ABSTRACT
Objective To detect the changes of mRNA isoforms in multiple cancer cell lines with dose of cisplatin. Methods Total RNA of the cells treated by cisplatin were abstracted 24 h after the treatment. mRNA isoforms of SRSF12 gene were detected by semiquantitative RT-PCR. The ratios of mRNA isoforms were analyzed by gel image software and statistical analysis. Results Under the cisplatin treatment, 2 mRNA isoforms of SRSF12 were detected in five cells except Caski cells,their ratios and relative mRNA levels were changed. With the increase of dose of cisplatin, the ratio of isoform-a was slightly increased; but the ratio of isoform-b was different, the changes were not obvious in the A549 and 293FT cells, the weaker expression was expressed in the H1299 and C33A cells, and the two isoforms were gradually weakening in the Siha cells. Conclution Under the cisplatin treatment in multiple cancer cells, the expression of SRSF12 shows tissue-specific and cell type-specific patterns .
ABSTRACT
Behavioral and molecular characterization of cell- type specific populations governing fear learning and behavior is a promising avenue for the rational identification of potential therapeutics for fear-related disorders. Identification of cell-type specific changes in neuronal translation following fear learning allows for targeted pharmacological intervention during fear extinction learning, mirroring possible treatment strategies in humans. Here we identify the central amygdala (CeA) Drd2-expressing population as a fear-supporting population that is molecularly distinct from other, previously identified fear-supporting CeA populations. Sequencing of actively translating transcripts of Drd2 neurons identifies mRNAs that are differentially regulated following fear learning including Npy5r, Rxrg, Sst5r, Fgf3, ErbB4, Fkbp14, Dlk1,Ssh3 and Adora2a. Direct pharmacological manipulation of NPY5R, RXR, and ADORA2A confirms their importance in fear behavior and validates the present approach of identifying pharmacological targets for the modulation of emotional learning.
ABSTRACT
Objective To investigate the cell-type-specific enhancer (CTSE) in HPV16 and its variation in cervical carcinoma. Methods CTSEs were detected by polymerase chain reaction (PCR) in 58 cervical carcinoma from Shaanxi province; in addition variation of CTSEs was analyzed through single-strand conformation polymorphisms (SSCP). Results HPV16 CTSEs were detectable in 34 of 58 (57%) specimens and mutant rate was 41%(14/34) and the main mutations of chosen randomly variant CTSE (CTSEv) happened at YY1 binding sites in addition to glucocoticoid response elements (GRE). Conclusion CTSE in some specimens of Shaanxi province was obviously different from that in HPV16 wild type and variant CTSE might affect the transcriptional regulation of LCR on viral P97, which regulates over-expression of viral oncogenes in cervical carcinoma.