association of hypoxiainducible factor α subunits with tsga10 transcripts in hela, mcf7 and mda-mb231- cell lines

Background: hypoxia is a common phenomenon in cancer cells. due angiogenesis and cell proliferation the hypoxia-inducible factor family (hifs) is the primary transcriptional factor to hypoxic stress. cancer-testis (ct) antigens are almost expressed in male germ cells, aberrantly expressed in some malignancies as well. the ct gene, tsga10, prevents the nuclear accumulation of hif-α and may be involved in organ-specific regulation of hypoxic gene expression during sperm maturation. tsga10 is supposed to regulate the hif expression in germ cells and cancer cells. the hif-α subunit has three isoforms, involved in oxygen transport, angiogenesis and tumor metastasis, detection of which is the subject of the current study. methods: three cell lines, mcf7, mda-mb-231 and hela were cultured, passaged and categorized into normal and synchronized groups. the cells were subjected to rna extraction and reverse-transcribed into cdnas. realtime rt-pcr was performed to amplify tsga10 and hif-α isoforms and hprt, as the normalizer gene, using appropriate primers. the rest and spss software were used for statistical analysis. results: the expression of the three isoforms of hif-α in hela cell line was higher than mcf7, and mcf7 was higher than mda-mb-231. moreover the expression relationship between hif-α isoforms and tsga10 was evaluated in each three cell lines. the results were significant in all cases with p =0.01. before and after synchronization in each three cell lines, the isoform expressions of hif-α and tasga10 were evaluated, and the results were revealed their dependent expression. the relationship between hif-α isoforms and tsga10 expression was compared with each other. the cell lines with less tsga10 expression had the higher expression of hif-α isoforms and vice versa, according to the extent of tsga10. conclusion: the significant relationship between expressions of tsga10 and hif-α isoforms is confirmed.