DNA polymerase beta (pol beta) provides most of the gap-filling synthesis at apurinic/apyrimidine sites of damaged DNA in the base excision repair pathway. A truncated form of the pol beta protein is expressed in colon and breast cancers. However, the role of the pol beta gene in lung cancer is not known. Thus, we investigated a possible occurrence of pol beta variants in primary lung tumors. The entire cDNA of pol beta obtained by RT-PCR amplification was analyzed for nucleotide sequencing in lung tumor and matched normal lung tissue of the same patient. Three types of variants were detected in squamous, non-small, or large cell carcinomas. The most common variant was a deletion of 87 bp from pol beta cDNA at a site corresponding to exon 11. In addition, a variant exhibiting deletions of 87 and 140 bp together with an insertion of 105 bp was identified in three lung tumors. This is the first report of the occurrence of pol beta variants, possibly splicing variants, in lung cancer. A truncated pol beta protein resulting from variant forms of the gene may impact the function of the enzyme and increase susceptibility to carcinogenesis.
In eukaryotic cells, DNA polymerase  (pol) carries out base-excision repair (BER) required for DNA maintenance, replication, recombination, and drug resistance. A specific deletion in one allele in the coding sequence of the pol gene occurs in colorectal and breast carcinomas.
Green synthesis of silver nanoparticles (AgNPs) is gaining momentum in the field of nano-research. Scoparia dulcis leaves were used as a reducing agent for the synthesis of silver nanoparticles from an aqueous solution of silver nitrate (AgNO 3 ). Synthesized AgNPs were characterized by UV-Vis spectroscopy, XRD, SEM with EDAX and TEM. UV-VIS surface plasmon resonance spectroscopy was observed at 430 nm. XRD data depicts that the NPs are crystalline in nature. The EDAX data indicate that 63.76% presence of Ag metal. The TEM & SEM results indicate that size of the AgNPs ranges from 15-25 nm. The results also support that spherical shape of the nanoparticles. In addition, the NPs are in polydispersed condition. The antimicrobial activities indicate significant inhibition of the growth of three pathogenic bacteria such as Pseudomonas ariginosa, Bacillua subtillis and Staphylococcus aureous. Cytotoxicity of this nanoparticle showed that this Ag-NP also has more cytotoxic effect on a lung cancer cell line, A549 cells compared to ovarian cancer cell line, PA1 indicating a possible therapeutic use of this AgNP.
In the base excision repair pathway, wild-type DNA polymerase beta (WT polbeta) provides most of the gap filling synthesis. A truncated polbeta protein (polbetaDelta), expressed in primary colorectal and breast tumors and in a primary culture of renal cell carcinoma, inhibits the gap filling synthesis and DNA binding activities of WT polbeta. However, a purified recombinant polbetaDelta does not inhibit a purified WT polbeta. To determine the dominant inhibitory activity of polbetaDelta, we examined interactions of purified polbetaDelta with X-ray cross complementing group 1 (XRCC1), poly(ADP-ribose) polymerase (PARP), and apurinic endonuclease (Ape) proteins. All of these proteins interact with polbetaDelta in vitro and in vivo. The polbetaDelta protein can fill one nucleotide gap by inserting a base at the AP site, whereas a presumed binary complex of polbetaDelta and XRCC1 cannot. However, this binary complex not only suppresses gap filling synthesis activity of WT polbeta but also binds more strongly to gapped DNA than WT polbeta bound to XRCC1. These results are the first to suggest that XRCC1 is directly involved in the dominant negative activity of truncated polbeta, possibly leading to the genomic instability characteristic of tumor cells.
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