ABSTRACT
DNA double-stranded break (DSB) is one of the most catastrophic damages of genotoxic insult. Inappropriate repair of DNA DSBs results in the loss of genetic information, mutation, and the generation of harmful genomic rearrangements, which predisposes an organism to immunodeficiency, neurological damage, and cancer. The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family. Recent discoveries have shown that human p53 gene encodes at least 12 isoforms. Different p53 members and isoforms play various roles in orchestrating DNA damage response to maintain genomic integrity. This review briefly explores the functions of p53 and its isoforms in DNA DSB repair.
ABSTRACT
Objective@#To investigate the effects of long non-coding RNA RP1-90L14.1 on the proliferation, migration and invasion of prostate cancer LNCaP cells and the expressions of GRIN2A and BACE2.@*METHODS@#Using RT-PCR, we detected the expression of RP1-90L14.1 in LNCaP and LNCaP-AI cells, transiently transfected the RP1-90L14.1 overexpression plasmid (the RP1-90L14.1 group) and vector plasmid (the LNCaP-NC group) into the LNCaP cells, and cultured the two groups of cells with ordinary medium and phenol red-free activated carbon adsorption medium (PRF-ACA). Then we examined the proliferation, migration and invasiveness of the cells by CCK-8 and Transwell, and determined the mRNA and protein expressions of GRIN2A and BACE2 by RT-PCR and Western blot.@*RESULTS@#The expression of RP1-90L14.1 was significantly higher in the LNCaP-AI than in the LNCaP cells (8.49 ± 0.43 vs 2.53 ± 0.95, P < 0.05), and so was that of LNCaP-RP1-90L14.1 in the RP1-90L14.1 than in the LNCaP-NC group after transfection (0.71 ± 0.22 vs 0.02 ± 0.01, P < 0.05). The optical densities (OD) of the cells were 51.95% and 50.69% higher in the RP1-90L14.1 than in the LNCaP-NC group after 72 hours of culture with ordinary medium and phenol red-free ACA (1.22 ± 0.08 vs 0.08 ± 0.05, P < 0.05; 0.79 ± 0.02 vs 0.53 ± 0.05, P < 0.05), and 51.72% and 60.23% higher in the former than in the latter after 96 hours (1.72 ± 0.07 vs 1.13 ± 0.05, P < 0.05; 1.18 ± 0.05 vs 0.73 ± 0.08, P < 0.05). The numbers of the migrating cells cultured with common medium and PRF-ACA were markedly higher in the RP1-90L14.1 than in the LNCaP-NC group after transfection (682.0 ± 42.7 vs 422.0 ± 37.1, P < 0.05; 419.0 ± 42.9 vs 251.0 ± 25.9, P < 0.05), and so were those of the invading cells (507.0 ± 22.2 vs 274.0 ± 19.6, P < 0.05; 352.0 ± 14.1 vs 216.0 ± 14.3, P < 0.05). Statistically significant differences were observed between the RP1-90L14.1 and LNCaP-NC groups in the mRNA and protein expressions of GRIN2A (5.13 ± 0.89 vs 2.09 ± 0.54, P < 0.05; 5.88 ± 0.29 vs 2.03 ± 0.22, P < 0.05) and BACE2 (5.82 ± 0.50 vs 2.53 ± 0.30, P < 0.05; 4.89 ± 0.19 vs 3.37 ± 0.13, P < 0.05).@*CONCLUSIONS@# lncRNA RP1-90L14.1 may play important roles in the proliferation, migration and invasiveness of prostate cancer cells. RP1-90L14.1 can promote the expressions of GRIN2A and BACE2 and may have an endogenous competitive relation with GRIN2A and BACE2.
ABSTRACT
DNA double-stranded break (DSB) is one of the most catastrophic damages of genotoxic insult. Inappropriate repair of DNA DSBs results in the loss of genetic information, mutation, and the generation of harmful genomic rearrangements, which predisposes an organism to immunodeficiency, neurological damage, and cancer. The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family. Recent discoveries have shown that human p53 gene encodes at least 12 isoforms. Different p53 members and isoforms play various roles in orchestrating DNA damage response to maintain genomic integrity. This review briefly explores the functions of p53 and its isoforms in DNA DSB repair.
Subject(s)
Animals , Humans , Mice , DNA Breaks, Double-Stranded , DNA Repair , Protein Isoforms , Physiology , Tumor Protein p73 , Physiology , Tumor Suppressor Protein p53 , Genetics , PhysiologyABSTRACT
In the human genome, there is a group of RNAs, called long non-coding RNA (lncRNA) with do not have the function of encoding proteins and whose transcript length is greater than 200 nucleotides. The disorders of lncRNAs are often involved in the occurrence and progression of malignant tumors. A large number of studies have indicated the aberrant expression of lncRNAs in prostate cancer (PCa) can regulate gene expressions at epigenetic, transcriptional and post-transcriptional levels and cause changes in the biological behaviors of PCa cells. Some lncRNAs have been shown to be closely related to the castration resistance of PCa. In recent years, a variety of lncRNAs have been detected in the PCa tissue, prostatic fluid, serum, and urine, and somehow influenced radiotherapy and chemotherapy of tumors. The expressions of some lncRNAs are also associated with disease prognosis. Thus, lncRNAs are expected to become new diagnostic markers and a therapeutic target for PCa. This review focuses on the roles and action modes and mechanisms of some lncRNAs as well as their potential value of clinical application in the diagnosis, treatment and prognosis of PCa.
ABSTRACT
<p><b>OBJECTIVE</b>Erectile dysfunction-no sexual life (ED-NS) is defined as the inability to have enough penile erection hardness and duration so as to have enough confidence in attempting sexual intercourse for more than six months. This study was to investigate the effect of daily low-dose tadalafil on ED-NS.</p><p><b>METHODS</b>We treated 35 ED-NS patients aged 17-35 (25.9 +/- 3.9) years with oral tadalafil at 5 mg qd for 3 months and followed them up for another 3 months after drug withdrawal. We obtained the scores of the patients on Self-estimation Index of Erectile Function-No Sexual Life (SIEF-NS) and compared them before and after medication and at 3 months after drug withdrawal.</p><p><b>RESULTS</b>The patients' SIEF-NS scores were 43.2 +/- 7.1 after medication and 42.1 +/- 7.4 at 3 months after drug withdrawal, both significantly higher than 21.2 +/- 5.9 before treatment (P < 0.05), though there was no significant difference between the former two scores (P > 0.05).</p><p><b>CONCLUSION</b>Daily medication of low-dose tadalafil can significantly improve the erectile function of the patients with ED-NS.</p>