis revealed a greater adjusted R2 of BMI versus plasma volume than of BMI PSA (0.569 vs 0.027). PSA was positively associated with the prostate volume and negatively with BMI and plasma volume (P<0.05). PSA mass was positively associated with prostate volume (P<0.05) but was not associated with BMI or plasma volume (P>0.05). PSA mass ratio was not associated with prostate volume (P>0.05) but negatively associated with BMI and plasma volume. Plasma volume and prostate volume, PSA, and PSA mass ratio (P<0.05), but not PSA mass (P>0.05), differed significantly among normal-weight, overweight, and obese patients., Conclusion: A higher BMI is associated with a greater plasma volume in BPH patients. In obese patients with BPH, a lower PSA concentration may result from hemodilution caused by a greater plasma volume, and PSA mass can eliminate the effect of obesity on PSA.

Objective: To investigate the effect of p53-regulated apoptosis-inducing protein 1 (p53AIP1) gene on the proliferation, cell cycle, apoptosis, invasion and migration of PC-3M human prostate cancer cells in vitro., Methods: The eukaryotic expression vector pDC316-p53AIP1 was constructed and confirmed by double enzyme digestion and PCR analysis. Then it was transfected into PC-3M human prostate cancer cells by Lipofectamine (TM) 2000. The expression of p53AIP1 protein was detected by Western blotting. The proliferation of PC-3M cells was tested by CCK-8 assay; the cell cycle and apoptosis rate were analyzed by flow cytometry combined with annexin V-FITC/PI staining; the effect of p53AIP1 on the cell invasion and migration was detected by Transwell(TM) assay. RESULTS The eukaryotic expression vector pDC316-p53AIP1 was constructed successfully. After transfected into PC-3M cells, Western blotting demonstrated that the protein p53AIP1 was effectively expressed. CCK-8 assay revealed that the proliferation of PC-3M cells was significantly inhibited by p53AIP1 (P<0.05). Flow cytometry indicated that the cells were arrested at S/G2-M phase (P<0.05) and cell apoptosis was evidently promoted (P<0.05). Transwell(TM) chamber experiments showed that p53AIP1 decreased the abilities of both invasion and migration of the cells (P<0.05)., Conclusion: The p53AIP1 inhibits the proliferation of PC-3M cells, arrests cell cycle at S/G2-M phase, decreases the abilities of invasion and migration and promotes cell apoptosis.